Adolescent anorexia nervosa, a psychiatric disease with high mortality, is often associated with bradycardia. We studied the vagal control of sinus node function in anorexic subjects, to investigate the mechanism of anorexic bradycardia. Cardiac vagal tone was determined in a group of 11 adolescent anorexic girls and in 11 age- and height-matched controls. Cardiac vagal tone in the anorexic patients was measured as the change in R-R interval in response to complete cholinergic blockade; in addition, non-invasive indices of cardiac vagal tone and baroreflex sensitivity were determined in both anorexic and control subjects. Cardiac vagal tone in anorexic subjects was 465 +/- 52 (SE) ms, about 30% higher than values reported for healthy subjects. Vagal tone values were directly related to percent weight loss (R = 0.69, P = 0.017). Non-invasive indices of both cardiac vagal activity and baroreflex sensitivity were significantly higher in the anorexic group as compared to controls; the percent increase of cardiac vagal tone, however, exceeded the increase of baroreflex sensitivity. Cardiac vagal hyperactivity significantly contributes to the bradycardia of anorexic subjects. The excess vagal activity is only partly explained by enhanced baroreflex sensitivity.
We investigated whether physiological variability in arterial baroreflex sensitivity (BRS) was related to differences in carotid elastic behavior among 19 young healthy subjects (age 18-26 yr). The diameter of the carotid artery (D) and its change during the arterial pulse (delta D) were monitored by a phase-locked echotracking device (UT-4 Hokanson), and pulse pressure (delta P) was measured in the brachial artery by sphygmomanometry. Distensibility coefficient (DC) for the common carotid artery was calculated using the formula DC = (2 x delta D/D)/delta P. Dynamic elastic parameters such as the maximum and mean rate of carotid artery expansion and the dominant harmonic frequency of the diameter curve were also determined. BRS was assessed by regressing R-F.intervals against systolic blood pressure, monitored by finger arterial pressure (FINAPRES), during an elevation of pressure, induced by intravenous bolus injection of phenylephrine. Using correlation and stepwise regression analysis, we found that BRS was significantly related to carotid artery distensibility (r = 0.778, P < 0.001) but was not related to any of the dynamic parameters of carotid pulsation.
We studied whether vasoactive drugs used to determine baroreflex sensitivity influence baroreceptor firing by affecting carotid sinus smooth muscle or simply by stretching the sinus wall through changes in pressure. In six young healthy subjects, the diameter of the carotid artery and its change with arterial pulse were measured with ultrasonography. Blood pressure was measured by Finapres. Phenylephrine and nitroglycerin doses were injected intravenously to raise and lower pressure by ∼15–25 mmHg. Carotid dimensions increased in all subjects during the phenylephrine-induced rise and decreased during the nitroglycerin-induced fall in pressure. Diastolic diameter changed more than systolic diameter; changes were significantly different from the control value (assessed by single-factor analysis of variance and Scheffé’s post hoc test). The systolic pressure-diameter relationship appeared to be nonlinear, with a steeper slope above than below baseline, and contributed significantly to the nonlinearity of the R-R interval-systolic pressure relationship. It is concluded that during drug-induced changes in blood pressure, baroreceptor activity in humans is influenced more by passive stretch than by local smooth muscle contraction.
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