Moxonidine-induced transient pressor response is mediated by both I1-imidazoline receptors and α2-adrenoceptors in anesthetized spontaneously hypertensive rats / 第二军医大学学报

Objective: Clonidine, by activating peripheral α-adrenoceptors, produces transient pressor response after i. v. injection in anesthetized animals. Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors, produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods: Female spontaneously hypertensive rats (SHRs, aged 14-16 weeks) were anesthetized with urethane. To observe the transient pressor responses, moxonidine 0. 1, 0. 3, 1. 0 mg/kg (intravenous, i. v.), 2.0 μg (intracerebroventricular, i. c. v.) and 1.0, 10.0 mg/kg (intragastric, i. g.) were administrated in different groups of rats. To evaluate the roles of α1-adrenoceptors, α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin (10.0 μg/kg), yohimbine (2.0 mg/kg), phentolamine (0.2 mg/kg), idazoxan (1.0 mg/kg) or yohimbine + idazoxan (2.0 mg/kg + 1.0 mg/kg) were intravenously given to the animals before moxonidine 0.3 mg/kg i. v.). Results: It was found that i. v. moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure. This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan, and completely blocked by the combination of yohimbine and idzaxon. Neither i. c. v. injection nor i. g. administration of moxonidine induced transient pressor responses. Conclusion: The transient pressor response of i. v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.

Complete transposition of the great arteries with severe pulmonary hypertension increses late mortality after artery switch operation / 中华胸心血管外科杂志

Objective The postoperative outcomes of transposition of the great arteries with severe pulmonary hypertension (PH) are still controversial. Based on relative large data, we evaluated the relationship between preoperative pulmonary hypertension and postoperative early and midterm clinical outcomes. Methods In this retrospective study, a cohort of consecutive patients with TGA was studied. One hundred and one patients underwent artery switch operation between February 2004 and October 2007. Preoperative medical records were reviewed. The mean follow-up period was 22.6 months. All artery switch operations were performed through a median sternotomy utilizing extracorporeal circulation. Deep hypothermia and circulatory arrest were used in 6 patients. After sternotomy, pulmonary arterial pressure was measured directly. According preoperative mean pulmonary pressure ( mPAP), patients were divided into three groups: normal group ( mPAP ＜25mmHg, n =43), moderate PH group ( mPAP between 25 to 50mmHg, n = 47) and severe PH group ( mPAP ≥50mmHg, n = 11 ). The methods of coronary anastomosis were "open trap door" ( 39 cases), "bay window" (61 cases) and "pulmonary artery tunnel" ( 1 case)techniques. Besides repairing of atrial septal defect and ventricular septal defect, ligation of patent ductus arteriosus, concomitsnt operations also involved mitral valvuloplasty (5 patients), tricuspid valvuloplasty (2 patients), pulmonary valvuloplasty (5 patients), pulmonary artery transplantation ( 1 patient ), subvalvular membrane resection ( 2 patients), widening of the right ventricular outflow tract ( 1 patient ) and collateral circulation occlusion ( 1 patient). The early and late postoperative results were compared among different groups. Results After operation, mPAP in severe PH group decreased from (61.2 ± 8.6 ) mmHg to ( 34.6 ± 13.6 ) mmHg( P ＜ 0.01 ). In moderate PH group it decreased from ( 34.5 ± 6.7 ) mmHg to ( 21.3 ± 5.6) mmHg( P ＜ 0.0l ). mPAP was not significantly changed in the control group. Operative mortality was 7.9% ( 8 patients ).The causes of early death were low output syndrome in 3 patients, septicemia in 4, central nervous system complications in 1.There was no difference in the postoperative complication rates among three groups. Also, no significant differences were found between groups regarding the early operative mortality (control group: 7.0%, moderate PH group: 8.5%, severe PH group:9.1%, P = 0.953 ). Combined abnormity contributed to postoperative death. Patients with ventricular septal defect and patent ductus arteriosus had a higher mortality rate. During follow-up 8 patients died: 5 in control group ( 11.6% ), 5 in moderate PH group ( 10.6% ) and 6 in severe PH group (54.5% ), P ＜ 0.01. Causes of midterm death were sudden death in 10, progressive heart failure in 4, pneumonia in 2. The rates of midterm mortality of the three groups were significantly different ( 11.6%,10.6% and 54.5% for control, moderate PH and severe PH group, respectively, P = 0.001 ). Kaplan-Meier survival analysis for patients with different age groups showed that survival rate in group with age older than 1 year was lower ( P = 0.029 ).Conclusion In TGA/PH patients, mPAP lower than 50 mmHg is suitable for artery switch operation and can get satisfying postoperative outcomes. If mPAP higher than 50 mmHg, even though the operation may decrease the pulmonary pressure, radical artery switch operation should not be recommended because of higher late mortality.

Renin gene polymorphisms and hypertension / 国际脑血管病杂志

With the constant deepening of the study in the genetic factors of eardio-cerebrovascular diseases, the relation between the renin-angiotensin system (RAS) gene polymorphisms and hypertension is increasingly receiving attention. As an important component of RAS, renin has received much concern in the genetic research of cardio-cerebrovascular diseases and its gene polymorphisrns have become the candidate genes of hypertension, coronary heart disease and stroke, etc.

Moxonidine-induced transient pressor response is mediated by both I1-imidazoline receptors and α2-adrenoceptors in anesthetized spontaneously hypertensive rats / 第二军医大学学报

Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.

Moxonidine-induced transient pressor response is mediated by both I1-imidazoline receptors and α2-adrenoceptors in anesthetized spontaneously hypertensive rats / 第二军医大学学报

Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.

Moxonidine-induced transient pressor response is mediated by both I1-imidazoline receptors and α2-adrenoceptors in anesthetized spontaneously hypertensive rats / 第二军医大学学报

Objective:Clonidine,by activating peripheral α-sbrenoceptors, produces transient pressor response after i.v.injection in anesthetized animals.Moxonidine, with at least 40-fold higher affinity to I1-imidazoline receptors than to α2-adrenoceptors,produces also a transient pressor response. This work was designed to investigate whether I1-imidazoline receptors are involved in this pressor effect of moxonidine. Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks)were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0mg/kg(intravenous,i.v),2.0μg(intracerebroventricular,i.c.v.)and 1.0,10.0mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of α1-adrenoceptors,α2-adrenoceptors and I1-imidazoline receptors in the transient pressor responses to moxonidine, prazosin(10.0μg/kg),yohimbine(2.0mg/kg),phentolamine(0.2mg/kg),idazoxan(1.0mg/kg)or yohimbine+idazoxan(2.0mg/kg+1.0mg/kg)were intravenously given to the animals before moxonidine 0.3mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin, but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g. administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v. moxonidine is mediated by both peripheral I1-imidazoline receptors and α2-adrenoceptors.

CT and MRI Appearances of Eclamptic Encephalopathy in Plateau / 实用放射学杂志

Objective To study CT and MRI findings of the eclamptic encephalopathy in plateau.Methods CT and MRI findings in 28 patients in plateau with eclamptic encephalopathy were retrospectively analyzed.Results CT and MRI appearances of eclamptism were as follow:normal in brain in 3 cases;cerebral edema in 18 cases,including slight encephaledema in 2 cases,focal encephaledema in 11 cases and diffuse encephaledema in 5 cases;cerebral hemorrhage in 6 cases and sinovenous thrombosis in 1 case.Conclusion CT and MRI scan are of significant value in diagnosis and treatment of eclamptic encephalopathy in plateau.

Moxonidine-induced transient pressor response is mediated by both I_1-imidazoline receptors and?_2-adrenoceptors in anesthetized spontaneously hypertensive rats / 第二军医大学学报

Objective:Clonidine,by activating peripheral?-adrenoceptors,produces transient pressor response after i.v. injection in anesthetized animals.Moxonidine,with at least 40-fold higher affinity to I_1-imidazoline receptors than to?_2-adreno- ceptors,produces also a transient pressor response.This work was designed to investigate whether I_1-imidazoline receptors are involved in this pressor effect of moxonidine.Methods:Female spontaneously hypertensive rats(SHRs,aged 14-16 weeks) were anesthetized with urethane.To observe the transient pressor responses,moxonidine 0.1,0.3,1.0 mg/kg(intravenous, i.v.),2.0?g(intracerebroventricular,i.c.v.)and 1.0,10.0 mg/kg(intragastric,i.g.)were administrated in different groups of rats.To evaluate the roles of?_1-adrenoceptors,?_2-adrenoceptors and I_1-imidazoline receptors in the transient pressor responses to moxonidine,prazosin(10.0?g/kg),yohimbine(2.0 mg/kg),phentolamine(0.2 mg/kg),idazoxan(1.0 mg/kg) or yohimbine+idazoxan(2.0 mg/kg+1.0 mg/kg)were intravenously given to the animals before moxonidine 0.3 mg/kg (i.v.).Results:It was found that i.v.moxonidine produced a greater pressor response than clonidine when producing a similar reduction of blood pressure.This effect of moxonidine was not influenced by prazosin,but was partly inhibited by yohimbine, phentolamine or idazoxan,and completely blocked by the combination of yohimbine and idzaxon.Neither i.c.v.injection nor i.g.administration of moxonidine induced transient pressor responses.Conclusion:The transient pressor response of i.v.mox- onidine is mediated by both peripheral I_1-imidazoline receptors and?_2-adrenoceptors.