Zaroff J G, Rordorf G A, Titus J S, Newell J B, Nowak N J, Torchiana D F, Aretz H T, Picard M H, Macdonald R L
Cardiac Units, Massachusetts General Hospital and Harvard Medical School, Boston, Ma 02114, USA.
Stroke. 2000 May;31(5):1136-43. doi: 10.1161/01.str.31.5.1136.
The pathophysiology of cardiac injury after subarachnoid hemorrhage (SAH) remains controversial. Data from animal models suggest that catecholamine-mediated injury is the most likely cause of cardiac injury after SAH. However, researchers also have proposed myocardial ischemia to be the underlying cause, as a result of coronary artery disease, coronary artery spasm, or hypertension and tachycardia. To test the hypothesis that SAH-induced cardiac injury occurs in the absence of myocardial hypoperfusion, we developed an experimental canine model that reproduces the clinical and pathological cardiac lesions of SAH and defines the epicardial and microvascular coronary circulation.
Serial ECG, hemodynamic measurements, coronary angiography, regional myocardial blood flow measurements by radiolabeled microspheres, 2D echocardiography, and myocardial contrast echocardiography were performed in 9 dogs with experimental SAH and 5 controls.
Regional wall motion abnormalities were identified in 8 of 9 SAH dogs and 1 of 5 controls (Fisher's Exact Test, P=0.02) but no evidence was seen of coronary artery disease or spasm by coronary angiography and of significant myocardial hypoperfusion by either regional myocardial blood flow or myocardial contrast echocardiography.
In this experimental model of SAH, a unique form of regional left ventricular dysfunction occurs in the absence of myocardial hypoperfusion. Future studies are justified to determine the cause of cardiac injury after SAH.
蛛网膜下腔出血（SAH）后心脏损伤的病理生理学仍存在争议。动物模型数据表明，儿茶酚胺介导的损伤是SAH后心脏损伤最可能的原因。然而，研究人员也提出心肌缺血是潜在原因，这是由于冠状动脉疾病、冠状动脉痉挛或高血压及心动过速所致。为了验证SAH诱导的心脏损伤在无心肌灌注不足的情况下发生这一假设，我们建立了一种实验犬模型，该模型可再现SAH的临床和病理心脏病变，并确定心外膜和微血管冠状动脉循环。
对9只患有实验性SAH的犬和5只对照犬进行连续心电图、血流动力学测量、冠状动脉造影、用放射性微球测量局部心肌血流量、二维超声心动图和心肌对比超声心动图检查。
9只SAH犬中有8只和5只对照犬中有1只出现局部室壁运动异常（Fisher精确检验，P = 0.02），但冠状动脉造影未发现冠状动脉疾病或痉挛的证据，局部心肌血流量或心肌对比超声心动图也未发现明显的心肌灌注不足。
在这个SAH实验模型中，在无心肌灌注不足的情况下出现了一种独特形式的局部左心室功能障碍。有必要进行进一步研究以确定SAH后心脏损伤的原因。
