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Abstract Introduction: Sticky platelet syndrome (SPS) is a prothrombotic condition characterized by increased platelet aggregation that causes arterial and venous thrombosis. Its diagnosis is reached by identifying increased aggregation using low concentrations of adenosine diphosphate and epinephrine in platelet aggregation tests. Objectives: To identify common mutations through exome sequencing in two patients from the same family diagnosed with SPS and, thus, contribute to the molecular study of this disease. Materials and methods: Descriptive study. In January 2018, exome sequencing was performed in a 10-year-old patient treated at Fundación HOMI (Bogotá D.C., Colombia), index case, and in one of his adult first-degree relatives, both with a history of thrombotic disease and diagnosed with SPS. Exome sequencing was performed at the Complexo Hospitalario Universitario de Santiago de Compostela (Spain) using the SureSelect Clinical Research Exome V2 software by Agilent. Results: Exome sequencing led to detect genetic variants in both cases when compared with the reference sequence. The following variant was identified in the two samples: a cytosine to thymine transition at position c.236 (NM_000174.4) of the glycoprotein (GP)Ib-IX-V complex platelet membrane receptor, which causes a heterozygous transition of the amino acid threonine to isoleucine (i.e., a transition from hydrophilic amino acid to a hydrophobic amino acid) at position p. 79 of the extracellular leucine-rich repeat domain of GPIba subunit of the (GP)Ib-IX complex, involving a conformational change of the main receptor of ligands IB alpha, which might result in platelet hyperaggregation and thrombosis. This variant has not been described in patients with SPS to date. Conclusion: The mutation identified in both samples could be related to SPS considering the importance of glycoprotein IX in platelet function.
Resumen Introducción. El síndrome de plaqueta pegajosa (SPP) es una condición protrombótica caracterizada por un incremento de la agregabilidad plaquetaria que causa trombosis arterial y venosa. Su diagnóstico se realiza al identificar el aumento de la agregabilidad utilizando bajas concentraciones de adenosín difosfato y epinefrina en pruebas de agregación plaquetaria. Objetivos. Identificar mutaciones comunes mediante secuenciación del exoma en dos pacientes de una misma familia con diagnóstico de SPP y, de esta forma, contribuir al estudio molecular de esta enfermedad. Materiales y métodos. Estudio descriptivo en el que se realizó secuenciación del exoma en un paciente de 10 años atendido en la Fundación HOMI (Bogotá, Colombia), caso índice, y en uno de sus familiares adultos en primer grado, ambos con antecedente de enfermedad trombótica y diagnosticados con SPP. La secuenciación del exoma se realizó en el Complexo Hospitalario Universitario de Santiago de Compostela (España) con el programa SureSelect Clinical Research Exome V2 de Agilent. Resultados. En la secuenciación del exoma se detectaron variantes genéticas en ambos casos en comparación con la secuencia de referencia. En las muestras de ambos pacientes se identificó una variante heterocigota consistente en una transición de citosina a timina en la posición c.236 (NM_000174.4) que provoca el cambio del aminoácido treonina por isoleucina en la posición p.79 del dominio extracelular repetitivo rico en leucina (subunidad GPIba del complejo de la glicoproteína Ib-IX-V) y que podría provocar el cambio conformacional del receptor principal del ligando Ib alfa, así como hiperagregación plaquetaria y trombosis. Esta variante no ha sido descrita previamente en pacientes con SPP. Conclusión. La mutación identificada en las muestras estudiadas podría estar relacionada con el SPP considerando la importancia de la glicoproteína IX en las funciones plaquetarias.
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Objective To investigate the relationship between the changes of plasma thromboxane B2 (TXB2),6-keto-prostaglandin 1 α (6k-PGF1 α) and positive platelet α-granule membrane glycoprotein (CD62P) in patients with acute cerebral infarction.Methods 160 patients with acute cerebral infarction (case group) and 80 healthy subjects were enrolled in our hospital from August 2016 to August 2018.The plasma levels of 6k-PGF1α,CD62P and TXB2 were measured and analyzed.Subgroup analysis was performed on patients with cerebral infarction with different trial of org 10172 in acute stroke treatment (TOAST) classification,National Institute of Health Stroke Scale (NIHSS) score,and prognosis outcome.Results The plasma levels of 6k-PGF1α,CD62P and TXB2 in the case group were significantly higher than those in the control group (P ＜ 0.05).The plasma levels of 6k-PGF1 α,CD62P and TXB2 in mild,moderate and severe groups were gradually increased (P ＜ 0.05).The plasma levels of 6k-PGF1 α,CD62P and TXB2 in patients with small infarction,mid-infarction and large infarction were also gradually increased,with statistically significant difference (P ＜ 0.05);plasma 6k-PGF1 α,CD62P,TXB2 levels in patients with good prognosis were significantly lower than those in poor prognosis group (P ＜ 0.05).Conclusions The levels of plasma TXB2,6k-PGF1α and CD62P in patients with acute cerebral infarction are elevated,and are closely related to the patient's condition and prognosis.
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Objective To evaluate the safety and efficacy of low-dose platelet glycoprotein Ⅱb/Ⅲa antagonist tirofiban on preventing reocclusion during mechanical thrombectomy (MT) for in situ thrombosis(IST).Methods It is a retrospective cohort study, and 112 patients treated with MT, from the Nanjing Prospective Stroke Registration, were enrolled from February 2014 to October 2014. During MT, if angiography after a successful recanalization(defined as Thrombolysis In Cerebral Infarction(TICI) 2b/3) showed residual stenosis at the site of occlusion, additional angiographies were made every 10 min for 30 min.Then, if angiography displayed reocclusion in the corresponding vessels, a repeat recanalization was operated, followed by a low dose intra-arterial tirofiban infusion. MRA or CT angiography (CTA) was implemented to identify intracranial atherosclerosis (ICAS) 5-7 days after the procedure. The patients with confirmed ICAS were enrolled in the IST group. The rest were enrolled in the non-in situ thrombosis (NIST) group.Results A total of 80 patients with acute cerebral infarction were enrolled in the study. IST rate was 32.5%(26/80).All IST patients were confirmed ICAS by follow-up vascular imaging. Instant reocclusion after successful recanalization was significantly more common in the IST group(57.7%(15/26) vs 3.7%(2/54);χ2=30.568, P=0.000) than in the NIST group.In the case of the efficacy and safety of low-dose intra-arterial tirofiban infusion, 82.6%(19/23) of the reocclusion patients eventually accomplished TICI 2b/3, the rest 17.4%(4/23) of the cases were intractable to the procedure and needed rescue stent implantation.The modified Rankin Scale scores in patients infusing tirofiban were superior to the unused patients in 90 days. There was no patient with symptomatic intracranial hemorrhage after the procedure. Conclusions Patients with IST have higher cerebrovascular reocclusion rate during MT. After MT, low-dose intra-arterial tirofiban infusion may prevent reocclusion, and the prognosis is better.
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Objective:To explore influence of preoperative tirofiban usage and using time on blood flow of infarct re-lated artery (IRA) in patients with acute ST elevation myocardial infarction (ASTEMI ) undergoing emergency di-rect percutaneous coronary intervention (PCI ) .Methods:A total of 266 ASTEMI patients undergoing direct PCI from Jan 2009 to Oct 2012 ,were randomly divided into tirofiban group (n=134 ,received preoperative tirofiban us-age for PCI) and routine treatment group (n=132 ,didn't receive tirofiban during PCI) .According to percutaneous using time of tirofiban tirofiban group was divided into <3h group (n= 63) and ≥3h group (n= 71) ;TIMI blood flow of IRA ,before and after PCI were compared among different groups .Results:Compared with routine treat-ment group before PCI ,there were significant rise in percentages of TIMI grade 3 (10.6% vs .20.9% ) in tirofiban group ,P=0.028 ;after PCI ,percentage of TIMI grade 3 in tirofiban group was more significantly rose than that of routine treatment group (78.8% vs .92.5% ,P=0.001);in tirofiban group ,blood flow of IRA before PCI in <3h group was significantly improved compared with ≥3h group (TIMI grade 2 + 3 ,63.5% vs .29.6% , P<0.01) . Conclusion:Early tirofiban usage can improve TIMI blood flow of IRA before and after PCI in ASTEMI patients , the earlier it′s used ,the more significant effect it has .
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Objective To investigate the effects of supplementing qi and activating blood circulation method(YQHX) on platelet inhibition rate and platelet membrane glycoprotein in elderly patients with unstable angina pectoris undergoing percutaneous coronary intervention(PCI).Methods Totally 177 elderly patients with unstable angina(qi deficiency and blood stasis syndrome) pectoris were randomized into two groups:90 cases in the treatment group and 87 cases in the control group.Both groups received conventional western medicinal treatment,for 14 days but YQHX was added to the treatment group.Platelet inhibition rate and platelet membrane glycoprotein were measured before and 14 days after treatment.Results After 14 days of treatment,the platelet inhibition rates induced by arachidonic acid (AA) and adenosine diphosphate (ADP) were significantly increased in the treatment group in comparison to pre-treatment and to control group respectively(P＜0.01).The prevalence of aspirin and clopidogrel resistance were lower in the treatment group than in the control group(8.9％ vs.21.8％,11.1％ vs.25.3％,both P＜0.05).After 14 days of treatment,the expression rates of CD62p,CD63 and PAC-1 were significantly lower in the treatment group than in pre-treatment and control group respectively (P＜0.01).Conclusions YQHX might effectively inhibit the platelet function and reduce the prevalence of aspirin and clopidogrel resistance in elderly patients with unstable angina pectoris undergoing the percutaneous coronary intervention.
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Objective To investigate the effect and significance of hyperbaric oxygenation in down-regulation of platelet membrane glycoproteins CD31 and CD62p in rats of traumatic brain injury (TBI).Methods Fifty-six SD rats were randomly distributed into TBI group,hyperbaric oxygenation group,and sham group by the lottery method.Furthermore,TBI group and hyperbaric oxygenation group were subgrouped at 6,48,and 96 hours.There were 8 rats per group.The rat models of severe TBI were induced by lateral fluid percussion.Levels of CD31 and CD62p were measured in all groups by flow cytometry.Results At 6,48 and 96 hours,expressions of CD31 (30.8 ± 8.9,32.5 ± 9.2 and 29.0 ±5.0) and CD62p (34.5 ±9.1,33.9 ±7.5 and 30.4 ±6.4) in TBI group were significantly higher than those (18.9-± 5.5,19.5 ± 6.1) in sham group (P ＜ 0.05).At 96 hours,expression of CD31 (22.7 ±5.5) in hyperbaric oxygenation group was significantly lower than 29.0 ± 5.0 in the TBI group (P ＜0.05).At 48 and 96 hours,expressions of CD62p (26.1 ± 5.8,23.6 ± 5.7) in hyperbaric oxygenation group were significantly lower than 33.9 ± 7.5 and 30.4 ± 6.4 in TBI group (P ＜ 0.05).Conclusions Platelet activation is enhanced in the acute phase after TBI.But platelet activation may be relieved with hyperbaric oxygenation,which is conducive to inhibiting microthrombosis and mitigating secondary brain injury after TBI.
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Objective To explore the pathogenic mechanism by detecting the expression of membrane glycoprotein in the platelets of nonmuscle myosin heavy chain 9 related disease (MYH9-RD)patients.Methods Periperal bloods were obtained from 11 MYH9-RD patients and 7 normal family members.Flow cytometry was used for detecting the expression of the platelet membrane glycoprotein including GP Ⅱ b/Ⅲa(CD41/61),GP Ⅰ a(CD49b),GP Ⅰ b/Ⅸ/Ⅴ (CD42a) GP Ⅰ b(CD42b) and GPⅣCD36).Results The expression fluorescence intensity of platelet membrane glycoprotein GP Ⅱ b/Ⅲ a CD41/61),GPⅠa(CD49b),GP Ⅰ b/Ⅸ/Ⅴ (CD42a) GP Ⅰ b(CD42b) and GPⅣ (CD36) are 653.7 ±192.7,420.0 ± 151.3,667.7 ± 371.3 and 236.4 ± 64.2 respectively,which are significantly higher than those in normal controls (406.7 ± 126.1,181.2 ± 29.3,271.4 ± 91.6 and 136.1 ± 23.5 ; P ＜ 0.01) ; The expression of GP Ⅰ a(CD49b) was lower in patients with MYH9-RD (139.1 ± 54.9) than that in normal controls (192.2 ± 143.4),but there was no significant difference (P ＞ 0.05).Conclusion In our study,the diverse clinical manifestations in patients with MYH9-RD is probably associated with the expression level of platelet membrane glycoprotein
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Platelet membrane glycoproteins play a key role in the processes of platelet adhesion,activation and aggregation and thrombosis.Many studies have shown that platelet membrane glycoprotein gene polymorphisms are associated with ischemic stroke.This article reviews the relationship between platelet membrane glycoprotein gene polymorphisms and ischemic stroke.
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Objective To analyze the efficacy and safety of tirofiban treatment combined with percutaneous coronary intervention (PCI) in the elderly with acute ST segment elevation myocardial infarction prospectively. Methods From May 2008 to May 2010, 106 patients who presented with acute STEMI within 12 hours from onset and received successful primary PCI were enrolled into the study. All patients had angiographic evidence of initial total occlusion of infarct-related artery and finally restored toTIMI3 flow after PCI. All patients were divided into tirofiban group (n = 54) and control group (n = 52) according to whether tirofiban was used or not. Assessment of myocardial perfusion included Myocardial Blush Grades (MBG), and the resolution of the sum of ST-segment elevation (sumSTR) at 90 minutes after the procedure. Left ventricular ejection fraction (EF) was measured one week later. Major adverse cardiac events in hospital and bleeding complications were also assessed. Results Baseline clinical and angiographic characteristics of the two groups were similar. Significant higher rates of MBG 3 were observed in the tirofiban group (88. 9% vs57. 7%, P ＜ 0.05). Patients received tirofiban were more likely to achieve higher sumSTR (70. 3% vs 42. 3%, P ＜0. 05). Ejection fraction was also markedly increased in tirofiban group than control group (56. 2 ± 7.6 vs 46. 7 ± 8. 5, P ＜ 0. 05). In-hospital major adverse cardiac events, it was not different between the two groups(P ＞0. 05). There were slightly more minor bleeding complications in tirofiban group compared with control(11.1% vs 6. 0%, P ＞0. 05). No patient had major bleeding or thrombocytopenia.Conclusions Tirofiban can further ameliorate microvascular perfusion and it is safe and feasible for patients with STEMI undergoing primary PCI.
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Objective To evaluate the clinical significance of antiplatelet antibody in patients with systemic lupus erythematosus complicated with thrombocytopenia.Methods Antiplatelet antibody (anti-GP Ⅱb/Ⅲa antibody, anti-GP Ⅰb/Ⅸ antibody, anti-GP Ⅰa/Ⅱ a antibody, anti-GP Ⅳ antibody) were detected by modified antigen capture ELISA. The positive rate of antiplatelet antibody between SLE complicated with thrombocytopenia group and without thrombocytopenia group before therapy were compared,and the positive rate of antiplatelet antibody before therapy and after therapy in SLE complicated with thrombocytopenia were compared,and the relevance between antiplatelet antibody and conditions in SLE complicated with thrombocytopenia were analyzed. Rank test and Chi square test were used for statistical analysis. Results The positive rate of anti-GP Ⅱb/Ⅲa antibody and anti-GP Ⅰb/Ⅸ antibody in SLE complicated with thrombocytopenia group before therapy was 50% and 67% respectively, however,the positive rate in SLE without thrombocytopenia group before therapy was 11% and 28% respectively,there was significant difference between the two groups (P＜0.05) and the positive rate of anti-GP Ⅱb/Ⅲa antibody and anti-GP Ⅰb/Ⅸ antibody in SLE complicated with thrombocytopenia group after therapy was 6% and 28% respectively, which was significantly lower than those before therapy (P＜0.05). In SLE complicated with thrombocytopenia group before therapy, there was significant relevance between anti-GP Ⅱb/Ⅲ a antibody and anti-GP[b/Ⅸ antibody, and there was significant relevance between these two antibodies and SLEDAI score,but no significant relevance between these two antibodies and ANA,dsDNA, ANCA. Neither anti-GPⅣ antibody nor anti-GP Ⅰ a/Ⅱ a antibody was detected in patients of this study. Conclusion The positive rate of antiplatelet antibody (anti-GP Ⅱb/Ⅲ a antibody, anti-GP Ⅰb/Ⅸ antibody) is significantly higher in patients with active systemic lupus erythematosus complicated with thrombocytopenia,and these two antibodies are significantly associated with clinical outcomes.
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Objective To investigate the differences of platelet membrane glycoprotein PAC-1 and CD62P expression in patients with cerebral small vessel disease and its subtype and large artery atherosclerotic stroke and to compare the traditional platelet activation markers and inflammatory chemokine platelet factor 4(PF4).Methods Peripheral blood platelet PAC-1,CD62P positive rates and serum PF4 concentration in 30 patients with large artery atherosclerotic stroke,45 patients with cerebral small vessel disease and 30 controls were detected using flow cytometry and enzyme-linked immunosorbent assay.The differences between the groups were compared.Results The PAC-1,CD62P positive rates and serum PF4 concentration in the large artery atherosclerotic stroke group were 63.21% ± 9.78%,55.91% ± 8.17%,and 30.55 ± 15.56 ng/ml,respectively.They were significantly higher than 40.65% ± 17.42%,36.49% ± 14.60%,and 12.59 ±5.57 ng/mlin the cerebral small vessel disease group(all P=0.000),and the latter was still higher than 13.55% ± 3.14%,9.00% ± 2.32%,and 4.95 ±2.82 ng/ml in the control group(all P = 0.000).There were significant differences in all the subtypes groups of cerebral small vessel disease between the PAC-1,CD62P positive rates and serum PF4 concentration.The leukoaraiosis with lacunar infarction group(n = 15;47.72% ±15.52%,43.75% ± 12.54%,and 13.96 ± 5.23 ng/ml)and the simple lacunar infarction group (n = 15;49.87% ± 14.65%,43.98% ± 10.55%,and 14.41 ± 5.53 ng/ml)was significantly higher than the simple lacmar infarction group(n = 15;24.44% ± 8.45%,21.74% ± 7.19%,and 9.40 ±4.99 ng/ml)(P =0.000,0.000,and 0.013,respectively).There was no significant difference between the forrner 2 groups(P = 0.658,0.952,and 0.858,respectively).The peripheral blood platelet PAC-1 positive rate had significant correlation with CD62P positive rate in patients with ischemic cerebral disease(r= 0.964,P= 0.000),and the serum PF4 concentration showed linier correlation with the PAC-1(r =0.846,P =0.000)and CD62P(r =0.857,P =0.000)positive rates.Conelusions The platelet membrane glycoprotein PAC-1 and CD62P expression showed linear correlation,and they were consistent with the changes of PF4 concentration.This sugested that platelet activation and its mediated inflammatory mechanisms played an important pathophysiological role in the processes of atherosclerosis and thrombosis.This mechanism had significant difference between the different lesion types.
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Objective To investigate the effects and the mechanism of tirofiban administration in myocardial ischemical reperfusion injury(MIRI) in patients with acute myocardial infarction(AMI) undergoing primary percutaneous coronary intervention(PCI). Method The study included 158 STEMI Patients who accepted primary PCI therapy and were randomly (random number) divided into two groups: tirofiban administration group and control group. Incidence of MIRI during PCI, Correct TIMI frame count(CTFC), ST segment resolution(STR), peak value and peak time of MB isoenzyme of creatine kinase( CK-MB), and incidence of major adverse cardiac events (MACE) during 30 days postoperation in both groups were measured. Results Tirofiban administration group was superior to control group in terms of incidence of MIRI, CTFC, STR, peak value and peak time of CK-MB, and incidence of MACE during 30 days postoperation (P < 0.05). Multiple factor logistic regression analysis indicated that intravenous tirofiban administration before primary PCI was the independently protective factor for MIRI. Conclusions Intravenous tirofiban administration in patients with STEMI before primary PCI can significantly decrease the incidence of MIRI,reduce myocardial damage and improve the prognosis.
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To investigate the role of platelet membrane glycoprotein (GP) Ib/Ⅸ/Ⅴ complex and its subunit GP Ibа in patients with hemorrhagic thrombopathy (HT), the expressions of GP lb/Ⅸ/Ⅴ complex and GP Ibа, defined as mean fluorescence intensity (MFI), were assessed by flow cytometry.The maximum aggregation of platelet was determined by turbidity method. These indicators were compared among 68 HT patients with the presenting complaint of hemorrhage, 33 well-controlled HT patients and 32 normal healthy subjects. The results showed that the MFI of GP lblIX/V complex and GP Ibct was markedly lower in HT patients with current hemorrhage than that in the healthy subjects, with difference being statistically significant (P<0.05). There was no significant difference in the expressions of GP lb/Ⅸ/Ⅴ complex and GP lbа between well-controlled HT patients and normal healthy subjects (P>0.05). It was concluded that the expression of GP Ib/Ⅸ/Ⅴ complex, the receptor of thrombin and yon Willebrand factor, was down-regulated in HT patients with current hemorrhage,which might result in the dysfunction of platelet aggregation and recurrence of HT.
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Objeetive To explore change of platelet glycoproteins Ⅵ(GPⅥ)in patients with type 2 diabetes mellitus and its clinical significance.Methods The surface expression of platelet glycoprotein Ⅵ was determined by flow cytometry in 56 patients with type 2 diabetes mellitus and 61 normal individuals.Plasma GP Ⅵ concentration was measured by ELISA in 30 patients with type 2 diabetes mellitus.Platelet surface CD62P was analyzed by flow cytometry and HbA1c was determined in Datients with type 2 diabetes mellitus.Results The geometric mean fluorescence of platelet surface GPⅥ in Datients with type 2 diabetes mellitus was 93.66±35.24,which was significantly enhanced compared with normal subjects (62.83±24.2)(t=-4.927,P＜0.05).Nine patients were positive in plasma GPⅥ among 30 Datients with type 2 diabetes mellitus.Plasma GP Ⅵ concentrations in 9 positive patients were conversely correlated with platelet surface GPⅥ expression(r=-0.633,P＜0.05).However,there was no correlation between platelet Surface CD62P and plasma HbA1c concentrations, and the correlation coemcient is -0.333 and -0.417,respectively(P＞0.05).There was no correlation between platelet surface GP Ⅵ expression with C062P and HbA1c in patients with type 2 diabetes mellitus and the conrrelation coefficient is -0.009 and -0.217,respectively(P＞0.05).Conclusions GPⅥ expression on platelet surface is elevated in Datients with type 2 diabetes mellitus and the determination of platelet surface GPⅥ and plasma GPⅥ concennlation may helP to prognosticate the risk of thrombotic events and may play an important role in evaluating platelet activation in patients with type 2 diabetes mellitus.
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Objective To discuss the role of platelet-actived factors and hepatic and renal function in the development of pre-eclampsia and eclampsia by detecting the levels of the GP Ⅱb/Ⅲa in the blood, Pt and hepatic and renal function of the patients with pre-eclampsia and eclampsia. Method GP Ⅱb/Ⅲa, Pt and hepatic and renal function were measured in the normal non-pregnancy women, normal late-pregnancy women and pre-eclampsia and eclampsia women. Results The level of GP Ⅱb/Ⅲa in patients with severe pre-eclampsia and eclampsia was higher than that in non-pregnancy, normal late-pregnancy and mild pre-eclampsia (P<0.01). The count of Pt in patients with severe pre-eclampsia and eclampsia was lower than that in non-pregnancy, normal late-pregnancy and mild pre-eclampsia (P<0.01). Except ALB, the hepatic and renal function had significant difference among severe pre-eclampsia and eclampsia, normal late-pregnancy and mild pre-eclampsia. Conclusion Detecting the GP Ⅱb/Ⅲa, Pt and hepatic and renal function have clinical significance in severe pre-eclampsia and eclampsia.
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RACIONAL: A lesão de isquemia e reperfusão hepática é um evento comum e responsável por considerável morbidade e mortalidade. OBJETIVO: Avaliar efeitos de inibidor da glicoproteína IIb/IIIa, cloridrato de tirofiban, nas alterações hepáticas e pulmonares da lesão de isquemia e reperfusão de fígado de ratos. MÉTODO: Vinte e três ratos Wistar divididos em três grupos: laparotomia (n = 6), isquemia e reperfusão que receberam solução fisiológica (n = 8), e submetidos a isquemia e reperfusão e tratados com o cloridrato de tirofiban (n = 9). Foram realizadas dosagens das aminotransferases e análise histológica hepática. Avaliação pulmonar foi realizada pelo teste do azul de Evans e pela dosagem tecidual da mieloperoxidase no parênquima pulmonar. A oxidação e fosforilação mitocondrial das células hepáticas também foram avaliadas. RESULTADOS: O grupo tratado com cloridrato de tirofiban apresentou menores níveis de aminotransferases, assim como alterações histológicas menos intensas. Avaliação pulmonar demonstrou diminuição no teste de azul de Evans no grupo tratado com cloridrato de tirofiban. Grupo tratado com cloridrato de tirofiban apresentou aumento significativo do estado 3 da respiração mitocondrial e das relações adenosina difosfato utilizado para fosforilação sobre o oxigênio consumido na reação e de coeficiente respiratório. CONCLUSÕES: O uso do cloridrato de tirofiban exerceu papel protetor da lesão hepática de isquemia e reperfusão e impediu o aumento da permeabilidade vascular secundária à lesão de reperfusão hepática.
BACKGROUND Hepatic ischemia-reperfusion injury is responsible for a considerable morbidity and mortality. Aim - To evaluate the effect of a platelet glycoprotein IIb/IIIa receptor inhibitor (tirofiban) on hepatic and pulmonary disturbances associated with hepatic ischemia-reperfusion injury. METHODS: Twenty-three Wistar rats divided in three groups: rats sham-operated (n = 6), rats submitted to ischemia-reperfusion that received saline solution (n = 8), and rats submitted to ischemia-reperfusion treated with 0.7 mg/kg of tirofiban (n = 9). Serum aminotransferases (AST and ALT) were also determined, and the study of hepatic tissue histology was carried out. The evaluation of the pulmonary disturbances was done using the Evans blue test and the tissular determination of myeloperoxidase. Hepatic mitochondrial oxidation and phosphorylation were also measured. RESULTS: There was an increase in the state 3 respiration, ADP/O ratio and respiration control rate in the group treated with tirofiban. This group had also lower levels of aminotransferases and the histological findings were significantly less intense. Pulmonary evaluation demonstrated decrease of the Evans blue test in the tirofiban group and an increase of its tissular determination of myeloperoxidase. CONCLUSION: The inhibition of glycoprotein IIb/IIIa receptor with tirofiban protected the hepatic disturbances and prevented the increase of pulmonary vascular permeability secondary to the ischemia-reperfusion injury of the liver.
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Animales , Ratas , Hígado/irrigación sanguínea , Pulmón/irrigación sanguínea , Inhibidores de Agregación Plaquetaria/uso terapéutico , Complejo GPIIb-IIIa de Glicoproteína Plaquetaria/antagonistas & inhibidores , Daño por Reperfusión/prevención & control , Tirosina/análogos & derivados , Permeabilidad Capilar/efectos de los fármacos , Modelos Animales de Enfermedad , Hígado/patología , Pulmón/patología , Mitocondrias Hepáticas/metabolismo , Mitocondrias Hepáticas/patología , Oxidación-Reducción , Peroxidasa/análisis , Ratas Wistar , Transaminasas/sangre , Tirosina/uso terapéuticoRESUMEN
@#Objective To explore the effect of aerobic exercise on platelet function in elderly patients with hypertension and type 2 diabetes.Methods81 elderly patients with hypertension and type 2 diabetes were divided into the routine treatment group (group A, n=41) and regular exercise group (group B, n=40). All patients of two groups were treated with routine treatment. The exercise with moderate intensity was performed in the group B for 3 months besides routine treatment. The platelet membrane glycoprotein CD62P, CD61 (Ⅲa) were detected by flow cytometric analysis and platelet aggregating ratio was measured before and after regular aerobic exercise.ResultsAfter three months, the systolic blood pressures were 166±3.6 mm Hg (group A) and 152±3.5 mm Hg (group B); the diastolic blood pressures were 93±4.2 mm Hg (group A) and 83±4.3 mm Hg (group B); the contents of blood glucose were 7.4±2.4 mmol/L (group A) and 6.3±1.9 mmol/L (group B); the positive percents of platelet membrane glycoproten CD62P were 27.3±2.2% (group A) and 21.5±3.3% (group B), CD61(Ⅲa) were 26.3±2.3% (group A) and 20.2±2.9% (group B) and platelet aggregation rates were 78.4±4.5% (group A) and 69.7±5.4% (group B), there was a significant difference between two groups ( P<0.05～0.01).ConclusionRegular aerobic exercise can decrease the positive percent of platelet membrane glycoprotein and platelet aggregation rate in elderly patients with hypertension and type 2 diabetes.
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Objective To investigate the change of platelet membrane glucoprotein CD62p,CD63 expression and platelet aggregation function in diabetes mellitus patients with retinopathy. Me-thods Platelet membrane glucoprotein CD62p and CD63 expression were analyzed by flow cytometry(FCM)and their adenosine diphosphate (ADP)-induced platelet aggregation function was determined in diabetes mellitus patients with retinopathy,and compared with those of diabetes mellitus patients without vascular disease,and normal controls.Results The positive rates of CD62p,CD63 and the rate of platelet aggregation function in diabetes mellitus patients with retinopathy were(8.74?3.01),( 9.38?3.25)and(58.9?9.7),significantly higher than those in normal controls 2.89?1.72(P
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Platelet membrane receptor glycoproteins (GP) are essential for the platelet activation process, and the genetic polymorphisms in the genes that encode platelet glycoproteins have been proposed to influence the risk of acute coronary syndrome and atherosclerosis. In this study, we investigated the role of GPIa, HPA-1 and HPA-3 polymorphisms as putative risk factors for myocardial infarction (MI) and the extent of coronary artery disease. We selected 1, 073 subjects who underwent coronary angiography; 242 had normal or minimal coronary atherosclerosis, and 831 patients had significant coronary artery disease (CAD). The genotype was determined by the methods of single base extension for C807T/G873A polymorphisms of GPIa, and restriction fragment length polymorphism for HPA-1 and HPA-3. The C807T and G873A polymorphisms of GPIa showed complete linkage in the Korean population. For HPA-1 gene polymorphism, only the HPA-1a/a (PlA1/A1) genotype was observed in 192 selected subjects from our study population. The distribution of GPIa (C807T/G873A) and HPA-3 genotypes did not differ significantly between normal subjects and CAD subjects. No significant association between MI and both gene polymorphisms was present. However, for the subgroup analysis of young male patients whose age was less than 56 years, the genotype frequency of HPA-3b/b was significantly lower in patients with MI compared to patients without a history of MI (7.5% vs. 20.0%, p=0.04). The odds ratio for HPA-3 b homozygosity versus the HPA-3a carrier was 0.32 (95% CI, 0.10- 0.99, p=0.04). Conclusively, HPA-3 polymorphism was associated with MI in Korean individuals younger than 56 years of age, but other polymorphisms of GP, which we studied, were not associated with both the extent of coronary atherosclerosis or MI.
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Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Enfermedad de la Arteria Coronaria/epidemiología , Frecuencia de los Genes , Predisposición Genética a la Enfermedad/epidemiología , Genotipo , Integrina alfa2/genética , Integrina beta3/genética , Corea (Geográfico) , Infarto del Miocardio/epidemiología , Glicoproteína IIb de Membrana Plaquetaria/genética , Polimorfismo Genético , Factores de RiesgoRESUMEN
Objective To investigate the expression and clinical value of platelet membrane glycoproteins CD 62p ,CD 63 in patients with type 2 diabetes mellitus (DM).Methods The levels of CD 62p ,CD 63 were measured by FCM in 64 cases of type 2 DM (31 cases with microangiopathy,33 cases without microangiopathy) and 30 normal individuals.Serial measurements were carried out in 16 patients before and after treatment.Results The levels of CD 62p ,CD 63 in type 2 DM were significantly higher than those in controls (P