Comparative effects of nitroglycerin on intestinal vascular capacitance and conductance.

BACKGROUND: Nitroglycerin (NTG) dilates capacitance veins and resistance arterioles, but its relative effects on veins and arterioles are not known. OBJECTIVES: To compare NTG-induced changes in capacitance and conductance. ANIMALS AND METHODS: Aortic, left ventricular and portal venous (P(port)) pressures, portal flow and relative changes in intestinal blood volume (IBV) ((99m)technetium blood-pool scintigraphy) were measured in seven isoflurane-anesthetized, splenectomized dogs. Changes in intestinal vascular capacitance and conductance (mean portal flow/[mean aortic pressure - mean P(port)]) were determined when NTG was continuously administered (0.8 to 150 microg/kg/min) into a jugular vein. Pressure-volume (ie, P(port)-IBV) curves were defined by impeding portal flow, and capacitance was defined as the IBV at P(port)=7.5 mmHg. RESULTS: At lower doses, NTG increased capacitance without increasing conductance, but conductance increased considerably with little further increase in capacitance at higher doses. Dose-response analysis revealed that the half-maximum capacitance effect was achieved at an NTG infusion rate of 3.5 microg/kg/min, whereas a rate of 35 microg/kg/min was required for the half-maximum conductance effect. CONCLUSIONS: At lower doses, NTG dilates capacitance vessels primarily, and that effect approaches its maximum before significant dilation of conductance vessels is manifest. However, at higher doses, the increase in conductance is substantial with little additional effect on capacitance.

Effects of acute volume loading and hemorrhage on intestinal vascular capacitance: a mechanism whereby capacitance modulates cardiac output.

BACKGROUND: Changes in intestinal vascular capacitance during acute volume loading and hemorrhage have not been described. OBJECTIVES: To determine the effects of volume loading and hemorrhage on the intestinal vascular pressure-volume relationship and cardiac output. PATIENTS AND METHODS: In 11 alpha-chloralose-anesthetized dogs, a pneumatic portal venous constrictor and catheter were positioned to increase and measure portal venous pressure (Ppv), respectively. Relative changes in intestinal blood volume (IBV) were determined by blood-pool scintigraphy and expressed as the percentage change from control values (taken as 100%). Ppv-IBV relationships were constructed by graded portal vein constriction. RESULTS: IBV and cardiac output increased by 60 6% and 178 48%, respectively, and Ppv increased from 5.8 0.9 mmHg to 13.2 1.8 mmHg after initial volume loading (40 mL/kg of an isotonic glucose-saline solution over 7 min). IBV gradually decreased and reached near-control values after 75 min. In seven dogs, hemorrhage (sufficient to decrease mean aortic pressure by 56 4%) decreased IBV and cardiac output to 88 4% and 52 3% of control values, respectively, and Ppv decreased to 3.2 0.8 mmHg. CONCLUSIONS: A sigmoid function curve defined the relationship between cardiac output and IBV. Cardiac output remained constant over a wide range (between approximately 95% and 135% of control IBV). Outside this range, insufficient dilation or constriction resulted in a marked increase or decrease in venous pressures and cardiac output. These data indicate that vasculature capacitance modulates cardiac output during acute volume loading and hemorrhage, thereby maintaining cardiac output relatively constant over a wide range of total vascular blood volume.