1. Mechanism of systemic vasodilation during normovolemic hemodilution.
- Author
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Doss DN, Estafanous FG, Ferrario CM, Brum JM, and Murray PA
- Subjects
- Amino Acid Oxidoreductases antagonists & inhibitors, Animals, Arginine analogs & derivatives, Arginine pharmacology, Blood Circulation drug effects, Blood Circulation physiology, Blood Pressure drug effects, Blood Pressure physiology, Blood Volume, Cardiac Output drug effects, Cardiac Output physiology, Decerebrate State, Heart Rate drug effects, Heart Rate physiology, Hydroxyethyl Starch Derivatives administration & dosage, Male, Nitric Oxide pharmacology, Nitric Oxide Synthase, Nitroarginine, Nitroprusside pharmacology, Rats, Rats, Sprague-Dawley, Reflex, Spinal Cord physiology, Stroke Volume drug effects, Stroke Volume physiology, Vascular Resistance drug effects, Vascular Resistance physiology, Hemodilution, Vasodilation physiology
- Abstract
In the nonfailing heart, normovolemic hemodilution increases cardiac output and decreases total peripheral resistance (TPR). Putative mechanisms mediating the decrease in TPR include reflex vasodilation and changes in the local regulation of blood flow. Our objectives were to determine whether ablation of reflex neural mechanisms or the inhibition of nitric oxide (NO) synthase, the enzyme responsible for the synthesis of the endothelium-derived relaxing factor (EDRF-NO), modulates the systemic vasodilator response to normovolemic hemodilution. Three groups of male Sprague-Dawley rats were subjected to acute normovolemic hemodilution, which was achieved by exchanging a volume of blood equivalent to 3.8% of body weight with hydroxyethyl starch. Hemodilution increased cardiac output and decreased TPR. Subsequent administration of the NO synthase inhibitor, L-nitroarginine (LNA), returned both cardiac output and TPR to control values. Pretreatment with LNA prior to hemodilution increased TPR, an effect that was partially reversed by the NO donor, sodium nitroprusside. In this setting, hemodilution failed to decrease TPR. After spinal cord destruction by "pithing," hemodilution decreased TPR to the same extent as that observed in intact rats. This hemodilution-induced decrease in TPR was abolished by the subsequent administration of LNA. These results indicate that neural reflexes do not modulate the systemic vascular response to hemodilution. Moreover, the systemic vasodilator response to hemodilution is abolished after inhibition of endogenous NO synthesis.
- Published
- 1995
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