Eades S C, Moore J N
Department of Large Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens 30602.
Am J Vet Res. 1993 Apr;54(4):586-90.
Stimulation of alpha 2 adrenergic receptors inhibits colonic motility and may constrict some peripheral vascular beds. Endotoxemia elicits release of sympathetic neurotransmitters and increases sympathetic nerve activity, which may result in stimulation of alpha 2 adrenergic receptors. The objective of this study was to determine whether blockade of alpha 2 adrenergic receptors would restore cecal motility and blood flow during endotoxemia in horses. Strain-gauge force transducers and ultrasonic flow probes were used to measure cecal and colonic mechanical activity and lateral cecal arterial blood flow. Intravenous infusion of endotoxin (cumulative dose of 0.03 mg/kg) significantly decreased cecal and right ventral colon contractile activity and lateral cecal arterial blood flow. Slow IV infusion of yohimbine (cumulative dose of 75 micrograms/kg) significantly attenuated those effects of endotoxin. On the basis of our findings, we concluded that endotoxemia causes cecal and proximal colonic ileus and cecal hypoperfusion via a mechanism that involves alpha 2 adrenergic receptors.
刺激α2肾上腺素能受体会抑制结肠蠕动，并可能使一些外周血管床收缩。内毒素血症会引发交感神经递质的释放并增加交感神经活性，这可能导致α2肾上腺素能受体受到刺激。本研究的目的是确定在马发生内毒素血症期间，阻断α2肾上腺素能受体是否能恢复盲肠蠕动和血流。应变片式力传感器和超声流量探头用于测量盲肠和结肠的机械活动以及盲肠外侧动脉血流。静脉输注内毒素（累积剂量为0.03 mg/kg）显著降低了盲肠和右腹侧结肠的收缩活动以及盲肠外侧动脉血流。缓慢静脉输注育亨宾（累积剂量为75微克/千克）显著减弱了内毒素的这些作用。基于我们的研究结果，我们得出结论，内毒素血症通过涉及α2肾上腺素能受体的机制导致盲肠和近端结肠肠梗阻以及盲肠灌注不足。
