Active vascular smooth muscle tone and venous membrane potentials during hemorrhage.
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.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004558:Electric Stimulation; D006470:Hemorrhage / Q000503:physiopathology*; D008297:Male; D008564:Membrane Potentials; D009129:Muscle Tonus; D009131:Muscle, Smooth, Vascular / Q000294:innervation / Q000503:physiopathology*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D014680:Veins / Q000503:physiopathology
D009638:Norepinephrine