Static and dynamic responses of carotid sinus baroreceptors in dogs with chronic volume overload.

Abstract

SUMMARY1. In this study we determined if there are any alterations in carotid sinus baroreceptor discharge in a model of heart failure in the dog.2. The left carotid sinus was isolated and perfused at 100 mmHg with a modified Krebs-Henseleit solution. Two groups of dogs were used: a normal group and a group with a chronic aorto-caval fistula (a.v.f.) of up to 20 weeks duration.3. The a.v.f. group had a significantly elevated heart rate and left ventricular end diastolic pressure as well as an increased arterial pulse pressure compared to normals. However, mean arterial pressure measured in the aortic arch was not significantly different.4. Carotid sinus pressure-discharge curves were constructed during increases in carotid sinus pressure by steps and by ramps of pressure change up to 200 mmHg/s. Carotid sinus diameter was also measured using sonomicrometer crystals.5. In six dogs from each group the sodium, potassium and water content of the right carotid sinus was measured.6. Several parameters of second order polynomial curves that were fitted to the data were compared between the two groups for step and ramp increases in pressure. These included maximum baroreceptor gain, threshold pressure and plateau pressure.7. Baroreceptor gain was significantly lower in the a.v.f. group for the step and lowest ramp rate pressure changes. Threshold pressure was significantly higher for the a.v.f. group for steps and the three slowest ramp rates. Plateau pressures were significantly higher for the steps and lowest ramp rate.8. The carotid sinus strain that was produced at any given carotid sinus pressure was not significantly different between the two groups. In addition, there was no difference in the sodium, potassium or water content of the carotid sinus between the two groups.9. It was concluded that there is a depression of the static discharge characteristics in this model of heart failure which is not due to an alteration in electrolyte or water content or to the compliance of the carotid sinus.

Baroreceptor Sensitivity During the Compensatory Phase of Left Ventricular Overloading

“…Although most previous studies have examined baroreceptor sensitiviy in congestive heart failure in the dog, [14][15][16] we assessed this issue in rabbits with AR, the animal model in which we previously described alterations in hemodynamics and -adrenergic receptors over the 4 weeks after left ventriocular overloading. 17 Myosin heavy chain isoenzyme composition, which has a central role in the pathophysiology of congestive heart failure, is similar in rabbits and humans.…”

“…Niebauer and Zucker showed that baroreceptor gain was lower in dogs with chronic volume overload induced by aortocaval fistula than in control dogs for both the step and lowest ramp rate pressure changes. 15 A steady-state method may have an advantage in assessing both vagal and sympathetic traffics whereas a ramp method essentially reflects vagal traffic. 33 Although several previous animal studies were undertaken in the anesthetized state, 6,15,16 we assessed baroreceptor-mediated reflex in the awake state to minicompared with that before production of AR (1.78±0.47 msec/mmHg).…”

“…15 A steady-state method may have an advantage in assessing both vagal and sympathetic traffics whereas a ramp method essentially reflects vagal traffic. 33 Although several previous animal studies were undertaken in the anesthetized state, 6,15,16 we assessed baroreceptor-mediated reflex in the awake state to minicompared with that before production of AR (1.78±0.47 msec/mmHg). The sensitivity was significantly decreased in the first week after production of AR (0.83±0.32 msec/mmHg, p<0.05).…”

“…14 Niebauer and Zucker examined the carotid sinus-discharge relationship by perfusing the carotid sinus with controlled pressure in dogs with aortocaval fistula, and found that the baroreceptor gain was lower and the threshold pressure was higher in dogs with chronic volume overload than in control dogs. 15 DibnerDunlap and Thames measured aortic and renal nerve activity during changes in blood pressure induced by phenylephrine and nitroglycerin infusions in anesthetized, ventricular-paced dogs. 16 They found that the gain of aortic nerve activity induced by blood pressure perturbation was decreased in dogs with heart failure, but was not the case for renal sympathetic efferent nerve activity.…”

“…There is accumulating evidence suggesting that arterial baroreceptor-mediated control and cardiopulmonary receptor-mediated control are altered in both human [10][11][12][13] and experimental heart failure, [14][15][16] but there are few studies concerning the compensatory process after acute left ventricular overloading. We previously demonstrated that left ventricular function progressively deteriorated, along with myocardial -adrenergic receptor down-regulation, depletion of catecholamines and an increase in plasma norepinephrine level, during the first week after production of aortic regurgitation (AR) in rabbits.…”