Lack of effect of low dose of nitroglycerin on splanchnic hemodynamic in patients with cirrhosis. Evidence for a decrease in cardiopulmonary baroreflex control

1988 ◽  
Vol 7 ◽  
pp. S62
1994 ◽  
Vol 266 (1) ◽  
pp. R27-R39 ◽  
Author(s):  
G. F. DiBona ◽  
L. L. Sawin

Efferent renal sympathetic nerve activity (ERSNA) is increased in the rat with low-cardiac-output congestive heart failure (CHF; myocardial infarction). Arterial and cardiopulmonary baroreflex control of ERSNA in CHF and control rats was examined. Cardiac index and arterial pressure were lower and total peripheral resistance index, left ventricular end-diastolic pressure, and heart-to-body weight ratio were higher in CHF than in control rats. Increases in left ventricular end diastolic pressure produced by intravenous volume loading failed to increase cardiac index in CHF rats as it did in control rats. Single-unit analysis of aortic baroreceptor nerve activity showed that CHF rats had higher pressure threshold, lower frequency at pressure threshold, and lower gain than control rats. Arterial baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. Single-unit analysis of vagal nerve activity showed that CHF rats had higher pressure threshold, lower frequency at saturation, and lower gain than control rats. Cardiopulmonary baroreflex control of ERSNA was attenuated; this was due to diminished gain of the afferent limb while the gain of the central portion of the reflex was normal. In the CHF rat, arterial and cardiopulmonary baroreflex control of ERSNA is markedly attenuated because of abnormalities in the periphery at the level of the aortic and cardiopulmonary receptors, respectively, and not in the central nervous system.


1997 ◽  
Vol 273 (2) ◽  
pp. R457-R471 ◽  
Author(s):  
J. L. Segar

The autonomic nervous system is intimately involved in regulating cardiovascular function. Sensing mechanisms dispersed throughout the circulation, including arterial baroreceptors, low pressure receptors, and chemosensitive receptors, continually evoke reflexes designed to maintain cardiovascular homeostasis. Although there is a growing body of knowledge regarding neural regulation of the adult cardiovascular system, characterization and understanding of these physiological systems during development is limited. This review highlights developmental changes in the arterial and cardiopulmonary baroreflex during fetal and postnatal life and contrasts the function of these responses with those seen in the adult. Baroreceptors are functional in the immature animal and reset toward higher pressure levels with maturation. In our ovine model, the sensitivity of the efferent limb of the baroreflex is greatest during fetal life and decreases with postnatal development. As in the adult, angiotensin II and arginine vasopressin interact with the sympathetic nervous system early during development to alter baroreflex control of the cardiovascular system. However, the extent to which these hormonal systems influence autonomic reflexes during the fetal and newborn period appears vastly different than in the adult. Endogenous angiotensin II significantly contributes to resetting of the arterial baroreflex early in life, whereas even high circulating levels of vasopressin have little effect on baroreflex function until adulthood. Finally, the ability of cardiopulmonary mechanoreceptors to regulate cardiovascular function is impaired early in development, in sharp contrast to the heightened sensitivity of the arterial baroreflex at this stage of maturation. The potential importance of these autonomic reflexes on cardiovascular function during the perinatal period is highlighted.


2016 ◽  
Vol 4 (13) ◽  
pp. e12859 ◽  
Author(s):  
Michael T. Mozer ◽  
Walter W. Holbein ◽  
Michael J. Joyner ◽  
Timothy B. Curry ◽  
Jacqueline K. Limberg

1985 ◽  
Vol 63 (6) ◽  
pp. 668-674 ◽  
Author(s):  
Thomas J. Ebert ◽  
Karel J. Kotrly ◽  
Eduards J. Vucins ◽  
Christine Z. Pattison ◽  
John P. Kampine

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