Hemorrhage‐induced increase in total peripheral resistance is blunted in conscious obese Zucker rats

Abstract

Obesity is associated with increased morbidity and mortality after severe hemorrhage. We hypothesize that in obesity, the blood pressure compensation following severe hemorrhage is impaired due to blunted neurohormonal responses. Mean arterial pressure (MAP) and heart rate (HR) in conscious lean (LZ) and obese Zucker rats (OZ) were monitored before and after injection of SNP or prazosin (iv.) to estimate baroreflex sensitivity or basal sympathetic tone, respectively. Severe hemorrhage (a loss of 35% of total blood volume) was induced in additional groups of conscious LZ and OZ. The MAP, HR, cardiac output (CO), total peripheral resistance (TPR), and plasma renin activity (PRA) were measured before and one hour after hemorrhage. Basal values for MAP, CO, TPR, and PRA were not different between conscious LZ and OZ. However, under basal conditions, prazosin resulted in a larger fall in MAP in OZ (134 ± 3 to 85 ± 4 mmHg) than in LZ (129 ± 4 to 96 ± 4 mmHg). In addition, baroreflex control of HR was impaired in OZ. Following hemorrhage, MAP and HR recovery were more complete in LZ than in OZ. CO was similar in both groups but MAP, TPR, HR, and PRA were significantly lower in OZ than in LZ (Table). These results indicate that the diminished recovery of MAP after hemorrhage in OZ is due to a blunted increase in TPR associated with impaired renin secretion and baroreflex activity. Supported by AHA‐12SDG12050525, NIH HL‐51971, and HL‐89581