Active vascular smooth muscle tone and venous membrane potentials during hemorrhage. Am J Physiol 1980 Feb;238(2):H144-52
Date
02/01/1980Pubmed ID
7361906DOI
10.1152/ajpheart.1980.238.2.H144Scopus ID
2-s2.0-0018978235 (requires institutional sign-in at Scopus site) 9 CitationsAbstract
To clarify mechanisms leading to failure of compensatory vascular tone in splanchnic blood vessels during prolonged hypotensive stress, anesthetized rats were maintained at a constant mean arterial pressure of 35 mmHg by hemorrhage into an external reservoir until 40% autoinfusion of maximum bled volume. In vivo intracellular membrane potentials (Em) of small intestinal mesenteric veins (300--500 micrometers) were measured before and during the compensatory (bleedout) and decompensatory (autinfusion) phases of the hypotensive period to assess the state of vascular smooth muscle (VSM) excitation. During the compensatory phase, Em decreased from -41 +/- 1 mV (prehemorrhage) to -31 +/- 2 mV, and small venous pressures decreased significantly. The onset of cardiovascular decompensation was associated with hyperpolarization (-53 +/- 3 mV), vasodilation, and return of venous pressure to control levels. Although direct electrical stimulation of the VSM and norepinephrine suffusion still produced constriction late in the hypotensive period, venoconstrictor responses to perivascular nerve stimulation failed progressively. This study indicates that failure of adrenergic neuromuscular transmission contributes significantly to the loss of compensatory VSM tone during hemorrhage.
Author List
Stekiel WJ, Willems WJ, Harder DR, Lombard JHMESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Electric Stimulation
Hemorrhage
Male
Membrane Potentials
Muscle Tonus
Muscle, Smooth, Vascular
Norepinephrine
Rats
Veins