Friedman H S, Lowery R, Shaughnessy E, Scorza J
Proc Soc Exp Biol Med. 1983 Dec;174(3):377-82. doi: 10.3181/00379727-174-41751.
The pathophysiology of alcohol-induced acute pancreatitis is not clear. Ischemic injury has been suggested as a possible mechanism. To examine the effects of ethanol on pancreatic and splanchnic blood flow, measurements were made in fasted, conditioned awake dogs before and after iv infusion of ethanol (1.7 g/kg). At 30 min blood ethanol concentration ranged between 60 and 150 mg/dl and at 60 min between 166 and 350 mg/dl. Although cardiac output, aortic pressure, left atrial pressure, and arterial pH did not change, pancreatic flow declined by 39 +/- 12 ml/min/100 g, P less than 0.05 (from 173 +/- 10 ml/min/100 g) at 30 min and was still depressed (by 27 +/- 12 ml/min/100 g, P less than 0.05) at 60 min. Concomitantly, hepatic arterial flow increased. While hepatic and pancreatic flow changed inversely, the correlation (r = -0.17) of these changes was not significant. At comparable blood ethanol concentrations in pentobarbital-anesthetized dogs hepatic arterial flow increased by 11 +/- 3 ml/min/100 g, P less than 0.01 (from 24 +/- 5 ml/min/100 g), but pancreatic flow did not change. Thus, in the awake dog at blood levels that would produce mild to moderate alcoholic intoxication in man, ethanol reduces pancreatic flow. Although hepatic flow increases concomitantly, the relationship of these changes appears to be independent.
酒精性急性胰腺炎的病理生理学尚不清楚。缺血性损伤被认为是一种可能的机制。为了研究乙醇对胰腺和内脏血流的影响，在禁食、适应环境的清醒犬静脉输注乙醇（1.7 g/kg）前后进行了测量。30分钟时血液乙醇浓度在60至150 mg/dl之间，60分钟时在166至350 mg/dl之间。虽然心输出量、主动脉压、左心房压和动脉pH值没有变化，但胰腺血流在30分钟时下降了39±12 ml/min/100 g，P<0.05（从173±10 ml/min/100 g降至），60分钟时仍处于较低水平（下降27±12 ml/min/100 g，P<0.05）。与此同时，肝动脉血流增加。虽然肝血流和胰腺血流呈反向变化，但这些变化的相关性（r = -0.17）并不显著。在戊巴比妥麻醉的犬中，当血液乙醇浓度相当时，肝动脉血流增加了11±3 ml/min/100 g，P<0.01（从24±5 ml/min/100 g升至），但胰腺血流没有变化。因此，在清醒犬中，在人体可产生轻度至中度酒精中毒的血液水平下，乙醇会降低胰腺血流。虽然肝血流同时增加，但这些变化之间的关系似乎是独立的。
