Kerr J C, Swan K G
Am J Physiol. 1981 Jan;240(1):G25-31. doi: 10.1152/ajpgi.1981.240.1.G25.
Adrenergic stimulation and blockade on inferior mesenteric arterial blood flow (Q) were measured in anesthetized rhesus monkeys. Control Q was 25 +/- 2 (mean +/- SE) ml/min; aortic and portal venous pressures were 121 +/- 5 and 6.5 +/- 1.0 mmHg. Calculated inferior mesenteric arterial resistance was 5.10 +/- 0.42 peripheral resistance units. Norepinephrine (N), 10(-3) to 1.0 microgram/kg intra-arterially, caused dose-dependent decreases in Q. Epinephrine (E) increased Q at 10(-3) microgram/kg in 60% of the animals studied and decreased Q at the higher doses (10(-2) to 1.0 microgram/kg). Isoproterenol (I) increased Q at all four doses studied. Ten-minute infusions of N and E (0.5 microgram x kg-1 x min-1) caused sustained decreases, and I caused sustained increases in Q. Autoregulatory escape was not observed. alpha-Adrenergic receptor blockade (phenoxybenzamine) attenuated the vasoconstrictor responses to N, but did not "reverse" the vasoconstrictor response to E (vasodilation). beta-adrenergic receptor blockade (propranolol) attenuated the vasodilator responses to I, but did not alter significantly the responses to E or N. These data indicate that in the monkey colonic circulation, alpha-adrenergic receptor stimulation causes vasoconstriction and beta-adrenergic receptor stimulation causes vasodilation.
在麻醉的恒河猴身上测量了肾上腺素能刺激和阻断对肠系膜下动脉血流量(Q)的影响。对照Q为25±2(平均值±标准误)ml/min;主动脉和门静脉压力分别为121±5和6.5±1.0 mmHg。计算得出的肠系膜下动脉阻力为5.10±0.42外周阻力单位。动脉内注射去甲肾上腺素(N),剂量为10⁻³至1.0微克/千克,可导致Q呈剂量依赖性下降。肾上腺素(E)在10⁻³微克/千克时使60%的受试动物的Q增加,而在较高剂量(10⁻²至1.0微克/千克)时使Q下降。异丙肾上腺素(I)在所有研究的四个剂量下均使Q增加。持续输注N和E(0.5微克·千克⁻¹·分钟⁻¹)10分钟导致Q持续下降,而I导致Q持续增加。未观察到自动调节逃逸现象。α-肾上腺素能受体阻断剂(酚苄明)减弱了对N的血管收缩反应,但未“逆转”对E的血管收缩反应(血管舒张)。β-肾上腺素能受体阻断剂(普萘洛尔)减弱了对I的血管舒张反应,但未显著改变对E或N的反应。这些数据表明,在猴结肠循环中,α-肾上腺素能受体刺激导致血管收缩,而β-肾上腺素能受体刺激导致血管舒张。