Adrenergic neurotransmission failure in isolated canine jejunal arteries during hemorrhagic shock.
This study was designed to determine if the effective vascular smooth muscle population and/or effective adrenergic innervation density varies as the dog moves from compensatory to decompensatory hemorrhagic shock. Jejunal arteries with adventitia intact were removed 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 and exposed to (1) periarterial electrical stimulation and, (2) exogenously supplied norepinephrine (NE). The results are consistent with the hypothesis that the visceral vascular decompensation occurring as a result of prolonged hemorrhagic hypotension is caused by an adrenergic neuroeffector transmission failure.
D000818:Animals; D001158:Arteries / Q000294:innervation; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D007583:Jejunum / Q000098:blood supply*; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D010477:Perfusion; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D013566:Sympathomimetics / Q000494:pharmacology*
D018377:Neurotransmitter Agents; D013566:Sympathomimetics; D009638:Norepinephrine