Vagal and sympathetic components of the heart rate reflex in chronic portal vein stenosis

被引:3
作者
Battarbee, HD [1 ]
Zavecz, JH [1 ]
Betzing, KW [1 ]
机构
[1] LOUISIANA STATE UNIV, MED CTR, DEPT PHARMACOL, SHREVEPORT, LA 71130 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 1995年 / 269卷 / 06期
关键词
portal hypertension; cirrhosis; adrenergic; cholinergic; portosystemic shunting; skeletal muscle;
D O I
10.1152/ajpgi.1995.269.6.G892
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 presser 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 presser 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 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 presser 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.
引用
收藏
页码:G892 / G901
页数:10
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