Clinical value of common laboratory indexes in evaluating infarct size of ischemic stroke / 中国医师杂志

Objective:To explore the level changes of common laboratory indexes in patients with ischemic stroke (IS) with different infarct sizes and their clinical application value.Methods:The baseline data of 237 patients hospitalized in Lanzhou University Second Hospital from June 2019 to December 2020 and their laboratory indicators within 24 hours of admission were collected. The patients were divided into lacunar group ( n=80) and infarct group ( n=157) according to the infarct area. The experimental indexes and clinical data of the two groups were compared. Binary logistic regression was used to screen the independent influencing factors of infarct size and establish a joint diagnostic model. The receiver operating characteristic (ROC) curve and model calibration chart were used to verify the clinical application value of each index. Results:The levels of cholesterol (CHO)/high density lipoprotein (HDL), low density lipoprotein (LDL)/HDL, neutrophil count, Cystatin C (Cys C), phosphorus (PHOS), indirect bilirubin (IBIL), LDL, apolipoprotein (ApoB), homocysteine (HCY), D-dimer, smoking, drinking, overweight and arterial stenosis in the infarct group were higher than those in the lacunar group (all P<0.05), and the levels of apolipoprotein A Ⅰ (ApoAⅠ)/ApoB, ApoAⅠ and carbon dioxide (CO 2) in the infarct group were lower than those in the lacunar group (all P<0.05). ApoA Ⅰ/ApoB and CO 2 were independent protective factors of infarct size (all P<0.05); Cys C, PHOS and IBIL were independent risk factors of infarct size (all P<0.05). The combined prediction model of CO 2, PHOS, IBIL, ApoA Ⅰ/ApoB and Cys C has good prediction efficiency for infarct area, and the area under the curve (AUC) of combined diagnosis was 0.739. Conclusions:Laboratory indicators are closely related to the infarct size of IS. The model developed in this study have good clinical value, which provides a new basis for IS evaluation and early warning.

Effects of pre-treatment with metoprolol and diltiazem on cerebral ischemia/reperfusion-induced injuries

Abstract Stroke is one of the most important health concerns worldwide. Calcium ions accumulation in the nerve cells and increase in the catecholamines level of the brain following cerebral ischemia/reperfusion (I/R) are accompanied by damaging effects. Therefore, the present study aimed to evaluate the effects of diltiazem, as a calcium channel blocker, and metoprolol, as a β-adrenoceptors antagonist, on I/R injury. In this study, 30 male Wistar rats were divided into control, I/R, metoprolol, diltiazem, and metoprolol plus diltiazem groups (n=6 in each). Metoprolol (1 mg/kg/day) and diltiazem (5 mg/kg/day) were injected intraperitoneally (i.p.) for 7 days before I/R induction. On day 8, the animals underwent ischemia by bilateral common carotid arteries occlusion for 20 min. Histopathological analysis showed a significant reduction in leukocyte infiltration in diltiazem, metoprolol, and diltiazem plus metoprolol treated rats compared with the I/R group (P<0.05, P<0.01, P<0.01, respectively). In addition, in all treated groups, myeloperoxidase activity and malondialdehyde levels in the brain tissue significantly declined compared with the I/R group (P<0.001). Furthermore, pre-treatment with diltiazem and metoprolol alone or in co-administration remarkably reduced infarct size following I/R (P<0.001). Overall, the results indicate the considerable neuroprotective effects of metoprolol and diltiazem in cerebral I/R.

The prognostic value of myocardial infarct size measured by cardiovascular magnetic resonance in patients with acute ST-segment elevation myocardial infarction / 中华内科杂志

Objective:To investigate the prognostic value of infarct size (IS) in patients with acute ST-segment elevation myocardial infarction (STEMI) underwent primary percutaneous coronary intervention (PCI).Methods:A total of 104 patients with acute STEMI who underwent primary PCI treatment in Shengjing Hospital of China Medical University from February 2017 to November 2018 were included in the present study. All patients underwent cardiovascular magnetic resonance (CMR) within one week after primary PCI treatment. The subjects were followed up for two years. Major adverse cardiac events (MACE) included new onset congestive heart failure and/or recurrent nonfatal myocardial infarction and/orcardiac death. The optimal IS cutoff value for MACE was determined by receiver operating character (ROC) curve. Based on the IS cutoff value, the patients were divided into the high IS group and the low IS group. Clinical characteristics between the two groups were compared. A cox regression model was used to analyze the prognostic value of IS in acute STEMI patients treated with primary PCI for the adverse events.Results:The IS cutoff value determined by ROC curve was 13.55%. 50 patients were in the high IS group (IS≥13.55%) and 54 patients were in the low IS group (IS<13.55%). More female patients [14 cases (28.0%) vs. 6 cases (11.1%)] were in the IS group, and a higher proportion of patients in the high IS group had anterior myocardial infarction [27 cases (54.0%) vs. 16 cases (29.6%)] or microvascular obstruction [32 cases (64.0%) vs. 16 cases (29.6%)]. White blood cell counts [11.25(8.90, 13.38) ×10 9/L vs. 9.25(7.58, 11.00) ×10 9/L], troponin I levels [50.63(16.56, 76.30)μg/L vs. 16.58(2.66, 38.42)μg/L] and brain natriuretic peptide levels [178.10(79.70, 281.95)μg/L vs. 79.60(42.83, 183.90)μg/L] in the high IS group were higher than those in the low IS group ( P<0.05), and left ventricular ejection fraction [(45.15±10.65)% vs. (51.95±12.91)%] in the high IS group was lower than that in the low IS group ( P<0.05). Multivariate Cox regression analyses showed that IS was independently associated with the risk of cardiac death in patients with acute STEMI two years after primary PCI( P=0.033, HR=1.075, 95% CI1.006-1.148). Every 1% increase in IS was associated with a 7.5% increase in cardiac death. Conclusions:Infarct size, measured by CMR within one week after primary PCI, is strongly associated with cardiac death in patients with acute STEMI two years after primary PCI. IS could be used as an index for the prognosis of patients with acute STEMI.

Correlation of serum calcium levels with infarct size and severity of stroke using NIHSS score in patients with acute ischemic stroke

Background: Normal cerebral membrane integration is important to maintain the cellular calcium homeostasis. Recent studies have suggested that elevated serum calcium levels at presentation correlates well with the infarct size and severity of stroke.Methods: A total of 73 patients with acute ischemic stroke satisfying inclusion and exclusion criteria were included in the study from November 1st 2017 to April 30th 2019 at a tertiary care centre in Kolar, Karnataka. Serum calcium (total, ionized and albumin corrected calcium) levels were measured at the time of presentation and compared with the infarct size and severity of stroke using NIHSS score (National Institute of Health Stroke Scale).Results: The levels of total calcium, albumin-corrected calcium, and ionized calcium were 9.13±0.89 mg/dL (range: 8.24-10.02), 9.56±0.82 mg/dL (range: 8.74-10.38), and 4.79±0.47 mg/dL (range: 4.3-5.2), respectively. Mean stroke size as measured on the CT scan was 47.38±17.7 cm (range: 21-88). Analysis revealed significant negative correlation between calcium levels (total, corrected, and ionized) and infarct size and severity of stroke.Conclusions: In this study, it was found that there was a statistically significant negative correlation between total, ionized and corrected calcium with the infarct size in patients with ischemic stroke and also the total calcium at presentation and severity of stroke calculated using NIHSS score.

Correlation of Serum Cholinesterase Level with the Severity and Prognosis of Acute Cerebral Infarction / 中国医科大学学报

Objective To investigate the relationship of serum cholinesterase(CHE) level with the severity and prognosis in patients with acute cerebral infarction. Methods A total of 325 patients with acute cerebral infarction were recruited as patients group,and another 101 healthy sub?jects were selected as control group. Velocity method was employed to detect the level of serum CHE. Patients with acute cerebral infarction were then divided into different groups according to the infarcts diameter and the modified Rankin scale(mRS)at 1 year post stroke. The collected data were analyzed statistically. Results The level of serum CHE in small and medium area infarction group was higher than control group(P<0.01);the level of serum CHE in large area infarction group was lower than control group(P<0.01);the level of serum CHE was negatively correlated with infarct size,NIHSS and the mRS score(r=-0.302,-0.232,-0.455,P<0.001). The level of CHE,age,NIHSS and infarcts diameter was identified as independent influence factors for prognosis of acute cerebral infarction. Conclusion Early phase of serum CHE level is closely related with the infarct size and illness severity index in patients with acute cerebral infarction,which could be an independent factor affecting the prognosis of cere?bral infarction.

The effect of S1PR2/3 during myocardial ischemia-reperfusion injury / 中国法医学杂志

Objective To observe the effect of S1PR2/3 on heart during myocardial ischemia-reperfusion (I/R) in rats. Methods Healthy adult male Sprague-Dawley rats were randomly divided into 7 groups: control group, sham operation group, IR group, IR group treated with DMSO, IR group treated with Cym5541( agonist of S1P3), IR group treated with Cay10444 (antagonist of S1P3), IR group treated with Cay10444/Jte-013 (antagonist both S1P3 and S1P2). In vivo model of myocardial ischemia-reperfusion was established. The hemodynamics, infarction area and mortality was recorded. Results Compared with IR, the S1PR3 antagonist group and S1PR2/3 antagonist group showed signiifcantly reduction of heart rate(HR) and increament left ventricular end-diastolic pressure(LVEDP)(P<0.05). In addition, the infarction area was increased in the S1PR3 antagonist group and S1PR2/3 antagonist treated group (55.7%:28.8%, 51.6%:28.8%), respectively. Treatment with S1PR3 agonist reduced the infarct size compared with IR group(18.6%:28.8%). Blocking S1P2/3 receptors increased IR-induced mortality signiifcantly (53%:22%, P<0.05). Conclusion S1PR2/3 have a beneifcial effect on heart. S1PR2 and S1PR3 were involved in the IR-induced SCD.

Protection of extract from pigeonpea leaves on myocardial ischemia reperfusion injury in rats / 中草药

Objective: To investigate the protective effects of pigeonpea leaves on myocardial ischemia reperfusion injury in rats. Methods: A model of myocardial ischemia reperfusion was established by ligating the anterior descending coronary arteries. Rats were administrated with extract from pigeonpea leaves (125, 200, and 500 mg/kg) before ischemia, and the size of myocardial infarction, arrhythmia score, and morphological changes of cardiomyocytes were determined. Results: Compared with the model group, pigeonpea leaves could reduce arrhythmia severity and incidence (P<0.05 or 0.01) and the size of myocardial infarction (P<0.05). Pigeonpea leaves could ameliorate the pathological lesion. Conclusion: Pigeonpea leaves have the protective effects on myocardial ischemia reperfusion injury in rats.

Effect of Immediate Hyperbaric Oxygen on Infarct Size in Rats after Focal Cerebral Ischemia / 中国康复理论与实践

@#Objective To investigate the effect of immediate hyperbaric oxygen on focal cerebral ischemia of rats. Methods Sprague-Dawly rats were randomly divided into control group (n=9), hyperbaric air group (n=9), hyperbaric oxygen group (n=9) and sham group (n=5). The middle cerebral arteries were occluded in the former 3 groups, while the hyperbaric air group and the hyperbaric oxygen group operated in the hyperbaric chamber, and the hyperbaric oxygen group accepted hyperbaric oxygen immediately after operation. All the rats were sacrificed 6 hours after operation and the percentage of volume of infarction in the brain slices was calculated. Results The percentage of infarction decreased in both hyperbaric oxygen group and hyperbaric air group compared with the control group (P<0.001), and decreased more in the hyperbaric oxygen therapy than in the hyperbaric air group (P<0.001). Conclusion Immediate hyperbaric oxygen therapy can reduce infarct size in rats after focal cerebral ischemia.

Effect of Immediate Hyperbaric Oxygen on Infarct Size in Rats after Focal Cerebral Ischemia / 中国康复理论与实践

Objective To investigate the effect of immediate hyperbaric oxygen on focal cerebral ischemia of rats. Methods Sprague-Dawly rats were randomly divided into control group (n=9), hyperbaric air group (n=9), hyperbaric oxygen group (n=9) and sham group (n=5). The middle cerebral arteries were occluded in the former 3 groups, while the hyperbaric air group and the hyperbaric oxygen group operated in the hyperbaric chamber, and the hyperbaric oxygen group accepted hyperbaric oxygen immediately after operation. All the rats were sacrificed 6 hours after operation and the percentage of volume of infarction in the brain slices was calculated. Results The per-centage of infarction decreased in both hyperbaric oxygen group and hyperbaric air group compared with the control group (P<0.001), and decreased more in the hyperbaric oxygen therapy than in the hyperbaric air group (P<0.001). Conclusion Immediate hyperbaric oxygen ther-apy can reduce infarct size in rats after focal cerebral ischemia.

Hypoxia training attenuates left ventricular remodeling in rabbit with myocardial infarction / 老年心脏病学杂志（英文版）

Objective Previous studies showed that hypoxia preconditioning could protect cardiac function against subsequent myo-cardial infarction injury. However, the effect of hypoxia on left ventricular after myocardial infarction is still unclear. This study therefore aims to investigate the effects of hypoxia training on left ventricular remodeling in rabbits post myocardial infarction. Methods Adult male rabbits were randomly divided into three groups: group SO (sham operated), group MI (myocardial infarc-tion only) and group MI-HT (myocardial infarction plus hypoxia training). Myocardial infarction was induced by left ventricular branch ligation. Hypoxia training was performed in a hypobaric chamber (having equivalent condition at an altitude of 4000 m, FiO214.9%) for 1 h/day, 5 days/week for four weeks. At the endpoints, vascular endothelial growth factor (VEGF) in the plasma was measured. Infarct size and capillary density were detected by histology. Left ventricular remodeling and function were as-sessed by echocardiography.Results After the 4-week experiment, compared with the group SO, plasma VEGF levels in groups MI (130.27 ± 18.58 pg/mL,P< 0.01) and MI-HT (181.93 ± 20.29 pg/mL,P< 0.01) were significantly increased. Infarct size in Group MI-HT (29.67% ± 7.73%) was deceased remarkably, while its capillary density (816.0 ± 122.2/mm2) was significantly increased. For both groups MI and MI-HT, left ventricular end-diastolic and end-systolic dimensions were increased whereas left ventricular ejection fraction was decreased. However, compared with group MI, group MI-HT diminished left ventricular end-diastolic (15.86 ± 1.09 mm,P< 0.05) and end-systolic dimensions (12.10 ± 1.20 mm,P< 0.01) significantly and im-proved left ventricular ejection fraction (54.39 ± 12.74 mm,P< 0.05).ConclusionHypoxia training may improve left ven-tricular function and reduce remodeling via angiogenesis in rabbits with MI.

An optimized modification of TTC staining method for better detection of myocardial ischemia-reperfusion injury in rats / 中国实验动物学报

Objective To evaluate an improved modification of TTC staining method for measuring myocardial in-farct size after ischemia-reperfusion in rats.Methods Twenty healthy SPF male 8-week-old SD rats were randomly divided into two groups:Group A with conventional TTC staining, and group B with the modified TTC staining method for measuring myocardial ischemia-reperfusion injury.The infarct size was caculated and the serum cTnI levels were determined.Results The infarcted myocardium was well detected in both groups A and B.There were no significant differences in the myocardial infarct sizes measured in the groups A and B (48.69 ±5.37 %vs.47.41 ±3.28%, P>0.05).There were no significant differences in the serum cTnI levels assayed in the groups A and B (4.51 ±0.88 ng/mL vs.4.70 ±0.71 ng/mL, P>0.05). But compared with the group A, the color contrast of stained myocardial slice and the distinguishing infarction area and non-infarction area were much clearer in the group B.Conclusions Our modified TTC staining technique using in vivo staining is an economic, convenient, fast and efficient method, being easy to control, time-saving and inexpensive, and enhances the staining effect in evaluating the size of myocardial ischemia/reperfusion injury more accurately.

Effects of Recombinant Human Erythropoietin on the Cardiac Function and Infarct Size after Myocardial Infarction in Rats / 昆明医科大学学报

Objective Ventricular remodeling mode after myocardial infarction in rats was used to investigate the effects of recombinant human erythropoietin (rHu-EPO) on hemodynamic,ventricular function and infarct size of left ventricle in rats with myocardial infarction, so as to find out the optimum time and protocol of EPO treatment for ventricular remodeling after myocardial infarction and provide evidence for clinical application of EPO. Methods Sixty healthy male Sprague Dawley rats were divided randomly and equally into 5 groups:sham group,simple cardiac remodeling after myocardial infarction group, the intervention groups of different drugs ( rHu-EPO in the intervention group and SB203580 group,rHu-EPO+SB203580,group) . Ligation was set at more than 1/3 points on the anterior descending coronary artery to make model of myocardial infarction in rats, and the rats were feeded for four weeks. Different drugs in the intervention groups were subcutaneously injected once before ischemia and twice a week after ischemia. Respectively, 24 hours, 2 weeks, and 4 weeks after ischemia, we detected the hemodynamic parameters, recorded the left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), maximal rate of left ventricular pressure (+dp/dt) and left ventricular pressure decline rate (-dp/dt), and recorded the synchronization of heart rate (HR) . The animals were sacrificed 4 weeks after ischemia, and the heart specimens were collected. The relative weight of left and right ventricle (LV/BW in the RV/BW) was calculated according to the left and right ventricular weight (LVW, RVW) . TTC and Evans blue staining was used to detect left ventricular infarct size, and pathological examination was used to observe the gross and microscopic morphological change. Results 24 hours after operation: Compared with the sham group, in simply cardiac remodeling after myocardial infarction group, rats' left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP) and left ventricular pressure maximum rise and fall rate (±dp/dt) was significantly abnormal,LVSP and ± dp/dt were significantly reduced, the LVEDP was significantly increased (P<0.05);compared with simply cardiac remodeling after myocardial infarction group, in the intervention groups (rHu-EPO in the intervention group, SB203580 group, rHu-the EPO + SB203580 group) rats' ± the dp /dt improved significantly (P<0.05) . After 2 weeks:compared with the sham group, in simple cardiac remodeling after myocardial infarction group rats’LVSP and LVEDP and ± dp/dt significant deterioration (P<0.05) ;compared with simply cardiac remodeling after myocardial infarction group, in the intervention group (rHu-EPO in the intervention group, SB203580 group, rHu-the EPO+SB203580 group) rats’± the dp/dt was significantly improved (P<0.05) . After 4 weeks:compared with the sham group, in simple cardiac remodeling after myocardial infarction group rats’LVSP and LVEDP and ± dp/dt significant deterioration (P<0.05) ; compared with simply cardiac remodeling after myocardial infarction group, in the intervention groups (rHu-EPO in the intervention group, SB203580 group, rHu-the EPO + SB203580 group) rats' ± the dp/dt was significantly improved (P<0.05) . Compared with the sham group, in simply cardiac remodeling after myocardial infarction group rats' LV/BW increased, the difference was statistically significant (P<0.05) . Compared with simply cardiac remodeling after myocardial infarction group,in the intervention group (rHu-EPO in the intervention group and SB203580 group, rHu-the EPO+SB203580 group) rats’LV/BW decreased, the difference was statistically significant (P<0.05 ) . Compared with simply after myocardial infarction cardiac remodeling group, in the intervention groups (rHu-EPO in the intervention group and SB203580 group,rHu-EPO+SB203580 group) rats’cardiac infarct size was significantly reduced (P<0.05). Conclusions rH-EPO can protect the heart function through improving the left ventricular systolic and diastolic function after AMI in rats.RH-EPO can suppress ventricular remodeling, through reducing ventricular relative weight and infarct size and promoting the renewal of capillary in infarction area after AMI in rats.

Effect of transplantation of bone marrow stem cells on myocardial infarction size in a rabbit model / 世界急诊医学杂志（英文）

@#BACKGROUND: Intravenous transplantation has been regarded as a most safe method in stem cell therapies. There is evidence showing the homing of bone marrow stem cells (BMSCs) into the injured sites, and thus these cells can be used in the treatment of acute myocardial infarction (MI). This study aimed to investigate the effect of intravenous and epicardial transplantion of BMSCs on myocardial infarction size in a rabbit model. METHODS: A total of 60 New Zealand rabbits were randomly divided into three groups: control group, epicardium group (group I) and ear vein group (group II). The BMSCs were collected from the tibial plateau in group I and group II, cultured and labeled. In the three groups, rabbits underwent thoracotomy and ligation of the middle left anterior descending artery. The elevation of ST segment>0.2 mV lasting for 30 minutes on the lead II and III of electrocardiogram suggested successful introduction of myocardial infarction. Two weeks after myocardial infarction, rabbits in group I were treated with autogenous BMSCs at the infarct region and those in group II received intravenous transplantation of BMSCs. In the control group, rabbits were treated with PBS following thoracotomy. Four weeks after myocardial infarction, the heart was collected from all rabbits and the infarct size was calculated. The heart was cut into sections followed by HE staining and calculation of infarct size with an image system. RESULTS: In groups I and II, the infarct size was significantly reduced after transplantation with BMSCs when compared with the control group (P<0.05). However, there was no significant difference in the infarct size between groups I and II (P>0.05). CONCLUSION: Transplantation of BMSCs has therapeutic effect on MI. Moreover, epicardial and intravenous transplantation of BMSCs has comparable therapeutic efficacy on myocardial infarction.

Partial role of nitric oxide in infarct size limiting effect of quercetin and rutin against ischemia-reperfusion injury in normal and diabetic rats.

Reperfusion injury is remarkable clinical issue that needs to be resolved as ischemia-reperfusion is a common phenomenon encountered in numerous clinical situations. The present communication report the involvement of nitric oxide (NO) in cardioprotection offered by flavonoids (rutin and quercetin) against myocardial ischemia reperfusion. Rutin produced better cardioprotection than quercetin in normal and diabetic rats. The observed cardioprotection offered with quercetin and rutin was partially abolished by prior administration of nitric oxide synthase inhibitor, L-NAME (N-nitro-L-arginine methyl ester) in both normal and diabetic rats. L-NAME abolished the cardioprotective actions of rutin more strongly than the cardioprotective actions of quercetin. However, mechanistic study with NOS inhibitor implied the possible partial role of nitric oxide in infarct size limiting effect of quercetin and rutin.

Cardioprotective effects of exogenous and endogenous hydrocortisone in the rabbit model of ischemia-reperfusion / Efectos cardioprotectores de la hidrocortisona exógena y endógena en el modelo isquemia-reperfusión de conejo

Reducing the infarct size in acute myocardial infarction is one of the most important goals driving new drug research and development. During the last two decades, many clinical studies have found cardioprotective effects of corticosteroids, but their exact role in ischemic preconditioning remains questionable. The aim of the present study was to determine the protective effects of hydrocortisone sodium succinate on myocardial preconditioning in rabbit hearts. Twenty-four male New Zealand rabbits were divided randomly & equally in four groups: 1) control, 2) Infarct, 3) Ischemic preconditioning (IP) and 4) Hydrocortisone (HYD). The HYD group received 50mg/kg Hydrocortisone 45min before major ischemia. Serum levels of cardiac troponin-T(cTNT) and cortisole were measured before and after the protocols. Triphenyl-tetrazolium chloride staining was used to determine the infarcted area. In the present study, exogenous hydrocortisone decreased infarct size by 53 percent in comparison to the infarct group. Serum level of cortisole was increased in the IP and HYD groups, and was significant in the HYD group (p<0.01). An increasing trend in cortisole level was associated with a decreasing trend in infarct size and cTNT in the IP and HYD groups (p>0.01). In conclusion, we showed that hydrocortisone has cardioprotective effects when injected before the onset of myocardial infarction. In addition, we have proposed for the first time that endogenous hydrocortisone may play a role in ischemic preconditioning phenomena.

La reducción del tamaño del infarto en el infarto agudo de miocardio es una de las metas más importantes que impulsan la investigación y el desarrollo de nuevos fármacos. Durante las dos últimas décadas, muchos estudios clínicos han encontrado efectos cardioprotectores de los corticosteroides, pero su papel exacto en el preacondicionamiento isquémico sigue siendo cuestionable. El objetivo del presente estudio fue determinar los efectos protectores de succinato sódico de hidrocortisona en el preacondicionamiento del miocardio en el corazón de conejo. Veinticuatro conejos neozelandeses machos fueron divididos al azar en cuatro grupos : 1) control, 2) infarto, 3) preacondicionamiento isquémico (PI) y 4) Hidrocortisona (HYD). El grupo HYD recibió 50 mg/kg de hidrocortisona 45 minutos antes de la isquemia mayor. Los niveles séricos de troponina cardíaca T (cTNT) y cortisol se midieron antes y después de los protocolos. Se utilizó la tinción cloruro de trifenil-tetrazolio para determinar el área infartada. En el presente estudio, la hidrocortisona exógena disminuyó el tamaño del infarto en un 53 por ciento en comparación con el grupo de infarto. Los niveles séricos de cortisol se incrementaron en los grupos IP y HYD, siendo significativa en el grupo de HYD (p <0,01). Un aumento en el nivel cortisol se asoció con la disminución del tamaño del infarto y la cTNT en los grupos IP y HYD (p> 0,01). En conclusión, hemos demostrado la hidrocortisona tiene efectos cardioprotectores cuando se inyecta antes de la aparición del infarto al miocardio. Además, hemos propuesto, por primera vez que la hidrocortisona endógena puede jugar un papel en los fenómenos de preacondicionamiento isquémico.

Cardioprotective effect of ornitho-kinin in an anesthetized, open-chest chicken model of acute coronary occlusion

The generation of bradykinin (BK; Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) in blood and kallidin (Lys-BK) in tissues by the action of the kallikrein-kinin system has received little attention in non-mammalian vertebrates. In mammals, kallidin can be generated by the coronary endothelium and myocytes in response to ischemia, mediating cardioprotective events. The plasma of birds lacks two key components of the kallikrein-kinin system: the low molecular weight kininogen and a prekallikrein activator analogous to mammalian factor XII, but treatment with bovine plasma kallikrein generates ornitho-kinin [Thr6,Leu8]-BK. The possible cardioprotective effect of ornitho-kinin infusion was investigated in an anesthetized, open-chest chicken model of acute coronary occlusion. A branch of the left main coronary artery was reversibly ligated to produce ischemia followed by reperfusion, after which the degree of myocardial necrosis (infarct size as a percent of area at risk) was assessed by tetrazolium staining. The iv injection of a low dose of ornitho-kinin (4 µg/kg) reduced mean arterial pressure from 88 ± 12 to 42 ± 7 mmHg and increased heart rate from 335 ± 38 to 402 ± 45 bpm (N = 5). The size of the infarct was reduced by pretreatment with ornitho-kinin (500 µg/kg infused over a period of 5 min) from 35 ± 3 to 10 ± 2 percent of the area at risk. These results suggest that the physiological role of the kallikrein-kinin system is preserved in this animal model in spite of the absence of two key components, i.e., low molecular weight kininogen and factor XII.

The effects of preconditioning with pioglitazone on infarct size and mitochondrial ATP-sensitive potassium channel in rats with ischemia-reperfusion / 中华急诊医学杂志

Objective To observe the effects of preconditioning with pioglitazone on infarct size and mito-chondrial ATP-sensitive potassium channel in rats with ischemia-repedusion, and to explore its possible mecha-nism. Method The whole experiment was divided into experiment Ⅰ and Ⅱ. In experiment Ⅰ, 24 rats were ran-domly divided into four groups (6 rats in each group): (1)Sham-operated (SO) group: the coronary artery of rat was threading without hgation, and the heart was removed by cutting immediately 4 hours later; (2) Isehemia-reperfusion (I/R) group: the rats were administered with 0.9% saline intravenously via caudal vein at 24 hours before iigating the left anterior descending branch of coronary artery for 30 minutes, and followed by reperfusion for 4 hours; (3)5-hydroxydecanoate plus pioglitazone(5HD+Pio) group: the rats were injected with 10 mg/kg 5-hy-droxydecanoate (the blocker of mitochondrial ATP-sensitive potassium channels,) at 24 hours before ligation, and 30 minutes later, 3 mg/kg pioglitazone was given in 5 minutes, and then the rats were subjected to ischemia for 30 minutes, followed by reperfusion for4 hours; (4)pioglitazone treatment group (Pio): the mrs were given 3 mg/kg pioglitazone at 24 hours before occlusion, and then they were treated as done in the 5HD+Pio group. In I/R, 5HD+Pio and Pio group, the hearts were removed by cutting after reperfusion. Western blotting was used to detect the protein expression of P38MAPK, .INK and NFκB P65. In experiment Ⅱ, 30 rats were randomly divided into five groups: SO, I/R, Pio, 5HD+Pio and 5-HD group (rats were treated as done in the rats of I/R group and were injected with 10 mg/kg 5-bydroxydecanoate 24 h before ischemia/reperfusion),and the size of myocardial in-farction and isehemia were measured after reperfusion. Statistical analyses were performed using SPSS10.0 soft-ware. Multiple comparisons were analyzed by one-way analysis of variance (SNK-q test). P<0.05 was consid-ered statistically significant. Results (1) The infarct size in i/R group was(34.93±5.55)%, while pioglita-zone reduced the infarct size to(20.24±3.93)% (P<0.05). There was no significant difference between I/R and 5-HD±Pio or 5-HD groups (P>0.05). Compared with the sham-operated group, the expression of P38MAPKmRNA, JNKmRNA and protein of P38MAPK, JNK and NFκB P65 in I/R increased (P<0.05). Com-pared with the I/R group, pioglitazone inhibited these undue expressions (P<0.05). Conclusions Pioglitazone could protect the heart from ischemia-reperfusion injury evidenced by reducing infarct size. These protective effects of pioglitazone may be related to opening mitochondrial ATP-seusitive potassium channels or downregulation of JNK and p38 MAPK signaling, leading to the overexpression of NFκB p65 activation.

The Effect of Hypercapnic Acidosis Preconditioning on Rabbit Myocardium / 华中科技大学学报（医学）（英德文版）

This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 aminals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO2 was maintained at the level of 40-50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO2 were 75-85,65-75, 55--65 mmHg,respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO2 to 40-50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis.Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5±11.5)% of the risk area in the control group and (42.4+7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%_+9.4%) (P<0.05 vs control group) and group A (31.0%±9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.

Time course of echocardiographic and electrocardiographic parameters in myocardial infarct in rats

In animal models the evaluation of myocardial infarct size in vivo and its relation to the actual lesion found post mortem is still a challenge. The purpose of the current study was to address if the conventional electrocardiogram (ECG) and/or echocardiogram (ECHO) could be used to adequately predict the size of the infarct in rats. Wistar rats were infarcted by left coronary ligation and then ECG, ECHO and histopathology were performed at 1, 7 and 28 days after surgery. Correlation between infarct size by histology and Q wave amplitude in lead L1 was only found when ECGs were performed one day post-surgery. Left ventricular diastolic and systolic dimensions correlated with infarct size by ECHO on day 7 post-infarction. On days 7 and 28 post-infarction, ejection indexes estimated by M-mode also correlated with infarct size. In summary we show that conventional ECG and ECHO methods can be used to estimate infarct size in rats. Our data suggest that the 7-day interval is actually the most accurate for estimation of infarct size by ECHO.

Nos modelos animais a medida do tamanho do infarto do miocárdio "in vivo" e sua relação com o tamanho da lesão encontrada no exame "pos-mortem" ainda é um desafio. A finalidade do presente estudo é verificar se um eletro (ECG) e ecocardiograma (ECO) rotineiros poderiam ser utilizados para predizer a extensão do infarto em ratos. Ratos Wistar foram infartados pela ligadura cirúrgica da artéria coronária descendente anterior e exames eletro, ecocardiográficos e histopatológicos foram realizados 1, 7 e 28 dias pós-infarto. Foi encontrada correlação entre o tamanho do infarto medido pela histopatologia e a amplitude da onda Q em D1 apenas nos ECGs realizados no primeiro dia após a cirurgia. Os diâmetros da cavidade ventricular esquerda medidos em sístole e em diástole pelo ECO correlacionaram-se com o tamanho do infarto no sétimo dia pós-infarto. Ainda mais, no sétimo e vigésimo oitavo dias pós-cirurgia, os índices sistólicos estimados pelo Modo M também se correlacionaram com o tamanho do infarto. Em resumo, nós mostramos que um ECG e ECO convencionais são capazes de estimar a extensão do infarto do miocárdio em ratos. Nossos dados sugerem que o tempo mais adequado para estimar o tamanho do infarto pelo ECO é 7 dias pós-cirurgia.

The Effect of Sufentanil on Myocardial Function and Coronary Flow in an Isolated-Heart Rat Model / 대한마취과학회지

BACKGROUND: Some opioids have been shown to attenuate an ischemia-reperfusion injury in an isolated-heart model. The aim of this study was to evaluate the effect of sufentanil on the cardiac function in isolated-heart models when given before and after prolonged periods of low flow ischemia. METHODS: Isolated rat hearts were stabilized for 30 minutes and subdivided into four groups (each n = 7). The control group was subjected to low flow ischemia (LFI 0.3 ml/min) of 5% dextrose water for 30 minutes, followed by perfusion with a modified Krebs solution at a constant pressure for 60 minutes. In the sufentanil groups, different sufentanil (12.5 mg/L, 25 mg/L, 50 mg/L) doses were administered with the modified Krebs solution after 30 minutes of stabilization until the end of the experiment with the exception of the LFI group. The left ventricular end systolic pressure (LVESP), dP/dt max, heart rate and coronary flow were measured. After reperfusion, the infarct size of all groups was measured. RESULTS: The control and the sufentanil groups had a lower LVESP, dP/dt max, coronary effluent flow and arrhythmia duration after ischemia and reperfusion than those before ischemia. The infarct sizes in the sufentanil groups were smaller than those in the control group. However the infarct sizes of the sufentanil groups were similar. CONCLUSION: Sufentanil reduces the infarct size but does not improve the post-ischemic functional dysfunction.