Shepherd A P, Pawlik W, Mailman D, Burks T F, Jacobson E D
Am J Physiol. 1976 Feb;230(2):298-305. doi: 10.1152/ajplegacy.1976.230.2.298.
To delineate the mechanism through which vasoactive compounds alter intestinal oxygen consumption and to determine the pharmacological nature of the receptors involved, we quantitated the effects of vasoconstrictors on arteriovenous oxygen difference and on vascular resistance in isolated constant-flow perfused canine small bowel. Norepinephrine (NE) and sympathetic stimulation (SS) increased vascular resistance and depressed O2 extraction. These effects were not altered by beta-blockade, but were abolished by alpha-blockade. Since capillary filtration coefficients at constant-pressure perfusion and 86Rb extraction at constant flow are reported to diminish during NE and SS, it follows that these agents reduce O2 extraction by an alpha-adrenergic closure of precapillary sphincters. Vasopressin had similar effects which were not affected by adrenergic blocking agents. Epinephrine (Epi) in high doses or after propranolol produced the same effects as NE and SS. By contrast, Epi in low doses increased O2 and 86Rb extraction. This response to low doses of Epi was not affected by phentolamine, but was reversed by propranolol. We conclude that Epi in high doses or after propranolol depresses intestinal O2 extraction by the same mechanism as NE and SS, but the mechanism through which Epi increases intestinal O2 extraction is unclear.
为了阐明血管活性化合物改变肠道氧消耗的机制,并确定所涉及受体的药理学性质,我们对血管收缩剂对离体恒流灌注犬小肠动静脉氧差和血管阻力的影响进行了定量研究。去甲肾上腺素(NE)和交感神经刺激(SS)增加了血管阻力并降低了氧摄取。这些作用不受β受体阻断的影响,但被α受体阻断所消除。由于据报道在NE和SS作用期间,恒压灌注时的毛细血管滤过系数和恒流时的86Rb摄取会降低,因此可以得出结论,这些药物通过α肾上腺素能使毛细血管前括约肌关闭来降低氧摄取。血管加压素具有类似的作用,且不受肾上腺素能阻断剂的影响。高剂量肾上腺素(Epi)或在普萘洛尔作用后产生与NE和SS相同的效果。相比之下,低剂量的Epi增加了氧和86Rb的摄取。这种对低剂量Epi的反应不受酚妥拉明的影响,但被普萘洛尔逆转。我们得出结论,高剂量肾上腺素或在普萘洛尔作用后的肾上腺素通过与NE和SS相同的机制降低肠道氧摄取,但肾上腺素增加肠道氧摄取的机制尚不清楚。