Malik A B, Loegering D J, Saba T M, Kaplan J E
Circ Shock. 1978;5(1):73-84.
The changes in cardiac output (Q), regional blood blow (Qr) and regional vascular resistance, and arterial pressure were studied in rats subjected to moderate (LD0) or severe (LD50) traumatic shock. Q and Qr were determined using microspheres at 15, 60 and 180 min posttrauma. Arterial pressure decreased in both groups at 15 min and recovered by 3 hr after sublethal (LD0) trauma, while arterial pressure did not return to control levels after LD50 trauma. Q decreased in both groups at 15 min and returned to control only in the LD0 trauma group by 3 hr. Cerebral, coronary, and hepatic arterial flows and resistances were maintained in both groups. Renal, intestinal, and splenic flows decreased and resistances increased in both groups by 15 min and returned to control levels by 3 hr only in the LD0 trauma group. Total hepatic and hepatic portal flows decreased at 60 min and returned to control levels at 3 hr after LD0 trauma, while there was significant depression in these parameters 3 hr after LD50 trauma. Therefore, sublethal and severe trauma resulted in early redistribution of flow favoring the coronary, cerebral, and hepatic arterial beds. However, renal, intestinal, splenic, and portal flows remained depressed only in severely traumatized rats, suggesting that continued hypoperfusion is a factor in the multiple organ failure and death following severe traumatic injury.
对遭受中度(LD0)或重度(LD50)创伤性休克的大鼠的心输出量(Q)、局部血流量(Qr)、局部血管阻力及动脉血压变化进行了研究。在创伤后15、60和180分钟使用微球测定Q和Qr。两组大鼠在创伤后15分钟时动脉血压均下降,在亚致死性(LD0)创伤后3小时恢复,而在LD50创伤后动脉血压未恢复至对照水平。两组在创伤后15分钟时Q均下降,仅在LD0创伤组中3小时后恢复至对照水平。两组的脑、冠状动脉和肝动脉血流及阻力均得以维持。两组在创伤后15分钟时肾、肠和脾血流量均减少,阻力增加,仅在LD0创伤组中3小时后恢复至对照水平。LD0创伤后60分钟时肝总血流量和肝门静脉血流量下降,3小时后恢复至对照水平,而在LD50创伤后3小时这些参数显著降低。因此,亚致死性和重度创伤导致早期血流重新分布,有利于冠状动脉、脑动脉和肝动脉床。然而,仅在重度创伤大鼠中肾、肠、脾和门静脉血流量仍处于较低水平,这表明持续的灌注不足是严重创伤性损伤后多器官功能衰竭和死亡的一个因素。