Hemorrhage alters plasma and cardiac enkephalins and catecholamines
in anesthetized dogs.
Mateo, Zaira, Leslie Napier, John F. Gaugl, Barbara A. Barron, and
James L. Caffrey.
Department of Physiology, University of North Texas Health Science
Center, Fort Worth, Texas 76107
APStracts 2:0270H, 1995.
Functional data obtained in this laboratory suggest that intrinsic
cardiac enkephalins may participate in circulatory regulation either
through the modification of vagal control of the heart or sympathetic
control of vasomotor tone. In the current study, plasma and
myocardial enkephalins were extracted, chromatographed and assayed in
samples obtained from anesthetized dogs under control conditions and
during two hours of hemorrhagic hypotension. Sufficient blood was
withdrawn to reduce and maintain mean arterial pressure at 40 mmHg.
Central venous blood samples were collected 15 minutes before and at
30 min intervals during the experiment. Arterial blood gases remained
stable throughout the experiment, pH declined to 7.1 and heart rate
rose gradually by 100 bpm. Plasma catecholamines were unchanged in
the two hour time-controls. Plasma norepinephrine and epinephrine
rose 6 and 100 fold respectively during the first hour of hypotension
and remained high through the second hour. All eight enkephalin
immunoreactivities (-irs) monitored were unchanged during observation
of the time-controls. Plasma met-enkephalin (ME) and Peptide-F both
gradually increased by 70-100% during the hypotension. Plasma met
-enkephalin-arg-phe (MEAP) and Peptide-B increased 10-30 fold during
the same interval. Proenkephalin and other large enkephalin
containing peptides though present, were unchanged in the circulation
during hypotension. Myocardial norepinephrine was concentrated 3:1 in
the atria and both atrial and ventricular contents were one third
lower after two hours hypotension. Proenkephalin and Peptide-B
accounted for more than 60% of the intrinsic cardiac enkephalins and
their ventricular concentrations were 3-4 X atrial concentrations.
Myocardial MEAP concentrations were 15-25 X comparable ME
concentrations in the same tissue extracts. Hypotension increased
Peptide-B and proenkephalin compared to controls. The increase was
consistent throughout the heart, thus maintaining the preferential
MEAP-ir concentration in the ventricles. Myocardial ME, MEAP and
Peptide-F were largely unchanged in hypotensives compared to time
-controls. The data demonstrate a preferential processing to or
retention of MEAP rather than ME-immunoreactive enkephalins in the
heart. The data also indicate that myocardial MEAP-ir enkephalins
respond to changes in the circulatory environment and they
subsequently appear in the plasma during hemorrhagic hypotension.
Received 31 October 1994; accepted in final form 13 June 1995.
APS Manuscript Number H961-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.