ENDOGENOUS OPIATE PEPTIDES MAY LIMIT NOREPINEPHRINE RELEASE DURING HEMORRHAGE

  • 1 January 1985
    • journal article
    • research article
    • Vol. 232  (3) , 656-660
Abstract
The involvement of the sympathetic nervous system in the cardiovascular response to hemorrhage and subsequent opiate receptor blockade was studied in conscious rabbits. Plasma catecholamines were measured by high-pressure liquid chromatography to indirectly assess sympathetic activity. Arterial blood samples were drawn at 4 times during the experiment: before hemorrhage; after a 15% blood loss; after mean arterial blood pressure decreased to < 40 mm Hg; and 2 min after an i.v. injection of naloxone (3 mg/kg) or saline. Rapid removal of 15% of the total blood volume (.simeq. 8 ml/kg) increased heart rate and plasma norepinephrine. Plasma epinephrine and blood pressure remained at control levels. Further hemorrhage (.simeq. 16 ml/kg) produced a sudden decrease in blood pressure and a large increase in plasma epinephrine. Plasma norepinephrine was not significantly different from the previous sample. Subsequent injection of naloxone significantly increased plasma norepinephrine and blood pressure compared to the saline-treated group. Plasma epinephrine was similar in the 2 groups. Naloxone may exert its pressor effect during hemorrhagic hypotension in the conscious rabbit by blocking a naturally occurring, opiate peptide-mediated inhibition of norepinephrine release. A peptidergic limit on sympathetic activity is responsible for the decrease in blood pressure seen during acute hemorrhage.