Contribution of the liver to thoracic duct lymph flow in a motionless subject.

To ascertain the contribution of the liver to thoracic duct lymph (TDL) flow in a resting subject, afferent hepatic blood flow was temporarily interrupted in dogs by placing an atraumatic clamp across the hepatoduodenal ligament containing the hepatic artery, portal vein and 80% of hepatic lymphatic drainage. To circumvent extrahepatic splanchnic venous sequestration, a side-to-side portacaval shunt (S-S-PCS) was constructed prior to interrupting blood flow. Portal venous pressure, cervical TDL flow, and total protein content were serially monitored. TDL and total protein after S-S-PCS was comparable to that recorded in dogs without celiotomy (0.60 +/- 0.17 ml/min and 3.4 +/- 0.5g/dl, respectively). Interruption of hepatic blood flow was associated with a fall in TDL flow (0.38 +/- 0.8ml; p less than 0.001) and protein content (2.8 +/- 0.7g/dl; p less than 0.01) and TDL/plasma protein ratio (0.58 +/- 0.7 to 0.48 +/- 0.05; p less than 0.01). These data suggest that in the absence of supplemental fluid administration or other exogenous stimulation, hepatic lymph contributes one-third of resting TDL flow.

A technical modification to improve experimental production of hepatogenic ascites.

Constriction of the thoracic inferior vena cava is a useful experimental maneuver to reproduce massive ascites. Unfortunately, the margin of safety of this technique is narrow in that too much constriction overly restricts venous return with subsequent shock and death, and lesser constriction is often associated with extensive venous collateralization via the azygos system and failure to sustain hepatic congestion. By combining azygos vein ligation with 50% constriction of the supradiaphragmatic inferior vena caval circumference at the time of the initial thoracotomy, we have found that intense hepatic congestion is sustained and that dogs consistently develop massive ascites within 2-3 weeks.

Oxygen exchange in the mesenteric microcirculation of the dog.

The relationships of O2 tension in mesenteric lymph (PmlO2) and mesenteric venous blood (PmvO2) to intestinal O2 delivery/O2 consumption (DO2/VO2) were examined after graded hemorrhage (10 dogs), stepwise increments in FIO2 (4 dogs), and regional infusion of papaverine (2 mg/min or IV glucagon (25 microgram/kg) (4 dogs). Measurements included superior mesenteric arterial flow (SMA-Q), PaO2, PmlO2, and arterial and mesenteric venous blood O2 content (CaO2, CmvO2). Intestinal DO2 was calculated as the product of SMA-Q and CaO2, and VO2 was calculated from the Fick equation [SMA-Q X (CaO2 - CmvO2)]. Graded hemorrhage lowered SMA-Q, DO2 and DO2/VO2 and increased splanchnic O2 extraction (CaO2 - CmvO2). Elevation of FIO2 increased PaO2, PmvO2, and PmlO2. Both PmlO2 and PmvO2 varied directly with DO2/VO2 and PaO2, but PmlO2 showed greater sensitivity to PaO2. Papaverine and glucagon both increased SMA-Q, DO2, CmvO2, and PmvO2, BUT PmlO2 rose after papaverine, indicating greater capillary perfusion, and fell after glucagon, suggesting diversion of mesenteric blood flow through arteriovenous shunts. Thus, either PmvO2 or PmlO2 is ordinarily an accurate measure of intestinal tissue oxygenation, but the disparate response after glucagon suggests that PmlO2 is a more reliable indicator.