Battarbee H D, Zavecz J H, Betzing K W
Department of Physiology, Louisiana State University Medical Center, Shreveport 71130, USA.
Am J Physiol. 1995 Dec;269(6 Pt 1):G892-901. doi: 10.1152/ajpgi.1995.269.6.G892.
The effects of portal hypertension and portosystemic shunting on autonomic components of the heart rate (HR) baroreflex and on skeletal muscle blood flow changes were investigated using the chronic portal vein-stenosed rat. Phenylephrine- and sodium nitroprusside-induced changes in mean arterial pressure (MAP), HR, and skeletal muscle conductance (SMC) were assessed before and after muscarinic or beta-adrenoceptor blockade. Stenosed rats had lower MAP than sham-operated rats (90 +/- 3 vs. 81 +/- 2 mmHg, P < 0.05), and their portal pressure was higher (7.4 +/- 0.5 vs. 13.9 +/- 1.0 mmHg, P < 0.005). Phenylephrine pressor responses were reduced in stenosed animals, their associated bradycardic responses were enhanced [-1.912 +/- 0.109 vs. -1.427 +/- 0.148 beats per minute (bpm)/mmHg, P < 0.01], and their SMC responses were diminished. Methylatropine abolished bradycardic responses and enhanced pressor responses without affecting SMC. After propranolol, reflex bradycardic responses in stenosed rats were less than in shams (-0.492 +/- 0.085 vs. -0.738 +/- 0.058 bpm/mmHg, P < 0.01), and their pressor and SMC responses became indistinguishable from shams. In contrast, tachycardic responses to nitroprusside-induced hypotension before propranolol were impaired in stenosed rats (-1.492 +/- 0.114 vs. -2.225 +/- 0.347 bpm/mmHg, P < 0.05), and their SMC responses were reduced. Muscarinic blockade did not affect HR or SMC responses to hypotension in either stenosed or sham rats. beta-Adrenoceptor blockade, however, prevented hypotension-induced tachycardia, enhanced nitroprusside depressor responses, and eliminated the between-group differences in SMC responses. These studies indicate that increased gain of the parasympathetic limb of the cardiac baroreflex was responsible for attenuated pressor responses to phenylephrine in portal vein-stenosed animals and that beta-adrenoceptors contributed to skeletal muscle vascular hyporesponsiveness to phenylephrine in portal-vein stenosed animals. Altered beta-adrenoceptor function also appears to contribute to impaired chronotropic and skeletal muscle conductance responses to hypotension.
利用慢性门静脉狭窄大鼠，研究门静脉高压和门体分流对心率（HR）压力反射的自主神经成分以及骨骼肌血流变化的影响。在毒蕈碱或β -肾上腺素能受体阻断前后，评估去氧肾上腺素和硝普钠诱导的平均动脉压（MAP）、HR和骨骼肌电导率（SMC）的变化。狭窄大鼠的MAP低于假手术大鼠（90±3 vs. 81±2 mmHg，P<0.05），其门静脉压力更高（7.4±0.5 vs. 13.9±1.0 mmHg，P<0.005）。去氧肾上腺素在狭窄动物中的升压反应降低，其相关的心动过缓反应增强[-1.912±0.109 vs. -1.427±0.148次/分钟（bpm）/mmHg，P<0.01]，并且其SMC反应减弱。甲基阿托品消除了心动过缓反应并增强了升压反应，而不影响SMC。普萘洛尔给药后，狭窄大鼠的反射性心动过缓反应小于假手术组（-0.492±0.085 vs. -0.738±0.058 bpm/mmHg，P<0.01），并且其升压和SMC反应与假手术组无差异。相反，在普萘洛尔给药前，狭窄大鼠对硝普钠诱导的低血压的心动过速反应受损（-1.492±0.114 vs. -2.225±0.347 bpm/mmHg，P<0.05），并且其SMC反应降低。毒蕈碱阻断对狭窄或假手术大鼠的HR或SMC对低血压的反应均无影响。然而，β -肾上腺素能受体阻断可防止低血压诱导的心动过速，增强硝普钠的降压反应，并消除两组之间SMC反应的差异。这些研究表明，心脏压力反射的副交感神经支增益增加是门静脉狭窄动物对去氧肾上腺素升压反应减弱的原因，并且β -肾上腺素能受体促成了门静脉狭窄动物骨骼肌血管对去氧肾上腺素的反应性降低。β -肾上腺素能受体功能改变似乎也导致了对低血压的变时性和骨骼肌电导率反应受损。
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