Nitric oxide mediates fluid accumulation during cardiopulmonary bypass

J Thorac Cardiovasc Surg. 1996 Jul;112(1):168-74. doi: 10.1016/s0022-5223(96)70193-9.

Abstract

Fluid accumulation during cardiopulmonary bypass may be related to the production of endogenous vasoactive substances. We investigated the role of nitric oxide in mediating fluid accumulation during cardiopulmonary bypass. Normothermic cardiopulmonary bypass was carried out for 3 hours in male Sprague-Dawley rats with constant, nonpulsatile flow and hemodilution. Fluid accumulation (rate of change of external reservoir volume) was measured under three experimental conditions: saline solution control (n = 8), L-arginine infusion (n = 6), and N-nitro-L-arginine methyl ester infusion (n = 6). At the end of the experiments, body weight and organ wet/dry ratios were examined. Percentage weight gain was 77% greater in the N-nitro-L-arginine methyl ester group and 23% less in the L-arginine group compared with control values. Fluid accumulation was increased with N-nitro-L-arginine methyl ester after 30 minutes (p < 0.01) and reduced with L-arginine after 120 minutes (p < 0.01) compared with control animals. Water content was significantly decreased in the heart, lung, skin, muscle and peritoneum in rats receiving L-arginine. These data suggest that endogenous nitric oxide plays an important role in minimizing fluid accumulation during cardiopulmonary bypass.

MeSH terms

  • Animals
  • Arginine / analogs & derivatives
  • Arginine / pharmacology
  • Body Fluids / physiology*
  • Body Water
  • Cardiopulmonary Bypass*
  • Edema / etiology*
  • Edema / physiopathology
  • Hemodynamics
  • Male
  • NG-Nitroarginine Methyl Ester
  • Nitric Oxide / biosynthesis
  • Nitric Oxide / physiology*
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Organ Size
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Nitric Oxide
  • Arginine
  • Nitric Oxide Synthase
  • NG-Nitroarginine Methyl Ester