Influence of nitroglycerin on splanchnic capacity and splanchnic capacity- cardiac output relationship

It has been postulated, but not tested directly, that nitroglycerin's venodilatory effects attenuate cardiac output. Thus, the present study examined the importance of changes in splanchnic capacity, as assessed by scintigraphy, in the regulation of cardiac output during nitroglycerin administration in 16 anesthetized pigs under conditions of carotid sinus denervation and cervical vagotomy. With nitroglycerin administration (0.5 mg/min iv) for 5 min, systemic arterial pressure decreased from 115 ± 7 to 95 ± 7 mmHg (P < 0.0001), portal vein pressure decreased from 9.0 ± 0.5 to 8.5 ± 0.5 mmHg (P < 0.0001), portal flow increased from 637 ± 49 to 668 ± 60 ml/min (P = 0.09), and transhepatic resistance decreased from 7.5 ± 1.5 to 6.5 ± 1.0 mmHg · min · l^-1 (P < 0.01), but cardiac output was unchanged (1,929 ± 126 to 1,890 ± 138 ml/min). Total splanchnic intravascular volume (VI) increased 1.6 ± 1.0% (P < 0.05, 14 ± 10 ml). This increase was due to an increment in extrahepatosplenic (mesenteric) VI (12.9 ± 1.9%, P < 0.0001), since splenic VI decreased (9.6 ± 2.8%, P < 0.0001) and hepatic VI did not change. After splenectomy, nitroglycerin infusions at doses of 0.5 and 2 mg/min were associated with increases in total splanchnic VI of 3.7 ± 1.2% (P < 0.0001, 30 ± 10 ml) and 7.6 ± 1.7% (P < 0.001, 59 ± 10 ml) due entirely to increases in mesenteric volume of 9.9 ± 2.7% (P < 0.0001) and 16.5 ± 1.9% (P < 0.0001), respectively, but cardiac output was unchanged at the end of infusion at either dose. Subsequent evisceration did not alter the cardiac output response at either dose. Thus, nitroglycerin administration is associated with an increment in total splanchnic VI due to active mesenteric venodilation and an increase in portal flow. The splanchnic VI changes do not affect cardiac output.