OBJECTIVE: Hypertensive patients having higher baseline peripheral resistance and sympathetic tone than normotensive patients may have aberrant responses to hemorrhage. In an attempt to further characterize this clinical observation, the authors compared the hemodynamic and metabolic responses to hemorrhage between spontaneously hypertensive rats (SHR) and normotensive rats (NTR). METHODS: Twenty adult rats (10 NTR and 10 SHR) were anesthetized with althesin via the intraperitoneal route. Femoral arteries were cannulated by cutdown. Twelve (6 SHR and 6 NTR) rats underwent controlled catheter hemorrhage of 25% of their total blood volumes. Eight rats (4 SHR and 4 NTR) served as nonhemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured prehemorrhage and then every 15 minutes for the next 120 minutes. Data were reported as mean +/- standard error of the mean (SEM). Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an alpha = 0.05. RESULTS: Immediately after hemorrhage, the SHR group experienced a significantly (p < 0.001) greater drop in MAP of 70 +/- 4% in the SHR vs 40 +/- 6% in the NTR. Blood pressure in the NTR returned to control values 15 minutes after hemorrhage, but the SHR remained relatively hypotensive for the entire length of the experiment. Base excess in the SHR decreased significantly (p < 0.004) by 8.2 +/- 2 mmol/L from control values, as compared with no changes in BE for the NTR. CONCLUSIONS: The authors observed significant differences in the response to hemorrhage between hypertensive and normotensive rats. Hypertensive rats experienced a more profound hemorrhagic shock insult than normotensives for the same degree of blood loss.
OBJECTIVE:Hypertensivepatients having higher baseline peripheral resistance and sympathetic tone than normotensive patients may have aberrant responses to hemorrhage. In an attempt to further characterize this clinical observation, the authors compared the hemodynamic and metabolic responses to hemorrhage between spontaneously hypertensiverats (SHR) and normotensive rats (NTR). METHODS: Twenty adult rats (10 NTR and 10 SHR) were anesthetized with althesin via the intraperitoneal route. Femoral arteries were cannulated by cutdown. Twelve (6 SHR and 6 NTR) rats underwent controlled catheter hemorrhage of 25% of their total blood volumes. Eight rats (4 SHR and 4 NTR) served as nonhemorrhage controls. Mean arterial pressure (MAP) and base excess (BE) were measured prehemorrhage and then every 15 minutes for the next 120 minutes. Data were reported as mean +/- standard error of the mean (SEM). Group comparisons were analyzed by ANOVA with repeated values post-hoc by Bonferroni. Statistical significance was defined by an alpha = 0.05. RESULTS: Immediately after hemorrhage, the SHR group experienced a significantly (p < 0.001) greater drop in MAP of 70 +/- 4% in the SHR vs 40 +/- 6% in the NTR. Blood pressure in the NTR returned to control values 15 minutes after hemorrhage, but the SHR remained relatively hypotensive for the entire length of the experiment. Base excess in the SHR decreased significantly (p < 0.004) by 8.2 +/- 2 mmol/L from control values, as compared with no changes in BE for the NTR. CONCLUSIONS: The authors observed significant differences in the response to hemorrhage between hypertensive and normotensive rats. Hypertensiverats experienced a more profound hemorrhagic shock insult than normotensives for the same degree of blood loss.