Adrenergic responses of gracilis arteries removed during hemorrhagic hypotension and shock.

Previous studies suggest that the gracilis vasculature responds to hypovolemic hypotension by constriction followed by vasodilation [Circ Shock 4:327, 1977; Circ Shock 6:43, 1979]. The objectives of the present study were to determine if the effective vascular smooth muscle population and/or adrenergic innervation density varies as the dog moves from compensatory into decompensatory shock. Gracilis arteries with adventitia intact were resected during four different stages of shock and compared to nonshocked vessels. All vessels were placed in a tissue chamber filled with warm (37 degrees C) Krebs-Henseleit solution and bubbled with 95% O2 and 5% CO2. Norepinephrine (NE) dose-response and periarterial electrical stimulation (ES) frequency-response studies were conducted. The maximum response to NE was not altered from control during either compensatory or decompensatory shock, but the maximum response to ES fell during compensatory and early decompensatory hypovolemic hypotension. The sensitivity of the innervated alpha receptors, as measured by the ES necessary to obtain a 50% maximal response (ES50), also fell below control during early decompensatory hypotension but returned to control values during early and late normovolemic shock, even though the sensitivity of the alpha receptors to NE (ED50) increased. These data support the suggestion that the skeletal muscle vascular decompensation occurring as a consequence of hemorrhage may be caused by a neuromuscular transmission failure.