摘要
家兔两侧顶骨部蜘网膜下腔注入抗凝兔血,从颅内压(ICP)升高到60mmHg至140mmHg时,颈内动脉血流量(ICABFV)急剧降低,颈交感神经自发性放电频率、血浆去甲肾上腺素和肾上腺素含量、动脉血压均急剧增高,与ICP升高前比较,相差均非常显著(P<0.01)。ICP140mmHg持续2～5min随着动脉血压降低,ICABFV进一步减少,在5～20min内动物死亡。左心房、室显著扩张,肺静脉淤血,发生了严重的出血性肺水肿。ICP升高时,由股动脉抽血使动脉血压保持在ICP升高前的水平,可以防止神经源性肺水肿(NPE)的发生。实验结果提示了ICP升高使脑血液供给急剧减少,引起交感神经兴奋性增高,儿茶酚胺释放增多,从而使动脉血压急剧升高,左心负荷过重,由于血液动力性机理,导致NPE的发生。
The neurogenic pulmonary edema (NPE) was produced consistently in rabbits by raising intracranial pressure (ICP) with an infusion of anticoagulat rabbit blood into subarachnoid space of the bilateral parietal regions. When ICP increased from 60mmHg to 140 mmHg, There was a rapid decrease in blood flow volume of the bilateral internal carotid arteries (ICABFV). At the same time, the frequency of cervical sympathetic discharge and the concentrations of plasma noradrenaline and adrenaline increased acutly accompanied by a rapid elevation of systemic arterial pressure (SAP). There was a decline in SAP and a further decrease in ICABFV and the animal died as ICP was sustained at 140mmHg for 5-20min. Autopsy revealed severe hemorrhagic pulmonary edema and the left ventricular and atrial enlargement. In the period of ICP rising, the NPE was prevented if SAP was kept at the baseline levels by withdrawing blood from femoral artery, The results suggest that decreased cerebral blood supply due to ICP rising is responsible for the massive sympathetic discharge and catecholamine release which contribute to SAP elevtion and left ventricular overload, the NPE is mediated by hemodynamic mechanism.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1991年第2期117-121,共5页
Chinese Journal of Pathophysiology
关键词
肺水肿
颅内压
病理
Intracranial pressure
Pulmonary edema
Sympathetic nerves system
Catecholaamines
Blood pressure
