Effect of stress adaptation on cyclic nucleotide content in myocardial tissue during acute ischemia/reperfusion

We studied the effect of adaptation to chronic immobilization stress on the contents of cyclic adenosine monophosphate and cyclic guanosine monophosphate in myocardial tissue during coronary occlusion and reperfusion. The contents of cyclic adenosine monophosphate and cyclic guanosine monophosphate in the ischemic area and nonischemic myocardium of unadapted rats increased during coronary artery ligation for 10 min. Reperfusion for 10 min was followed by an increase in the content of cyclic adenosine monophosphate. During coronary occlusion, the content of cyclic adenosine monophosphate in the myocardium of stress-adapted rats increased less significantly than in control animals. No significant differences were found in the content of cyclic guanosine monophosphate in control and adapted rats. Our results suggest that poor response of the myocardial cyclic nucleotide system to ischemia/reperfusion in adapted animals is associated with the antiarrhythmic and cardioprotective effect of adaptation. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 145, No. 5, pp. 525–528, May, 2008     

Effects of central opiate and serotoninergic structures on heart rhythm during acute myocardial ischemia

Electrostimulation of the central gray matter in the sylvian aqueduct and nucleus raphe magnus produced an antiarrhythmic effect during acute myocardial ischemia. Stimulation and blockade of opiate receptors in the central amygdaloid nucleus and lateral hypothalamus with dalargin and naloxone induced the same effect. Destruction of the central gray matter in the sylvian aqueduct and nucleus raphe magnus decreased electrical stability of ischemic myocardium.     

Effect of adaptation to stress and periodic hypoxia on cardiomyocyte resting and acting potentials in the isolated heart during ischemia and reperfusion

Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. N. A. Testemitsianu Kishinev Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. R Paleev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 12, pp. 573–575, December, 1991.     

Disturbance of mechanisms maintaining the resting potential of cardiomyocyte membranes during stress and its prevention

Central Research Laboratory, Irkutsk Medical Institute. Laboratory of Pathophysiology of the Heart, Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR N. R. Paleev.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 110, No. 10, pp. 363–365, October, 1990.     

Comparison of the effect of adaptation to stress and to high altitude hypoxia on resistance of the heart to reperfusion injury after total ischemia

Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 112, No. 7, pp. 18–20, July, 1991.     

Comparative study of activation of lipid peroxidation after electrical destruction of the myocardium and during early development of acute myocardial infraction in experiments on dogs

Professorial Surgical Department and Central Research Laboratory, I. P. Pavlov First Leningrad Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR F. G. Uglov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 6, pp. 601–603, June, 1991.     

Effect of bradykinin and morphine on sensomotor cortical neurons in rats

Acute experiments on rats showed that bradykinin, injected by microiontophoresis, activates sensomotor cortical neurons in rats. Morphine, administered in the same way, prevents the development of the bradykinin effect. Bradykinin, it is suggested, acts on opiate receptors in cerebral cortical neurons.Laboratory of Pharmacology of the Nervous System, Institute of Pharmacology, Academy of Medical Sciences of the USSR. Laboratory of Emotions and Emotional Stresses, P. K. Anokhin Institute of Normal Physiology, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov). Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 86, No. 10, pp. 450–452, October, 1978.     

急性心肌缺血时连接蛋白43降解对传导速度影响的研究

目的：探讨急性短时间缺血时心肌细胞连接蛋白43(Cx43)的降解对缺血心肌电传导速度的影响。方法：16只犬随机分为正常对照组(n=4)和缺血组(n=12), 缺血组结扎冠状动脉1h造成急性心肌缺血, 测定缺血区心肌电传导速度, 应用激光共聚焦显微镜技术和荧光免疫组织化学方法对缺血心肌Cx43含量进行定量检测。结果：(1)急性心肌缺血时Cx43迅速降解, 心肌电传导速度明显下降；(2)缺血区各局部传导速度与该部位Cx43像素密度呈明显正相关；(3)出现持久传导阻滞的区域其Cx43降解程度均大于50%。结论： 急性短时间(1 h)缺血时Cx43的降解已经开始对心肌传导速度产生明显的影响, 而局部心肌Cx43的严重降解将导致该区域出现持久传导阻滞。     

Interaction between zones of the sensomotor cortex and hypothalamus during the formation of pain stress

Cross-correlation analysis of the tension rhythm in various zones of the sensomotor cortex relative to the posterior hypothalamus showed that during pain stress there is an increase in the phase shifts accompanied by a decrease in the cross-correlation coefficients. These changes varied within the sensomotor cortex. At the focus of maximal activity for pain projections (posteriorly to the bregma) they were less marked than outside it, especially in the more anterior zones of the cortex (anteriorly to the bregma).Laboratory of General Physiology of the Central Nervous System, Institute of Normal and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician P. K. Anokhin. [deceased]). Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 78, pp. 26–27, August, 1974.     

GYY4137 protects against myocardial ischemia and reperfusion injury by attenuating oxidative stress and apoptosis in rats

Hydrogen sulfide（H₂S） is a gasotransmitter that regulates cardiovascular functions.The present study aimed to determine the protective effect of slow-releasing H₂S donor GYY4137 on myocardial ischemia and reperfusion（I/R） injury and to investigate the possible signaling mechanisms involved.Male Sprague-Dawley rats were treated with GYY4137 at 12.5 mg/（kg·day）,25 mg/（kg·day） or 50 mg/（kg·day） intraperitoneally for7 days.Then,rats were subjected to 30 minutes of left anterior descending coronary artery occlusion followed by reperfusion for 24 hours.We found that GYY4137 increased the cardiac ejection fraction and fractional shortening,reduced the ischemia area,alleviated histological injury and decreased plasma creatine kinase after myocardial I/R.Both H₂S concentration in plasma and cystathionine-γ-lyase（CSE） activity in the myocardium were enhanced in the GYY4137 treated groups.GYY4137 also decreased malondialdehyde and myeloperoxidase levels in serum,attenuated superoxide anion level and suppressed phosphorylation of mitogen activated protein kinases in the myocardium after I/R.Meanwhile,GYY4137 increased the expression of Bcl-2 but decreased the expression of Bax,caspase-3 activity and apoptosis in the myocardium.The data suggest that GYY4137 protects against myocardial ischemia and reperfusion injury by attenuating oxidative stress and apoptosis.