Does acute hyperglycemia alter rat aortic depressor nerve function?
Does acute hyperglycemia alter rat aortic depressor nerve function?
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DOI：
10.1590/s0100-879x2007001100017
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发表时间：
2007-11-01
影响因子：
2.3
通讯作者：
Salgado, H.C.
中科院分区：
文献类型：
--
作者：
Huber, D.A.;Carmo, J.M. do;Salgado, H.C.
由于目前尚不清楚高血糖在反射弓的什么部位，即传入、中枢神经系统或传出，影响压力感受器反射功能，本研究通过平均动脉压-降压神经活动曲线(S形回归拟合)或平均动脉压与降压神经活动之间的交叉频谱分析，研究了短期(30分钟)高血糖对主动脉降压神经功能的影响。麻醉雄性Wistar大鼠静脉推注0.25m L，然后以1m L/h的速度输注30 m in 30%葡萄糖(n=14)。对照组注射0.9%生理盐水(N=14)或30%甘露醇(N=14)。葡萄糖显著升高血糖和血浆渗透压(P<；0.05)。平均动脉压在输注葡萄糖、生理盐水或甘露醇后没有改变。开始输注葡萄糖、生理盐水或甘露醇前、后10分钟和30分钟，平均动脉压与神经活动曲线一致。用控制性失血诱导动脉压缓慢振荡(0.3 Hz)，并对动脉压和主动脉神经活动进行交叉频谱分析。计算传递函数大小(降主动脉神经活动/平均动脉压在频域的比值)作为降主动脉神经增益的指标。在诱发或自发的动脉压振荡期间，所有组的传递函数大小都是相似的。总之，本研究通过两种不同的评估压力感受器功能的方法证明，短期(30分钟)高血糖不会改变主动脉降压神经的活动。
Because it is not known where in the reflex arch, i.e., afference, central nervous system or efferences, hyperglycemia affects baroreflex function, the present study examined the effect of short-term ( 30 min) hyperglycemia on aortic depressor nerve function measured by a mean arterial pressure vs aortic depressor nerve activity curve, fitted by sigmoidal regression, or by cross-spectral analysis between mean arterial pressure and aortic depressor nerve activity. Anesthetized male Wistar rats received an intravenous bolus ( 0.25 mL) injection, followed by 30 min of infusion ( 1 mL/h) of 30% glucose ( N = 14). Control groups received a bolus injection and infusion of 0.9% saline ( N = 14), or 30% mannitol ( N = 14). Glucose significantly increased both blood glucose and plasma osmolarity ( P < 0.05). Mean arterial pressure did not change after glucose, saline or mannitol infusion. Mean arterial pressure vs nerve activity curves were identical before and 10 and 30 min after the beginning of glucose, saline or mannitol infusion. Slow ( 0.3 Hz) oscillations of arterial pressure were induced by controlled bleeding, and cross-spectral analysis was applied to arterial pressure and aortic nerve activity. Transfer function magnitude ( aortic depressor nerve activity/mean arterial pressure ratio in the frequency domain) was calculated as an index of gain of the aortic depressor nerve. Transfer function magnitude was similar in all groups during induced or spontaneous oscillations of arterial pressure. In conclusion, the present study demonstrates, by means of two different approaches for assessing baroreceptor function, that aortic depressor nerve activity was not altered by short-term ( 30 min) hyperglycemia.