Effects of portacaval shunt and portacaval transposition on hepatocellular and hepatic reticuloendothelial cell activity in the dog.

UNLABELLED: Quantitative reduction of portal blood flow following a portacaval shunt (PCS) adversely affects hepatocyte function, but does not alter HRES activity [L. P. Edgcomb , J. A. Knol , and F. E. Eckhauser . J. Surg . Res. 33: 233, 1982]. To determine whether similar changes occur after qualitative alteration of portal blood flow, portacaval transpositions (PCT) were constructed in six conditioned mongrel dogs. Estimated hepatic blood flow (EHBF) was determined scintigraphically by the rate of hepatic uptake of a 500-microCi dose of 99mTc -sulfur colloid (Tsc). Hepatic reticuloendothelial cell (RES) phagocytic (PI) and degradative (DI) indices were calculated from the half-time blood disappearance of 131I-labeled RES test lipid emulsion, and the half-time urine appearance of free 131I, respectively. Opsonic activity (OI) was determined by gelatin latex particle agglutination and normalized to control values. Hepatocellular function was assessed by serial determinations of albumin (Alb), and pyruvic and glutamic oxaloacetic transaminases (SGPT and SGOT). All studies were performed prior to and at 3, 6, and 9 weeks following PCS or PCT. CONCLUSIONS: In the dog, neither PCS nor PCT adversely affected HRES activity. Hepatocellular function and OI remained unchanged following PCT but deteriorated significantly after PCS. Observed changes in hepatocyte function and OI following PCS suggest that hepatocellular integrity and serum opsonic activity may be interrelated.

In vitro observations of greater saphenous vein valves during pulsatile and nonpulsatile flow and following lysis.

A significant number of saphenous vein femoral-popliteal bypass graft failures have been attributed to flow abnormalities caused by venous valves. Seventy-seven greater saphenous vein valves were observed and photographed through a 0-degree choledochoscope during pulsatile and nonpulsatile flow. No valve was seen to lie flat against the vein wall. With pulsatile flow the valves were noted to close during diastole. Stasis was noted within the valve cusps. Twenty-three valves produced photographs of sufficient quality to allow measurement of the luminal obstruction caused by the valves. This valvular obstruction represented 61% +/- 12% of the total vein lumen. Fifty venous valves were lysed by five different techniques: the microscissors, the Connolly vein stripper, the Mills valvulotome, the venotomy valvulectomy of Hall, and eversion valvulectomy. The first three methods created valvular incompetence, but flaps of valve cusps were observed to disturb flow and place potentially thrombogenic surfaces within the vein lumen. Valvulectomy, whether by venotomy or eversion, removed the valve cusps satisfactorily.

Low molecular weight dextran in experimental pancreatitis: effects on pancreatic microcirculation.

UNLABELLED: Although low molecular weight (LMW) dextran has been said to decrease the lethality of experimental acute pancreatitis (AP) by reversing stasis in the pancreatic microcirculation, the actual mechanism(s) of action is unknown. This investigation was designed to measure the effects of low molecular weight dextran on pancreatic capillary flow (QCAP) and arteriovenous shunt flow (QAVS), and on pancreatic oxygen consumption (O2CP) following bile-trypsin-induced AP in dogs. Total pancreatic blood flow (QT) was measured with an electromagnetic flow probe on the superior pancreaticoduodenal artery (SPDA). QAVS was measured by liver trapping of 99mTc-albumin microspheres after SPDA injection. QCAP was calculated as QT minus QAVS. Seventeen dogs were treated with lactated Ringer's (LR) solution at 6.5 ml/kg/hr; 10 dogs were treated with LMW dextran 10% in normal saline at 1.5 ml/kg/hr plus LR at 5.0 ml/kg/hr. Mean arterial and central venous pressures remained constant throughout the 4-hr experiment. In the dogs receiving LR only, QT decreased from 42.7 to 24.4 ml/min (P less than 0.001); QAVS remained constant at 1.35 +/- 0.04 ml/min. During the first 30 min O2CP decreased from 1.17 to 0.76 ml O2/min (P less than 0.05) and remained constant thereafter. LMW dextran treatment altered none of these hemodynamic or metabolic parameters significantly. CONCLUSIONS: bile trypsin AP in the dog causes significant decreases in QT and QCAP without altering QAVS. The decrease in O2CP in association with a constant QAVS suggests a metabolic block to oxygen uptake at the cellular level. Continuous infusion of LMW dextran at a dose of 1.5 ml/kg/hr in the dog does not reverse these abnormalities.

Parastomal ileal conduit hemorrhage and portal hypertension.

An analysis of six cases of parastomal ileal conduit hemorrhage in patients with portal hypertension is presented. The presence of coexisting esophageal varices, documented in only one of six cases (17%), suggest preferential retrograde portal flow through mesenteric venous (as opposed to coronary-azygos) collateral channels. Venous phase mesenteric angiography offers the best diagnostic specificity and provides inferential evidence regarding overall liver blood flow. Operative therapy should be based on assessment and understanding of the splanchnic circulatory derangements which accompany intrahepatic portal obstruction.