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糖尿病中的压力反射功能障碍。II. 糖尿病兔压力反射受损部位。

Baroreflex dysfunction in diabetes mellitus. II. Site of baroreflex impairment in diabetic rabbits.

作者信息

McDowell T S, Hajduczok G, Abboud F M, Chapleau M W

机构信息

Cardiovascular Center, University of Iowa, Iowa City.

出版信息

Am J Physiol. 1994 Jan;266(1 Pt 2):H244-9. doi: 10.1152/ajpheart.1994.266.1.H244.

DOI:10.1152/ajpheart.1994.266.1.H244
PMID:8304505
Abstract

In our companion paper [T. S. McDowell, M. W. Chapleau, G. Hajduczok, and F. M. Abboud, Am. J. Physiol. 266 (Heart Circ. Physiol. 35): H235-H243, 1994] we report that baroreflex-mediated bradycardia is impaired in diabetic rabbits. The purpose of the present study was to identify the site of impairment. Diabetes was induced in rabbits by alloxan (90-100 mg/kg iv; n = 7). Alloxan-treated rabbits that remained normoglycemic (n = 8) and rabbits given saline instead of alloxan (n = 4) served as controls. Twenty-four weeks after administration of alloxan or saline, rabbits were anesthetized with alpha-chloralose. Aortic baroreceptor and renal sympathetic nerve activity (RSNA) were recorded during phenylephrine- and nitroglycerin-induced changes in arterial pressure. The slope of the baroreceptor pressure-activity relation was not significantly different in diabetic rabbits (1.3 +/- 0.3%/mmHg, n = 7) compared with either alloxan-treated (1.3 +/- 0.1%/mmHg) or saline-treated normoglycemic rabbits (1.2 +/- 0.2%/mmHg). The slope of the arterial pressure-RSNA relation was not significantly different in diabetic rabbits (-3.5 +/- 0.3%/mmHg, n = 7) compared with the alloxan-treated normoglycemic rabbits (-3.0 +/- 0.4%/mmHg, n = 8) and was greater than that in saline-treated normoglycemic rabbits (-1.9 +/- 0.3%/mmHg, n = 4; P < 0.05). The decreases in heart rate in response to electrical stimulation (10 V, 2 ms, 0.5-16 Hz) of the cut peripheral end of the right cervical vagus were similar in diabetic and alloxan-treated normoglycemic rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在我们的配套论文中[T. S. 麦克道尔、M. W. 沙普洛、G. 哈伊杜佐克和F. M. 阿博德,《美国生理学杂志》266卷(心脏循环生理学35):H235 - H243,1994年],我们报道糖尿病兔压力感受性反射介导的心动过缓受损。本研究的目的是确定受损部位。用四氧嘧啶(90 - 100毫克/千克静脉注射;n = 7)诱导兔患糖尿病。血糖保持正常的经四氧嘧啶处理的兔(n = 8)以及注射生理盐水而非四氧嘧啶的兔(n = 4)作为对照。给予四氧嘧啶或生理盐水24周后,用α - 氯醛糖麻醉兔。在去氧肾上腺素和硝酸甘油诱导动脉压变化期间记录主动脉压力感受器和肾交感神经活动(RSNA)。与经四氧嘧啶处理的兔(1.3 +/- 0.1%/毫米汞柱)或注射生理盐水的血糖正常兔(1.2 +/- 0.2%/毫米汞柱)相比,糖尿病兔压力感受器压力 - 活动关系的斜率(1.3 +/- 0.3%/毫米汞柱,n = 7)无显著差异。与经四氧嘧啶处理的血糖正常兔(-3.0 +/- 0.4%/毫米汞柱,n = 8)相比,糖尿病兔动脉压 - RSNA关系的斜率(-3.5 +/- 0.3%/毫米汞柱,n = 7)无显著差异,且大于注射生理盐水的血糖正常兔(-1.9 +/- 0.3%/毫米汞柱,n = 4;P < 0.05)。糖尿病兔和经四氧嘧啶处理的血糖正常兔对右侧颈迷走神经切断外周端的电刺激(10伏,2毫秒,0.5 - 16赫兹)的心率下降相似。(摘要截断于250字)

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