Shanlin R J, Sole M J, Rahimifar M, Tator C H, Factor S M
Department of Physiology, University of Toronto, Ontario, Canada.
J Am Coll Cardiol. 1988 Sep;12(3):727-36. doi: 10.1016/s0735-1097(88)80065-2.
Intracranial pressure was increased in 59 rats by inflating a subdural balloon to a total mass volume of 0.3 ml. The increase in intracranial pressure ranged from 75 to greater than 500 mm Hg. With few exceptions, mean arterial pressure increased to as high as 227 mm Hg during the increase in intracranial pressure. Significant increases in plasma catecholamines, major electrocardiographic changes and a considerably shortened survival time were observed only in the rats that demonstrated an increase in mean arterial pressure greater than 50 mm Hg. A perfusion study with liquid silicone rubber (Microfil) revealed dilated irregular myocardial vessels with areas of focal constriction consistent with microvascular spasm. Histologic examination of the myocardium revealed widespread patches of contraction band necrosis and occasional contraction bands in the smooth muscle media of large coronary arteries. These observations suggest that myocardial damage after suddenly increased intracranial pressure resulted both from exposure to toxic levels of catecholamines and from myocardial reperfusion. Extension of these studies to humans suggests that a detailed assessment of myocardial function should be performed in victims of severe brain injury. Myocardial dysfunction may be a major determinant of the patient's prognosis or may render the heart unsuitable for transplantation.
通过向硬膜下气囊充气至总体积0.3 ml，使59只大鼠颅内压升高。颅内压升高范围为75至大于500 mmHg。除少数例外，颅内压升高期间平均动脉压升高至高达227 mmHg。仅在平均动脉压升高大于50 mmHg的大鼠中观察到血浆儿茶酚胺显著增加、主要心电图改变和生存时间显著缩短。用液态硅橡胶（Microfil）进行的灌注研究显示心肌血管扩张且不规则，有局灶性狭窄区域，符合微血管痉挛。心肌组织学检查显示广泛的收缩带坏死斑以及大冠状动脉平滑肌中层偶尔出现的收缩带。这些观察结果表明，颅内压突然升高后的心肌损伤是由接触毒性水平的儿茶酚胺和心肌再灌注共同导致的。将这些研究扩展到人类表明，应对重度脑损伤患者进行详细的心肌功能评估。心肌功能障碍可能是患者预后的主要决定因素，或者可能使心脏不适合移植。
