CAROTID BAROREFLEX CONTROL DURING HEMORRHAGE IN CONSCIOUS AND ANESTHETIZED DOGS

The hypothesis was tested that carotid baroreflex gain is increased af ter 20% hemorrhage. The baroreceptor reflex responses to changes in ca rotid sinus pressure (CSP) were measured in control, 20% hemorrhage, a nd reinfusion conditions in three experimental groups: conscious intac t (n = 7), anesthetized intact (n = 8), and anesthetized vagotomized ( n = 8) dogs. Mean arterial pressure (MAP), heart rate (HR), cardiac ou tput (CO), stroke volume (SV), and calculated total peripheral resista nce (TPR) responses to changes in CSP were measured. At any given CSP, MAP, CO, and SV all decreased significantly with the 20% hemorrhage, as reflected by a downward shift in the reflex characteristic curve wi th no change in overall reflex range or gain. In contrast, TPR and HR responses to CSP were not significantly altered by 20% hemorrhage; ref lex curves and gains were comparable to control conditions. In the con scious intact dogs, the maximal reflex gain, G(max), for the MAP respo nse was -1.365 +/- 0.25, -1.298 +/- 0.33, and -1.324 +/- 0.25 in contr ol, 20% hemorrhage, and reinfusion conditions, respectively, and was n ot significantly altered by hemorrhage. In the same group, the G(max) for the HR response was -1.792 +/- 0.65, -1.709 +/- 0.33, and -1.986 /- 0.67 in control, 20% hemorrhage, and reinfusion conditions, respect ively; baroreflex gain on HR was not increased with hemorrhage. Plasma arginine vasopressin (AVP), an increase in which has been proposed to augment baroreflex gain, increased from a control level of 0.98 +/- 0 .27 to 9.66 +/- 2.67 pg/ml during 20% hemorrhage in the conscious inta ct dogs; despite the increase in plasma AVP during hemorrhage, augment ation of baroreflex gain was not observed. These results suggest that baroreflex control of multiple efferent mechanisms is not augmented af ter a 20% decrease in blood volume.