Hepatic arterial and portal flow in cardiogenic and hemorrhagic shock in awake dogs.

The changes in liver blood flow produced by experimental cardiogenic and hemorrhagic shock are relatively unexplored. Fifteen unanesthetized dogs in which electromagnetic blood flow transducers had been implanted on the common hepatic artery and portal vein were subjected to acute myocardial infarction by mercury embolization of the circumflex coronary artery. Another group of ten dogs were bled to an arterial pressure of 40 mmHg and maintained at that level for 2 hours before reinfusion. Six additional dogs in which blood flow transducers had been implanted on the superior mesenteric artery and portal vein also were subjected to hemorrhage. In three of the six, phenoxybenzamine was infused directly into the superior mesenteric artery 45 minutes prior to bleed-out. During cardiogenic shock, both hepatic arterial and protal venous flow fell. However, whereas protal flow continued to fall, eventually stabilizing at values 36 +/- 3% of control, hepatic arterial flow subsequently rose, reaching values 93 +/- 9% above control. Total liver blood flow, after an initial decline to 53 +/- 4% of control levels rose as a result of the increased hepatic arterial flow to 73 +/- 4% of control values. During hemorrhage, both hepatic arterial and protal venous flows decreased as aortic pressure fell. Within 5 minutes of reinfusion, hepatic arterial flow surpassed its control values. Portal flow also increased but, on a percentage basis, not to so great an extent. Flow in hepatic artery remained high for 40 minutes after reinfusion, whereas portal flow rapidly decreased to levels seen at the end of hemorrhage. In hemorrhage without alpha-adrenergic receptor blockade the superior mesenteric bed constricted, thereby supporting systemic pressure. With alpha-adrenergic blockade, however, mesenteric flow became pressure-dependent and no longer acted as a homeostatic mechanism.