Korean J Physiol Pharmacol.
1998 Jun;2(3):345-351.
Nitric oxide impairs the recovery from hemorrhagic hypotension in
conscious rats
- Affiliations
-
- 1Department of Physiology, School of Medicine, Catholic University of Taegu-Hyosung, Taegu 705-716, Korea.
Abstract
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The role of nitric oxide (NO) in the hemorrhagic hypotension was
examined using a NO synthase inhibitor, Nomega-nitro-L-arginine methyl
ester (L-NAME), in conscious rats, The rats were bled at a constant
rate (2 ml/kg/min) through a femoral arterial catheter until the mean
arterial pressure (MAP) was reduced by 50 mmHg. We studied the
responses to hemorrhage under normal condition (Control) and after the
pretreatment with 3 doses of L-NAME (1.6, 8, 40 mg/kg i.v. of NOX1.6,
NOX8, and NOX40, respectively). Intravenous bolus injection of L-NAME
produced a sustained increase in MAP and decrease in heart rate (HR).
During hemorrhage, the MAP fell faster in the NOX8 and NOX40-treated
groups than in Control group, but the control group showed same
response to NOX1.6. HR greatly increased in NOX groups. The recovery
from hemorrhagic hypotension was slowed in the control group, which was
not treated with L-NAME. In comparison with the control group, NOX8 and
NOX1.6-treated groups registered a significant recovery in MAP during
the 15 min recovery period, but NOX40 brought about only a slight
increase in MAP. NO precursor, L-arginine (150 mg/kg i.v.), produced
significant bradycardia responses before and after hemorrhage and
significant depressor response only after hemorrhagic hypotension
regardless of pretreatment with L-NAME. These data suggest that the
role of NO in blood pressure regulation is greater after hemorrhagic
hypotension than basal condition, but the effect of NO can be
detrimental to the recovery from hemorrhagic hypotension. In addition,
the bradycardia response of L-arginine provides indirect evidence that
NO may inhibit sympathetic activity, especially after hemorrhagic
hypotension.