Arner A, Bialojan C, Brückner U B, Frost-Arner L, Messmer K, Rüegg J C
Department of Physiology II, University of Heidelberg, Germany.
Pflugers Arch. 1993 Oct;425(1-2):82-9. doi: 10.1007/BF00374507.
The influence of prolonged ischaemia on the regulation of contraction in the myocardium and in the smooth muscle of coronary arteries was investigated. Chemically skinned preparations were used which enabled the contraction to be studied with the environment of the contractile filaments controlled. Myocardial ischaemia was produced in anesthetized adult beagle dogs by occlusion of the left anterior descending artery for 3 h and followed by 30 min reperfusion. Myocardial tissue and segments from coronary arteries were obtained from the ischaemic infarcted wall region ("in vivo ischaemic") and compared with control preparations from perfused coronary arteries and from the free wall of the left ventricle. Coronary and myocardial preparations were also obtained from the heart after a 3 h period in vitro under anoxic conditions at 37 degrees C ("in vitro ischaemic") simulating a state of extreme ischaemia. Control myocardial fibres were fully relaxed at pCa (-log-[Ca2+]) 9 and developed 24 +/- 5% (n = 7) of maximum force at intermediate calcium concentration (pCa 5.5). In contrast, the in vivo and in vitro ischaemic preparations produced force at pCa 9 (28 +/- 13 and 39 +/- 8%, respectively, n = 5 and 7) and showed an increased force development at pCa 5.5 (53 +/- 11 and 75 +/- 5%). The in vivo and in vitro ischaemic coronary arteries relaxed more slowly following calcium removal than control vessels. The in vitro ischaemic vascular preparations developed active force at pCa 9 and showed increased levels of myosin light chain phosphorylation and reduced phosphatase activity.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了长时间缺血对心肌和冠状动脉平滑肌收缩调节的影响。使用化学去膜制剂，使得能够在收缩细丝环境可控的情况下研究收缩。通过结扎成年麻醉比格犬的左前降支动脉3小时，随后再灌注30分钟来产生心肌缺血。从缺血梗死壁区域（“体内缺血”）获取心肌组织和冠状动脉节段，并与来自灌注冠状动脉和左心室游离壁的对照制剂进行比较。还从在37℃缺氧条件下体外培养3小时后的心脏获取冠状动脉和心肌制剂（“体外缺血”），模拟极端缺血状态。对照心肌纤维在pCa（-log-[Ca2+]）9时完全松弛，在中等钙浓度（pCa 5.5）时产生最大力的24±5%（n = 7）。相比之下，体内和体外缺血制剂在pCa 9时产生力（分别为28±13%和39±8%，n = 5和7），并且在pCa 5.5时显示出更大的力产生（53±11%和75±5%）。体内和体外缺血的冠状动脉在去除钙后比对照血管松弛得更慢。体外缺血的血管制剂在pCa 9时产生主动力，并且显示出肌球蛋白轻链磷酸化水平增加和磷酸酶活性降低。（摘要截短为250字）
