Baroreflex Testing Research Articles

Attenuation of arterial baroreflex control of renal sympathetic nerve activity during lidocaine infusion in alpha–chloralose–anesthetized dogso

The purpose of this study was to identify the relationship between sensitivity of arterial baroreflex and plasma concentrations of lidocaine. Using twelve mongrel dogs anesthetized with alpha-chloralose, the left kidney was exposed retroperitoneally, and renal sympathetic nerve activity was recorded continuously. Lidocaine was infused in four different doses: 2 mg.kg BW-1 bolus + 100 micrograms.BW-1 x min; 3 mg.kg BW-1 bolus + 200 micrograms.kg BW-1 x min; 6 mg.kg BW-1 bolus + 400 micrograms.kg BW-1 x min; and 12 mg.kg BW-1 + 800 micrograms.kg BW-1 x min. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after beginning lidocaine infusion. Plasma lidocaine concentrations determined by high performance liquid chromatography revealed that the steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at plasma concentrations of lidocaine below 5 micrograms.ml-1. However, cardiac and sympathetic baroreflex sensitivity were significantly attenuated (P < 0.01) when plasma lidocaine concentrations were well above human convulsion levels (10 micrograms.ml-1). The results indicate that hemodynamic derangement observed in the lidocaine-induced central nervous system toxicity is, at least in part, due to the attenuated arterial baroreflex.

Prognostic value of baroreflex sensitivity testing after acute myocardial infarction.

Disturbances of autonomic function are recognised in both the acute and convalescent phases of myocardial infarction. Recent studies have suggested that disordered autonomic function, particularly the loss of protective vagal reflexes, is associated with an increased incidence of arrhythmic deaths. The purpose of this study was to compare the value of differing prognostic indicators with measures of autonomic function and to assess the safety of arterial baroreflex testing early after infarction. As part of a prospective trial of risk stratification in post-infarction patients arterial baroreflex sensitivity, heart rate variability, long term electrocardiographic recordings, exercise stress testing, and ejection fraction were recorded between days 7 and 10 in 122 patients with acute myocardial infarction. During a one year follow up period there were 10 arrhythmic events. Baroreflex sensitivity was appreciably reduced in these patients suffering arrhythmic events (1.73 SD (1.49) v 7.83 (4.5) ms/mm hg, 95% confidence interval (CI) 4.8 to 7.3, p = 0.0001). Significant correlations were noted with age (r = -0.68, p less than 0.001) but not left ventricular function. When baroreflex sensitivity was adjusted for the effects of age and ventricular function baroreflex sensitivity was still considerably reduced in the arrhythmic group (2.1 v 7.57 ms/mm Hg, p less than 0.0001). Depressed baroreflex sensitivity carried the highest relative risk for arrhythmic events (23.1, 95% CI 7.7 to 69.2) and was superior to other prognostic variables including left ventricular function (10.4, 95% CI 3.3 to 32.6) and heart rate variability (10.1, 95% CI 5.6 to 18.1). No major complications were noted with baroreflex testing and in particular no patients developed ischaemic or arrhythmic symptoms during the procedure. Disordered autonomic function as measured by depressed baroreflex sensitivity or reduced heart rate variability was associated with an increase incidence of arrhythmic events in post-infarction patients. Baroreflex testing can be safely performed in the immediate post-infarction period.

Normotensive Diabetic BB/W Rats Show Enhanced Reflex Tachycardia

Spontaneously diabetic BB/W rats were compared with age-matched regular Wistar and nondiabetic BB/W rats to determine whether the presence of diabetes would alter cardiovascular regulation appreciably. Systolic and mean blood pressures measured with the tail-cuff method from 12 to 26 wk of age tended to be slightly higher in diabetic than nondiabetic BB/W rats, but the differences were not significant. Mean pressures recorded from indwelling catheters in the same rats at 28 wk of age also did not differ significantly, thereby verifying that the diabetic rats were not hypertensive. To measure baroreflex sensitivity, heart-rate responses were elicited reflexly by elevating blood pressure with phenylephrine or lowering it with sodium nitroprusside. Although reflex bradycardia elicited with phenylephrine was the same, reflex tachycardia elicited with sodium nitroprusside was more pronounced in diabetic BB/W than other rats. Underlying autonomic mechanisms were then assessed by repeating the baroreflex tests after either cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Magnitude of reflex bradycardia after inhibition by either cholinergic or beta-adrenergic blockade still did not differ between rat groups but that of reflex tachycardia remained significantly stronger in diabetic BB/W than other rats. These results collectively show that, although diabetic BB/W rats remained normotensive, they had enhanced reflex tachycardia that persisted even after efferent autonomic blockade. The failure to develop higher pressures with time further indicates that without additional manipulation, these rats cannot be used experimentally to simulate the simultaneous presence of hypertension in diabetic patients.

Differential age-dependent attenuation of reflex tachycardia by verapamil in rats

To determine if verapamil alters baroreflex function differently depending on age, reflex heart rate responses to intravenous infusions of phenylephrine or sodium nitroprusside were compared in conscious 5- and 14-month-old rats before and after daily oral administration of verapamil (100 mg/kg) for 6 days. The effects of verapamil on parasympathetic and sympathetic mediation of heart rate were also assessed by repeating baroreflex tests after treatment with either propranolol or atropine. All reflex heart rate responses were initially smaller in 14- than in 5-month-old rats. Regardless of age, magnitude of reflex bradycardia or the effects on it of either cholinergic or β-adrenergic blockade, were unaffected by verapamil. By contrast, reflex tachycardia which was attenuated in both age groups, was decreased further by subsequent cholinergic or β-adrenergic blockade in 5-month-old rats, but only by cholinergic blockade in 14-month-old rats. These findings suggest that while verapamil did not affect autonomic mediation of reflex bradycardia, it reduced that of reflex tachycardia differently depending on age. Whereas it attenuated both sympathetic and parasympathetic mediation of reflex tachycardia in 5-month-old rats, it attenuated only sympathetic mediation in 14-month-old rats.

Autonomic regulation of reflex bradycardia in rats declines with age

Heart rate responses, elicited reflexly by elevating blood pressure with phenylephrine or lowering it with sodium nitroprusside, were compared in groups of rats aged 4 and 14 months. All tests were done while the rats were awake to avoid artefacts due to anesthesia. Parasymphatetic and sympathetic contributions were assessed by repeating baroreflex tests after cholinergic blockade with atropine or β-adrenergic blockade with propranolol. Magnitude of reflex bradycardia was initially smaller in the 14-month-old rats than in the younger rats thereby indicating that baroreflex sensitivity had diminished with age. After β-adrenergic or cholinergic blockade, adjusted means (obtained by covariance analysis) for reflex tachycardia did not differ significantly between rat groups, but those for reflex bradycardia were significantly smaller in the 14-month-old rats than in the younger rats. Selective attenuation of reflex bradycardia after either cholinergic or β-adrenergic blockade indicates that concurrent parasympathetic activation and sympathetic withdrawal during reflex bradycardia were also reduced in 14-month-old rats. These results suggest that as autonomic mediation of reflex bradycardia diminishes with age, old rats may no longer be able to slow the heart as easily whenever blood pressure rises, but they can still accelerate it whenever blood pressure falls.

Enhanced sympathetic mediation of chronotropic baroreflexes in old Sprague—Dawley rats

We compared reflex heart rate responses elicited during intravenous infusions of phenylephrine or sodium nitroprusside in conscious 4- and 24-month-old male Sprague—Dawley rats to determine whether baroreflex regulation changes with age. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or β-adrenergic blockade with propranolol. Basal blood pressures always tended to be higher, while corresponding heart rates were lower, in old than in young rats. Reflex bradycardia (but not tachycardia) was initially weaker in 24-month-old rats as were reductions in both reflex bradycardia and tachycardia after cholinergic blockade. On the other hand, the reduction in reflex tachycardia following β-adrenergic blockade in old rats was more pronounced and almost equal to that produced by combined cholinergic and β-adrenergic blockade. From these results we conclude that with old age in male Sprague—Dawley rats, just as has been shown previously in Fischer 344 rats, predominant efferent pathways for regulating heart rate reflexes are also altered to become almost exclusively β-adrenergic or sympathetic.

Mediation of reflex tachycardia becomes exclusively β-adrenergic in old Fischer 344 rats

To study how baroreflex regulation changes with age we compared reflex heart rate responses elicited in awake Fischer 344 rats of different ages during intravenous infusions of phenylephrine or sodium nitroprusside. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or β-adrenergic blockade with propranolol. Basal heart rates always tended to be lower in old than in young rats, but the differences became statistically significant only after β-adrenergic or combined cholinergic and β-adrenergic blockade. Most reflex heart rate responses (i.e. except reflex tachycardia in males during depressor responses to sodium nitroprusside) were initially weaker in old than in younger rats. Reflex bradycardia and tachycardia were reduced equally in both age groups after cholinergic blockade, but were reduced more in old than in young rats after β-adrenergic blockade. β-adrenergic blockade alone reduced reflex tachycardia as much as did combined blockade thereby suggestng that the predominant neural mechanism was β-adrenergic. Taken altogether these reuslts are compatible with the interpretation that efferent pathways for mediating heart rate reflexes in Fischer 344 rats are altered with age such that as parasympathetic mediation diminishes, residual mediation particularly of reflex tachycardia, becomes almost exclusively β-adrenergic or sympathetic.

Effects of high-frequency jet ventilation on arterial baroreflex regulation of heart rate.

Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ventilation (CPPV) on arterial baroreflex regulation of heart rate. Systolic arterial pressure and right atrial pressure were measured using indwelling catheters. Electrocardiogram (ECG) and mean airway pressure were continuously monitored. Lung volumes were measured using two linear differential transformers mounted on thoracic and abdominal belts. Baroreflex testing was performed by sequential intravenous bolus injections of phenylephrine (200 micrograms) and nitroglycerin (200 micrograms) to raise or lower systolic arterial pressure by 20-30 Torr. Baroreflex regulation of heart rate was expressed as the slope of the regression line between R-R interval of the ECG and systolic arterial pressure. In each mode of ventilation the ventilatory settings were chosen to control mean airway pressure and arterial PCO2 (PaCO2). In HFJV a tidal volume of 159 +/- 61 ml was administered at a frequency of 320 +/- 104 breaths/min, whereas in CPPV a tidal volume of 702 +/- 201 ml was administered at a frequency of 13 +/- 2 breaths/min. Control values of systolic arterial pressure, R-R interval, mean pulmonary volume above apneic functional residual capacity, end-expiratory pulmonary volume, right atrial pressure, mean airway pressure, PaCO2, pH, PaO2, and temperature before injection of phenylephrine or nitroglycerin were comparable in HFJV and CPPV. Baroreflex regulation of heart rate after nitroglycerin injection was significantly higher in HFJV (4.1 +/- 2.8 ms/Torr) than in CPPV (1.96 +/- 1.23 ms/Torr).(ABSTRACT TRUNCATED AT 250 WORDS)

Nutrient control of cardiac rate in infant rats: role of arterial baroreceptors

A surgical procedure is described for the deafferentation of carotid sinus (CS) and aortic depressor (AD) baroreceptors in 2-wk suckling rats. Baroreflex testing in unanesthetized pups showed that cardiac rate responses to acute elevations of blood pressure were reduced to less than 9% of controls after combined denervation (CSAD), 28% after AD and 47% after CS denervation at 4 h. After 24 h of nutrient deprivation, resting cardiac rates of sham operated controls fell a mean of -148 beat/min, significantly more than CS, AD, or CSAD groups (P less than 0.01). Baroreflex test responses in individuals correlated significantly with their later responses to nutrient deprivation (r = 0.67, P less than 0.01). There were no significant differences in base-line cardiac rate, systolic blood pressure, or cardiac rate during 24 h intragastric milk infusion between deafferented and control pups. These experiments suggest that arterial baroreceptors are important in the cardiovascular adjustments after nutrient deprivation in suckling rats.

Effects of 1000 Rads 60 Co on Baroreceptor Reflex Responses to Phenylephrine and Carotid Occlusion in Monkeys

Failure of the baroreceptor reflex mechanisms has been proposed as a basis for the early hypotension seen in monkeys after high-dose, whole-body irradiation. The present work involved the testing of baroreflex sensitivity by carotid occlusion and phenylephrine injection before and after 1000 rads60 Co in nine unanesthetized, restrained monkeys. During the early postradiation minutes, at the time of deepest hypotension, both of the baroreflex tests revealed depressed baroreflex sensitivity (diminished blood pressure and heart rate responses). After 8-15 min postirradiation, the phenylephrine, but not the occlusion, test demonstrated a reversal to significant baroreflex hypersensitivity which persisted 24 hr or more. Early shifts in the set level relation between blood pressure and heart rate also occurred after irradiation. No failure of the baroreflex mechanisms was evident, in contradiction to a previous finding.