Benarroch E E, Schmelzer J D, Ward K K, Nelson D K, Low P A
Department of Neurology, Mayo Clinic, Rochester, Minnesota 55905.
Am J Physiol. 1990 Aug;259(2 Pt 2):R371-5. doi: 10.1152/ajpregu.1990.259.2.R371.
The cardiovascular responses to sympathomimetic agents, the norepinephrine (NE) content in peripheral tissues, and the tissue content and cardiovascular effects of neuropeptide Y (NPY) were examined in anesthetized adult rats with guanethidine-induced sympathectomy (GuSx). We observed blunted pressor responses to tyramine, exaggerated pressor responses to phenylephrine, and markedly reduced NE contents in the atrium, femoral artery, superior cervical ganglion (SCG), and sciatic and vagus nerves. When tyramine responses were corrected for the NE content in the SCG, GuSx rats were similar to controls. A depletion of NPY levels in tissue resulted in an increased sensitivity to the pressor effects of intravenous NPY administration. GuSx, therefore, reproduces findings of postganglionic adrenergic failure in humans. Responses to the administration of sympathomimetic agents may reflect the degree of noradrenergic denervation. NPY may be a potential marker of chronic postganglionic sympathetic denervation in cardiovascular tissue.
在接受胍乙啶诱导的交感神经切除术(GuSx)的成年麻醉大鼠中,研究了对拟交感神经药的心血管反应、外周组织中的去甲肾上腺素(NE)含量以及神经肽Y(NPY)的组织含量和心血管效应。我们观察到对酪胺的升压反应减弱、对去氧肾上腺素的升压反应增强,并且心房、股动脉、颈上神经节(SCG)以及坐骨神经和迷走神经中的NE含量显著降低。当根据SCG中的NE含量校正酪胺反应时,GuSx大鼠与对照组相似。组织中NPY水平的耗竭导致对静脉注射NPY升压作用的敏感性增加。因此,GuSx再现了人类节后肾上腺素能衰竭的表现。对拟交感神经药给药的反应可能反映了去甲肾上腺素能去神经支配的程度。NPY可能是心血管组织中慢性节后交感神经去神经支配的潜在标志物。