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交感肾上腺素能阻滞对狒狒操作性条件反射性血压升高的影响。

Sympathetic adrenergic blockade effects upon operantly conditioned blood pressure elevations in baboons.

作者信息

Goldstein D S, Harris A H, Brady J V

出版信息

Biofeedback Self Regul. 1977 Mar;2(1):93-105. doi: 10.1007/BF01001722.

Abstract

Sympathetic adrenergic nervous activity during operantly conditioned hypertension was evaluated by assessing the effects of specific alpha-(phentolamine or phenoxybenzamine) and beta- (propranolol) adrenergic blockers in baboons reinforced for increasing diastolic pressure in daily, 12-h sessions. In the first 10 min of control (no blockade) sessions, mean heart rate increased 24 bpm (21%) above the value for the 10 min immediately prior to the beginning of the sessions; systolic pressure increased 27 mm Hg (22%) and diastolic pressure increased 24 mm Hg (31%). Beta-blockade eliminated the tachycardia but did not attenuate the increased blood pressure. Alpha-blockade did not attenuate the increased blood pressure significantly either. Combined alpha- and beta-blockade did significantly attenuate the increase in diastolic pressure, but consistent, significant increases in systolic pressure (17 mm Hg, 17%) and diastolic pressure (16 mm Hg, 26%) still occurred. The results support the participation of the sympathetic adrenergic nervous system in producing operantly conditioned blood pressure changes, but the results are also consistent with the additional participation of nonadrenergic factors in operantly conditioned hypertension.

摘要

通过评估特定的α-(酚妥拉明或酚苄明)和β-(普萘洛尔)肾上腺素能阻滞剂对狒狒的影响,来评估操作性条件性高血压期间交感肾上腺素能神经活动。这些狒狒在每天12小时的实验中,因舒张压升高而得到强化。在对照(无阻断)实验的前10分钟,平均心率比实验开始前紧挨着的10分钟的值增加了24次/分钟(21%);收缩压升高了27毫米汞柱(22%),舒张压升高了24毫米汞柱(31%)。β-阻断消除了心动过速,但并未减弱血压升高。α-阻断也未显著减弱血压升高。联合α-和β-阻断确实显著减弱了舒张压的升高,但收缩压(17毫米汞柱,17%)和舒张压(16毫米汞柱,26%)仍持续出现显著升高。结果支持交感肾上腺素能神经系统参与产生操作性条件性血压变化,但结果也与非肾上腺素能因素额外参与操作性条件性高血压一致。

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