The effect of AT1 receptor antagonist on chronic cardiac response to coronary artery ligation in rats.
The effect of AT1 receptor antagonist on chronic cardiac response to coronary artery ligation in rats.
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AT1受体拮抗剂对大鼠冠状动脉结扎慢性心脏反应的影响。
DOI：
10.1016/s0008-6363(95)00244-8
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发表时间：
1996
影响因子：
10.8
通讯作者：
Karel Rakusan
中科院分区：
文献类型：
--
作者：
T. Sladek;Jarmila Sladkova;František Kolář;F. Papoušek;N. Cicutti;B. Korecky;Karel Rakusan
目的：研究at1受体拮抗剂氯沙坦对实验性梗死后血流动力学和形态学变化的影响。方法：结扎成年雄性大鼠冠状动脉形成实验性梗死。在实验性梗塞大鼠和假手术动物中，氯沙坦治疗与未治疗的对照组进行了比较。结果：心肌梗死患者左室发育压及正、负（dP/dt）max显著降低，左室舒张末压（LVEDP）、舒张常数τ和右室收缩压（RVSP）显著升高。氯沙坦治疗可降低梗死心脏LVEDP、舒张常数τ和RVSP。梗死大鼠右心室重量显著增加；这被氯沙坦减弱了。氯沙坦治疗对梗死面积无显著影响。形态学数据显示梗死心脏毛细血管供应减少，特别是在梗死附近区域；氯沙坦治疗后下降不太明显。未治疗组近梗死区毛细血管密度由2826/mm2降至1471/mm2，而治疗组由2982/mm2降至2037/mm2。与未治疗的大鼠相比，治疗动物的肌细胞与毛细血管之比同时显著降低（0.87至0.67），这似乎表明氯沙坦治疗后形成了新的毛细血管通道。LVEDP在未治疗的动物中依赖于梗死的大小，而在治疗的动物中没有。LVEDP与毛细血管密度密切相关。结论：实验性心肌梗死大鼠心室收缩力降低、舒张时间延长、冠状动脉毛细血管密度降低，证实并扩大了以往有关该模型的报道。此外，我们发现氯沙坦治疗后血液动力学和冠状血管生成改善的证据。
Objective:The aim was to study the effect of the AT1receptor antagonist losartan on hemodynamic and morphometric changes following experimental infarction.Methods:Experimental infarction was produced in adult male rats by ligating the coronary artery. Treatment with losartan was compared to untreated controls, in rats with experimental infarction and sham-operated animals.Results:Infarcted hearts were characterized by significant decreases in left ventricular developed pressure, as well as positive and negative (dP/dt)max, whereas left ventricular end-diastolic pressure (LVEDP), relaxation constant τ and right ventricular systolic pressure (RVSP) significantly increased. Treatment with losartan decreased the LVEDP, the relaxation constant τ and RVSP in the infarcted hearts. Right ventricular weight significantly increased in rats with infarction; this was attenuated by losartan. Infarct size was not significantly influenced by losartan treatment. Morphometric data revealed decreased capillary supply in infarcted hearts, especially in regions close to infarction; the decrease was less pronounced after losartan treatment. Capillary density in near infarct region decreased from 2826/mm2to 1471/mm2in untreated animals but in the treated animals it decreased from 2982/mm2to only 2037/mm2. Simultaneous significant decrease in myocyte-to-capillary ratio in treated animals compared to untreated rats (0.87 to 0.67) seems to indicate formation of new capillary channels after losartan treatment. LVEDP was dependent on the size of infarction in untreated but not in treated animals. A close correlation between LVEDP and capillary density was found.Conclusions:Decreased ventricular contractility, prolonged relaxation and decreased coronary capillary density in rat experimental cardiac infarction confirm and amplify previous reports dealing with this experimental model. Moreover, we have found evidence of improved hemodynamics and coronary angiogenesis after losartan treatment.
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DOI：
--
发表时间：
1994
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Reddy,ST;Herschman,HR
通讯作者：
Herschman,HR
影响因子：
37.8
作者：
PFEFFER, MA;PFEFFER, JM;FINN, P
通讯作者：
FINN, P
在心力衰竭大鼠模型中，直接血管紧张素 II 阻断与转化酶抑制相比的血流动力学效应。
影响因子：
3.2
作者：
Raya,TE;Fonken,SJ;Lee,RW;Daugherty,S;Goldman,S;Wong,PC;Timmermans,PB;Morkin,E
通讯作者：
Morkin,E
血管紧张素 II 产生的新血管形成。
DOI：
--
发表时间：
1985
期刊：
The Journal of laboratory and clinical medicine
影响因子：
--
作者：
Fernandez,LA;Twickler,J;Mead,A
通讯作者：
Mead,A
影响因子：
--
作者：
PFEFFER, JM;PFEFFER, MA;BRAUNWALD, E
通讯作者：
BRAUNWALD, E