PubMed · 9581535
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1998. A protective factor.. https://pubmed.ncbi.nlm.nih.gov/9581535/
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Respiratory activity phasically alters membrane potentials of preganglionic vagal and sympathetic motoneurones and continuously modulates their responsiveness to stimulatory inputs. The most obvious manifestation of this 'respiratory gating' is respiratory sinus arrhythmia, the rhythmic fluctuations of electrocardiographic R-R intervals observed in healthy resting humans. Phasic autonomic motoneurone firing, reflecting the throughput of the system, depends importantly on the intensity of stimulatory inputs, such that when levels of stimulation are low (as with high arterial pressure and sympathetic activity, or low arterial pressure and vagal activity), respiratory fluctuations of sympathetic or vagal firing are also low. The respiratory gate has a finite capacity, and high levels of stimulation override the ability of respiration to gate autonomic responsiveness. Autonomic throughput also depends importantly on other factors, including especially, the frequency of breathing, the rate at which the gate opens and closes. Respiratory sinus arrhythmia is small at rapid, and large at slow breathing rates. The strong correlation between systolic pressure and R-R intervals at respiratory frequencies reflects the influence of respiration on these two measures, rather than arterial baroreflex physiology. A wide range of evidence suggests that respiratory activity gates the timing of autonomic motoneurone firing, but does not influence its tonic level. I propose that the most enduring significance of respiratory gating is its use as a precisely controlled experimental tool to tease out and better understand otherwise inaccessible human autonomic neurophysiological mechanisms.
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In this communication, the altered homeostatic theory will be discussed and updated, and evidence will be presented that the premises of the theory might permit improvement of the prevention of ischemic heart disease (IHD). This hypothesis, first described in 1999, argues that IHD is due basically to an inappropriate shift of homeostasis, and the theory includes the position that S-RV directly induces symptoms. In contrast, the standard approach to IHD is based fundamentally on two principles: that atherosclerosis is due fundamentally to lipid abnormalities, and that symptoms in IHD are due to obstructive complications of atherosclerosis in epicardial coronary arteries. Suggestions for prevention stem from the altered homeostatic theory's different basic conceptualization of this disorder, and it seems reasonable that accepted basic pathogenetic mechanisms help shape measures to prevent IHD. Many of the theory's positions for preventing IHD parallel standard views, but the theory's basic premises have resulted in significant differences between the standard and the theory's overall approach to the prevention of IHD. Positions for the prevention of IHD include: the possibility that any preventative factor can improve any risk factor, the use of substitute preventative factors to counter unmodifiable or difficult to correct risk factors, underestimation of the risk of IHD by the standard position in individuals with normal lipid levels but multiple other risk factors, the probable relative overemphasis of the risk factor of cholesterol, the value of a national program to reduce the incidence of multiple disorders with similar risk factors, an alternate approach to the use of statins, and the value of an evolutionary approach to preventing IHD and other disorders.