Crissinger K D, Kvietys P R, Granger D N
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130-3932.
Am J Physiol. 1988 Apr;254(4 Pt 1):G560-5. doi: 10.1152/ajpgi.1988.254.4.G560.
Stimulation of sympathetic fibers or infusion of norepinephrine (NE) into the superior mesenteric artery (SMA) leads to an initial decrease in intestinal blood flow, which is followed by a return of flow toward the base-line value (autoregulatory escape) despite continued nerve stimulation or NE infusion. Although the mechanisms responsible for "autoregulatory escape" have not been defined, accumulation of vasodilator metabolites is frequently invoked to explain this phenomenon. Inasmuch as histamine and adenosine exist in high concentrations in the intestinal mucosa and both are potent vasodilators, we examined the effects of chlorpheniramine (an H1 blocker) and adenosine deaminase (degrades adenosine) on autoregulatory escape from NE infusion. In autoperfused piglet intestinal preparations, we measured SMA blood flow and the arteriovenous oxygen difference during intra-arterial NE infusion before and after blockade with chlorpheniramine or adenosine deaminase. Adenosine deaminase pretreatment increased the peak vasoconstrictor and reduced the steady-state escape responses to NE infusion. Chlorpheniramine did not affect either the vasoconstrictor or escape responses. The oxygen uptake changes induced by NE infusion were not dramatically modified by either treatment. These results indicate that adenosine but not histamine is responsible for at least part of the escape of intestinal blood flow from NE infusion.
刺激交感神经纤维或向肠系膜上动脉（SMA）内注入去甲肾上腺素（NE）会导致肠血流量最初减少，尽管持续进行神经刺激或注入NE，但随后血流量会恢复至基线值（自动调节逃逸）。尽管尚未明确导致“自动调节逃逸”的机制，但血管舒张代谢产物的积累常被用来解释这一现象。鉴于组胺和腺苷在肠黏膜中浓度很高，且二者均为强效血管舒张剂，我们研究了氯苯那敏（一种H1阻滞剂）和腺苷脱氨酶（降解腺苷）对NE注入后自动调节逃逸的影响。在自体灌注的仔猪肠道制备物中，我们在使用氯苯那敏或腺苷脱氨酶阻断前后，测量了动脉内注入NE期间的SMA血流量和动静脉氧差。腺苷脱氨酶预处理增加了血管收缩峰值，并降低了对NE注入的稳态逃逸反应。氯苯那敏对血管收缩或逃逸反应均无影响。两种处理均未显著改变NE注入引起的氧摄取变化。这些结果表明，腺苷而非组胺至少部分地导致了肠血流量从NE注入中的逃逸。
