Nicorandil, a KATP Channel Opener, Attenuates Ischemia-Reperfusion Injury in Isolated Rat Lungs.

PURPOSE: Nicorandil is a hybrid between nitrates and KATP channel opener activators. The aim of this study was to evaluate the nicorandil's effects on ischemia-reperfusion (IR) lung injury and examine the mechanism of its effects. METHODS: Isolated rat lungs were divided into 6 groups. In the sham group, the lungs were perfused and ventilated for 150 min. In the IR group, after perfusion and ventilation for 30 min, they were interrupted (ischemia) for 60 min, and then resumed for 60 min. In the nicorandil (N) + IR group, nicorandil 6 mg was added before ischemia (nicorandil concentration was 75 µg ml-1). In the glibenclamide + N + IR group, the L-NAME (Nω-Nitro-L-arginine methyl ester) + N + IR group and ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) + N + IR group, glibenclamide 3 µM, L-NAME 100 µM, and ODQ 30 µM were added 5 min before nicorandil administration, respectively. We measured the coefficient of filtration (Kfc) of the lungs, total pulmonary vascular resistance, and the wet-to-dry lung weight ratio (WW/DW ratio). RESULTS: Kfc was significantly increased after 60 min reperfusion compared with baseline in the IR group, but no change in the sham group. An increase in Kfc was inhibited in the N + IR group compared with the IR group (0.92 ± 0.28 vs. 2.82 ± 0.68 ml min-1 mmHg-1 100 g-1; P < 0.01). Also, nicorandil attenuated WW/DW ratio was compared with IR group (8.3 ± 0.41 vs. 10.9 ± 2.5; P < 0.05). Nicorandil's inhibitory effect was blocked by glibenclamide and ODQ (P < 0.01), but not by L-NAME. CONCLUSIONS: Nicorandil attenuated IR injury in isolated rat lungs. This protective effect appears to involve its activation as KATP channel opener as well as that of the sGC-cGMP pathway.

Effect of lidocaine cream analgesia for chest drain tube removal after video-assisted thoracoscopic surgery for lung cancer: a randomized clinical trial.

BACKGROUND AND OBJECTIVES: Pain management makes an important contribution to good respiratory care and early recovery after thoracic surgery. Although the development of video-assisted thoracoscopic surgery (VATS) has led to improved patient outcomes, chest tube removal could be distressful experience for many patients. The aim of this trial was to test whether the addition of lidocaine cream would have a significant impact on the pain treatment during chest tube removal from patients who had undergone VATS for lung cancer. METHODS: This clinical trial was a double-blind randomized study. Forty patients with histologically confirmed lung cancer amenable to lobectomy/segmentectomy were enrolled. All patients had standard perioperative care. Patients were randomly assigned to receive either epidural anesthesia plus placebo cream (placebo, Group P) or epidural anesthesia plus 7% lidocaine cream cutaneously around the chest tube insertion site and on the skin over the tube's course 20 min (Group L) before chest drain removal. RESULTS: Visual analog scale (VAS) scores were higher in Group P (median 5, IQR, 3.25-8) than in Group L (median 2, IQR, 1-3). Pain intensities measured using a PainVision system were also higher in Group P (median 296.7, IQR, 216.9-563.5) than Group L (median 41.2, IQR, 11.8-97.0). VAS scores and the pain intensity associated with chest drain removal were significantly lower in Group L than Group P (p=0.0002 vs p<0.0001). CONCLUSION: Analgesia using lidocaine cream is a very simple way to reduce the pain of chest tube removal after VATS. TRIAL REGISTRATION NUMBER: UMIN000013824.

Neuroprotective Effects of Fasudil, a Rho-Kinase Inhibitor, After Spinal Cord Ischemia and Reperfusion in Rats.

BACKGROUND: Excessive Rho/Rho-kinase pathway activation occurs subsequent to stroke. We examined the neuroprotective effects of pre- and posttreatment with fasudil (a Rho-kinase inhibitor) in a rat transient spinal cord ischemia-reperfusion model under normothermic conditions. METHODS: After approval by our animal research committee, male Sprague-Dawley rats were assigned to 1 of 6 groups: pre- and postcontrol (C); pre- and postfasudil (F); and pre- and postsham (S). Fasudil (10 mg/kg) or normal saline was administered intravenously over 30 minutes before ischemia in the pre-F or pre-C groups, and over 30 minutes after reperfusion in the post-F or post-C groups. Sham groups were not subjected to ischemia. Ischemia was induced by aortic occlusion using a balloon catheter combined with hypotension for 10 minutes. Neurologic deficit scores (NDS; 0-8 points) were assessed 1, 7, and 14 days after ischemia, and then histopathologic outcomes were assessed. RESULTS: NDS 7 and 14 days after ischemia in the pre-F group (median [range]; 3.5 [2-6] and 2.5 [0-6]) were lower than those in the pre-C group (5.5 [4-7] and 4.5 [4-6]; P = .046 and P = .049), whereas NDS in the post-F group and in the post-C group were not different. The numbers of intact neurons in the gray matter in the pre- and post-F groups (mean ± standard deviation [95% confidence interval]: 25 ± 7 [20-30] and 16 ± 5 [12-19]) were greater than those in the pre- and post-C groups (11 ± 5 [7-14] and 9 ± 3 [7-11]; P < .001 and P = .002). The number of intact neurons in the post-F group (16 ± 5 [12-19]) was lower than the number in the post-S group (26 ± 2 [24-29]; P < .001). The percentages of vacuolation in the white matter in the pre- and post-F groups (21.5 ± 8.4 [15.5-27.5] and 13.6 ± 7.4 [8.3-18.9]) were lower than those in the pre- and post-C groups (43.7 ± 10.4 [36.3-51.1] and 40.6 ± 12.3 [31.8-49.4]; P < .001 and P < .001). CONCLUSIONS: Our results demonstrated that intravenous fasudil administered before ischemia improved both neurologic and histopathologic outcomes even 14 days after ischemia, while fasudil administered postinsult improved histopathologic outcomes only in normothermic rats. Fasudil may be a relevant pretreatment paradigm for planned procedures at risk for spinal cord ischemia.

Recovery From Ropivacaine-Induced or Levobupivacaine-Induced Cardiac Arrest in Rats: Comparison of Lipid Emulsion Effects.

BACKGROUND: Lipid emulsion treatment appears to have application in the treatment of local anesthetic-induced cardiac arrest. To examine whether the efficacy of lipid resuscitation in the treatment of local anesthetic-induced cardiac arrest is affected by lipophilicity, the effects of lipid infusions were compared between levobupivacaine-induced (high lipophilicity) and ropivacaine-induced (lower lipophilicity) rat cardiac arrest model. METHODS: A total of 28 female Sprague-Dawley rats were anesthetized using sevoflurane, which subsequently underwent tracheostomy, followed by femoral artery and vein cannulation. Two hours after the discontinuation of sevoflurane, either levobupivacaine 0.2% (n = 14) or ropivacaine 0.2% (n = 14) was administered at a rate of 2 mg/kg/min to the awake rats. When the pulse pressure decreased to 0, the infusion of local anesthetic was discontinued, and treatment with chest compressions and ventilation with 100% oxygen were immediately initiated. The total doses of local anesthetics needed to trigger the first seizure and pulse pressure of 0 mm Hg were calculated. The 2 groups were each subdivided into a lipid emulsion group (n = 7) and a control group (n = 7). In the lipid emulsion group, 20% lipid emulsion was administered intravenously (5 mL/kg bolus plus continuous infusion of 0.5 mL/kg/min), while in the control group, the same volume of normal saline was administered. Chest compressions were discontinued when the rate-pressure product had increased by more than 20% of baseline. RESULTS: The cumulative doses of levobupivacaine and ropivacaine that produced seizures and 0 pulse pressure showed no significant difference. Mean arterial blood pressure (MAP) values were higher in the levobupivacaine group than in the ropivacaine group after resuscitation was initiated (P < .05). In levobupivacaine-induced cardiac arrest, heart rate and MAP values were higher in the lipid group than in the control group after starting resuscitation (P < .05); all rats in the lipid group achieved spontaneous circulation (rate-pressure product >20% baseline), while only 2 of 7 rats in the control group achieved spontaneous circulation at 10 minutes. In ropivacaine-induced cardiac arrest, there were no significant differences in heart rate and MAP between the lipid and control groups from the start of resuscitation to 10 minutes; spontaneous circulation returned in 6 of 7 lipid group rats, but in only 2 of 7 control group rats at 10 minutes. CONCLUSIONS: Lipid emulsion treatment was more effective for levobupivacaine-induced cardiac arrest than for ropivacaine-induced cardiac arrest. Although lipid therapy is also effective for ropivacaine-induced cardiac arrest, it takes more time than in levobupivacaine-induced cardiac arrest. This suggests that the lipophilicity of local anesthetics influences the efficacy of lipid infusion when treating cardiac arrest caused by these drugs.

The suppressive effects of landiolol administration on the occurrence of postoperative atrial fibrillation and tachycardia, and plasma IL-6 elevation in patients undergoing esophageal surgery: A randomized controlled clinical trial.

STUDY OBJECTIVE: To determine whether perioperative landiolol administration suppresses postoperative atrial fibrillation (AF) and the plasma cytokines elevation in patients undergoing esophageal cancer surgery. DESIGN: A prospective, randomized controlled trial. SETTING: Akita University Hospital, Akita, Japan, from April 2012 to January 2015. PATIENTS: Forty American Society of Anesthesiologists grade I-II patients undergoing elective esophagectomy. INTERVENTIONS: Patients were randomly divided into two groups, landiolol group (landiolol: 5µg/kg/min) and control group (the same volume of covered saline). Landiolol or saline was infused continuously from the induction of anesthesia until next morning. MEASUREMENTS: We examined the new onset of AF and sinus tachycardia, and measured plasma concentrations of cytokines (IL-1ß, IL-6, IL-8, IL-10, and TNF-α) just before surgery, at the end of surgery, the next day, and 2days after surgery. Data (mean±SD) were analyzed using two-way ANOVA followed by the Bonferroni"s test for post hoc comparison; a P<0.05 was considered statistically significant. MAIN RESULTS: Demographic data were similar between the landiolol and the control groups. The incidence of AF was significantly lower in the landiolol group (1/19=5.3%) compared with the control group (7/20=35%) as well as sinus tachycardia (landiolol group, 0/19=0% vs. control group, 5/20=25%). Plasma IL-6 level at the end of surgery was significantly lower in the landiolol group compared with the control group, but the other plasma cytokines levels were similar between the two groups during the entire study period. CONCLUSIONS: Perioperative landiolol administration suppressed the incidence of new-onset of AF as well as sinus tachycardia, and the plasma IL-6 elevation in patients undergoing esophageal cancer surgery.

Evaluation of postoperative pregabalin for attenuation of postoperative shoulder pain after thoracotomy in patients with lung cancer, a preliminary result.

OBJECTIVE: Thirty-one to 97% of patients who undergo thoracotomy for lung cancer experience ipsilateral shoulder pain, marring the otherwise excellent relief provided by thoracic epidural analgesia. The aim of this study was to test whether the addition of pregabalin to the treatment for shoulder pain would provide a significant benefit. METHODS: Twenty patients undergoing thoracic surgery for lung cancer were enrolled in the control group between May 2012 and December 2012, and 20 patients were enrolled in the pregabalin group between January 2013 and July 2013, consecutively. All patients had standard pre- and intraoperative care. Patients received pregabalin 150 mg po POD 1 and then non-steroidal anti-inflammatory drugs (NSAIDs) po 2 h later (pregabalin group), or they received only NSAIDs po at exactly the same times (control group). Pain severity was then measured using a 100-mm visual analog scale (VAS) scoring system. RESULTS: The VAS scores indicated that patients in the pregabalin group had significantly less shoulder pain on postoperative day (POD) 2 than those in the control group (control: 27.9 ± 28.1 vs. pregabalin: 11.8 ± 14.4; p = 0.030). No differences in pain were observed between the two groups on other POD. There were significant differences on only POD 2 in the patients with shoulder pain immediately after surgery. Three of the pregabalin-treated patients showed mild somnolence. CONCLUSIONS: Postoperative administration of pregabalin provided significant relief of postoperative shoulder pain during earlier POD after thoracic surgery for lung cancer when received multimodal analgesia in combination with NSAIDs.

Combination of oral clonidine and intravenous low-dose ketamine reduces the consumption of postoperative patient-controlled analgesia morphine after spine surgery.

OBJECTIVE: Because ketamine, clonidine, and morphine modulate nociceptive pain, coadministration of these drugs would augment the activity of postoperative analgesic drugs. The purpose of this study was to evaluate the effects of coadministration of ketamine and clonidine on postoperative morphine consumption in patients after spine surgery. METHODS: The patients undergoing spine surgery were allocated randomly to one of the four study groups, which are as follows: group M (n = 12), intravenously (IV) administered patient-controlled analgesia (PCA) morphine alone; group MK (n = 12), IV-PCA morphine plus intra- and postoperative ketamine; group MC (n = 13), IV-PCA morphine plus oral clonidine premedication; group MCK (n = 12), IV-PCA morphine plus intra- and postoperative ketamine and clonidine premedication. The patients in the MC and MCK groups received 4 µg/kg clonidine orally, whereas those in the MK and MCK groups received IV bolus of ketamine (10 mg) at a rate of 2 mg/kg/hour during anesthesia. Patients were arranged to use IV-PCA mode for administration of drugs, which was programmed to deliver a bolus dose of 2-mg morphine (groups M and MC), or boluses of 2-mg morphine and 2-mg ketamine (groups MK and MCK). Scores of visual analog scale (VAS) for pain, morphine requirement, vital signs, nausea, sedation, and other side effects were followed up to 60 hours after surgery. RESULTS: Although there were significant differences in VAS pain scores at rest 24-48 hours after the surgery, the VAS pain score at movement was similar among the groups. The number of PCA request and cumulative morphine requirement were significantly lower in the MCK group than in the M group. CONCLUSION: This study results show that the administration of perioperative low-dose ketamine combined with clonidine premedication could reduce the consumption of postoperative PCA morphine following spine surgery.

[Comparative performance of Airway Scope, Trueview EVO2, and Fibertech video laryngoscope used by inexperienced medical students in a simulated manikin with normal and difficult airways].

BACKGROUND: Many kinds of video-typed laryngoscopes are widely used for tracheal intubation in many clinical situations. The present study was performed to compare the ease in the use of the Airway Scope (AWS), Trueview EVO2 (TVE), and Fibertech Video Laryngoscope (FVL). METHODS: Twenty-seven inexperienced medical students used AWS, TVE and FVL in a simulated manikin with normal and difficult airways. We measured the time of tracheal intubation and start of ventilation, performance levels of tracheal intubations, dental clicks, difficulty of tracheal intubation, and ease of tracheal intubation, and performer's liking. RESULTS: The use of TVE was associated with the longest time to tracheal intubation with dental click and ventilation than the other devices in normal and difficult airways, whereas the performance levels of tracheal intubation were similar among the three devices. VAS score (easy to use) and the degree of liking were lower in AWS than TVE. CONCLUSIONS: This study suggests that inexperienced medical students would perform tracheal intubation using AWS in a short time without dental click in a simulated manikin.

Neuroprotective effects of selective ß-1 adrenoceptor antagonists, landiolol and esmolol, on transient forebrain ischemia in rats; a dose-response study.

Although selective beta-1 adrenoceptor antagonists are known to provide neuroprotective effects after brain ischemia, dose-response relationships of their neuroprotective effects have not been examined. The present study was conducted to evaluate whether the degree of brain protection against transient forebrain ischemia would be influenced by different doses of selective beta-1 adrenoceptor antagonists, esmolol and landiolol, in rats. Adult male S.D. rats received intravenous infusion of saline 0.5 ml/h, esmolol 20, 200, 2,000 µg/kg/min, or landiolol 5, 50, 500 µg/kg/min. Infusion was initiated 30 min prior to ischemia and continued for 24h. Ten-minute forebrain ischemia was induced by hemorrhagic hypotension and occlusion of the bilateral carotid arteries. Neurological and histological examinations were performed. Neurological deficit scores at 1, 4 and 7 days were lower, and the number of intact neurons in CA1 hippocampal region was larger in the rats treated with esmolol and landiolol after ischemia, compared with saline-treated rats (P<0.05), whereas no difference was found among different doses of esmolol and landiolol. These results suggested that selective beta-1 adrenoceptor antagonists improved neurological and histological outcomes following forebrain ischemia in rats, irrespective of their doses.

Neuroprotective effects and suppression of ischemia-induced glutamate elevation by ß1-adrenoreceptor antagonists administered before transient focal ischemia in rats.

BACKGROUND: ß-Adrenoreceptor antagonists provide neuroprotective effects after focal cerebral ischemia in experimental settings. This study was conducted to compare the neuroprotective effects of low-dose and high-dose of selective ß1-adrenoreceptor antagonists in rats after focal cerebral ischemia. We also investigated whether glutamate and norepinephrine contribute to neuroprotection of the ß-adrenoreceptor antagonists. METHODS: Sprague-Dawley rats were subjected to 120 minutes middle cerebral artery occlusion. The rats received intravenous infusion of saline 0.5 mL/h, esmolol 200, esmolol 2000, landiolol 50, or landiolol 500 µg/kg/min. Infusion of all the drugs were started 30 minutes before ischemia and continued for 24 hours. Neurological deficit scores were evaluated at 1, 4, and 7 days, whereas the brains were removed and stained at 7 days after ischemia. In the esmolol 200, and landiolol 50 µg/kg/min groups of additional rats, glutamate and norepinephrine concentrations in the striatum were measured separately by microdialysis during ischemia (glutamate, 120 min; norepinephrine, 110 min) and reperfusion (40 min). RESULTS: Neurological deficit scores were smaller in rats treated with esmolol or landiolol than in saline-treated rats at 1, 4, and 7 days. The cortical and striatal infarct volumes were smaller in rats receiving ß-adrenoreceptor antagonists than in the saline-treated rats. There were no significant differences in neurological score or infarct volume between the groups receiving the different doses of ß1-adrenoreceptor antagonists. The area under the curve of glutamate in the esmolol-treated or landiolol-treated rats was significantly smaller than that in the saline-treated rats, whereas no significant differences were noted in the norepinephrine concentration among the groups. CONCLUSIONS: This study indicates that the improvement in neurological and histologic outcomes by selective ß1-adrenoreceptor antagonists after transient focal cerebral ischemia is partly attributed to attenuation of glutamate release.

[Comparison of levobupivacaine and ropivacaine for postoperative epidural analgesia].

BACKGROUND: Levobupivacaine is a long acting local anesthetic with less cardiovascular toxicity. Recently we can use levobupivacaine for postoperative analgesia. We retrospectively compared levobupivacaine with ropivacaine for the postoperative epidural analgesia in patients undergoing gynecological abdominal surgery. METHODS: The patients who had received epidural and general anesthesia from October 2008 to April 2009 were allocated into two groups. Analgesia intensity, the time to receive the first analgesic, and the number of times to use the additional analgesics were observed for three postoperative days. RESULTS: There was no difference in demographic data between the levobupivacaine and ropivacaine groups. In the levobupivacaine group (n=23) the patient received epidural 0.24% levobupivacaine and fentanyl, while the patients in the ropivacaine group (n=43) epidural 0.19% ropivacaine and fentanyl, at the rate of 3.5 ml x hr(-1). The volume of epidural fentanyl was similar between the groups. The time from the end of surgery to receive the first analgesic was longer in the levobupivacaine group than in the ropivacaine group. The number of the patients who did not require additional analgesia was greater in the levobupivacaine group than in the ropivacaine group. The patients who received metocropramide to treat nausea were fewer in the levobupivacaine group, compared with the ropivacaine group. CONCLUSIONS: These results suggest that the use of epidural 0.24% levobupivacaine in the patients undergoing the gynecological surgery is superior to the use of 0.19% ropivacaine.

Post-treatment with selective ß1 adrenoceptor antagonists provides neuroprotection against transient focal ischemia in rats.

We have reported the neuroprotective effects of pre-treatment with beta-adrenoceptor antagonists on the cerebral infarction at 1 and 7 days after focal ischemia in rats. However, the protective effect of post-treatment with beta-adrenoceptor antagonists has not been investigated yet. This study was conducted to evaluate the post-treatment effects of selective beta(1)-adrenoceptor antagonists in the rat focal cerebral ischemia. Halothane anesthetized, normothermic adult male Sprague-Dawley rats were subjected to 2h of middle cerebral artery occlusion (MCAO) using the intraluminal suture technique confirmed by laser Doppler flowmetry. Rats received intravenous infusion of saline 0.5 mL/h, esmolol 200 microg/kg/min, or landiolol 50 microg/kg/min (n=8 in each group). Infusion was initiated 30 min after MCAO and continued for 24h. Rats were allowed to survive for 7 days, and the neurological deficit score was evaluated at 1, 4 and 7 days after reperfusion. The brains were removed and stained with triphenyltetrazolium chloride at 7 days after reperfusion. Neurological deficit scores were lower in the rats treated with esmolol or landiolol, compared with saline-treated rats at 1 day as well as 4 and 7 days. The infarct volumes of cortical and striatum were less in the rats receiving beta-adrenoceptor antagonists than in saline-treated rats (P<0.05). The current study indicates that administration of selective beta1-adrenoceptor antagonists after the onset of ischemia also improved neurological and histological outcomes following transient focal cerebral ischemia in rats.

Esmolol and landiolol, selective beta1-adrenoreceptor antagonists, provide neuroprotection against spinal cord ischemia and reperfusion in rats.

BACKGROUND: Paraplegia is a devastating and unpredictable complication occasionally resulting from surgery of the thoracic and thoracoabdominal aorta. Because ultrashort-acting selective beta(1)-adrenoreceptor antagonists provide neuroprotective effects after brain ischemia, we hypothesized that they would also ameliorate spinal cord injury after transient ischemia and reperfusion in rats. METHODS: Male Sprague-Dawley rats were randomly assigned to one of the following 4 groups: saline (received IV infusion of 0.9% saline at a rate of 0.5 mL/h, n = 8), esmolol (esmolol 200 microg/kg/min, n = 8), landiolol (landiolol 50 microg/kg/min), or sham surgical (n = 6). Infusion of saline or drugs was initiated 30 minutes before spinal cord ischemia and continued for the subsequent 24-hour reperfusion. Spinal cord ischemia was induced by intraaortic balloon occlusion combined with proximal arterial hypotension for 10 minutes. The spinal cord was then reperfused for 24 hours. Ischemic injury was assessed in terms of the motor deficit index score of the hindlimb and the number of viable motor nerve cells in the anterior spinal cord at 24 hours after reperfusion. RESULTS: The motor deficit index scores were significantly lower in the esmolol and landiolol groups compared with the saline group (P < 0.05). Histopathologic evaluation of the spinal cord showed less damage in the esmolol and landiolol groups than in the saline group (P < 0.05). CONCLUSIONS: These data show that ultrashort-acting selective beta(1)-adrenoreceptor antagonists can reduce neurological injury in a rat model of spinal cord ischemia-reperfusion.

[An index of cerebral perfusion: noninvasive monitoring of regional cerebral oxygen saturation by use of near-infrared spectroscopy (NIRS, NIRO) or NIRS cerebral oximetry (INVOS)].

Noninvasive monitoring of regional cerebral oxygen saturation has been introduced in clinical settings for estimation of cerebral perfusion and cerebral blood flow. In this article, I have described several issues regarding the usefulness and clinical limitations associated with the use of these monitors, as well as relevant information on basic principles of monitoring. At present, there is not enough clinical data concerning critical levels of measured variables that are essential for safe perioperative management of patients susceptible for cerebral ischemia.

[Risk management for neurosurgical anesthesia].

Even a trivial increase in intracranial pressure is likely to induce cerebral ischemia, hernia, and neurogenic pulmonary edema in patients with intracranial hypertension. In this article, I have described several issues that are essential for safe perioperative management in patients undergoing neurosurgical procedures for treatment of subarachonoid hemorrhage, and intracerebral and subdural hematoma, as well as relevant information on basic physiology and pathology of the brain.

Intravenous dexmedetomidine decreases lung permeability induced by intracranial hypertension in rats.

BACKGROUND: Intracisternal dexmedetomidine (Dex) attenuates cardiac dysfunction in rats with intracranial hypertension (ICH). However, the effects of IV Dex on cardiac function and lung permeability during ICH have not been evaluated. We tested the hypothesis that IV Dex attenuates hemodynamic changes and decreases lung permeability induced by ICH in rats. METHODS: Halothane-anesthetized and mechanically ventilated rats were divided into four groups. In two groups, a subdural balloon catheter was inflated for 60 s to produce ICH. Arterial blood gas analysis was performed before and 30 min after ICH. Mean arterial blood pressure, heart rate (HR) and intracranial pressure were monitored for 30 min. The Dex group (n = 8) received IV Dex 80 microg/kg, followed by 6 microg.kg(-1).min(-1) (40 microg/mL) for 10 min and the control group (n = 8) received IV saline 2 mL/kg, followed by at 0.15 mL.kg(-1).min(-1) for 10 min. Surgery was performed without ICH with Dex (Sham-Dex group, n = 5) and without Dex (Sham-control, n = 5). In all groups, pulmonary permeability was measured using a modification of the Evans blue dye extravasation technique. IV Evans blue dye 20 mg/kg was administered 2 h before being killed and Evans blue dye in plasma and lung tissue was quantified by dual-wavelength spectrophotometric analysis. RESULTS: There were no significant differences in basal arterial blood pressure, HR, and Pao(2) among groups. In the control group, ICH resulted in transient increases in mean arterial blood pressure and HR, followed by a rapid decline and a plateau. In the Dex group, mean arterial blood pressure showed a transient increase and subsequent, rapid decrease to baseline, whereas HR did not change during ICH. Pao2 was higher in the Dex group than in the control group after ICH [138 (127-169) vs 78 (59-124) mm Hg, median (range), P < 0.01]. The pulmonary permeability index was lower in the Dex group than the control group [430 (182-450) vs 570 (427-1170), P < 0.01]. It was however, higher in the Sham-Dex group than the Sham-Control group [25 (24-35) vs 6 (4-7), P < 0.01]. CONCLUSIONS: Prophylactic IV Dex decreases lung permeability as well as hemodynamic changes induced by ICH in rats.

[Emergent percutaneous coronary intervention therapy after renal transplantation].

A 54-year-old man was scheduled for renal transplantation. There was no cardiac event except ST-segment depression during surgery. One hour after surgery, the patient complained of a chest pain, and received immediate percutaneous coronary intervention therapy, which was successfully performed. We need close monitoring after surgery even if the patients have no cardiac complication before surgery.