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The hemodynamic basis of neurogenic hypertension was studied in unanesthetized rabbits 10 minutes to 30 days after sinoaortic denervation (SAD). The fractional distribution of 86Rb to body tissues was determined and used to calculate regional blood flow from the value of cardiac output obtained from an arterial dilution curve of the indicator. Sham-operated rabbits served as controls. Increased cardiac output was a major hemodynamic component of SAD hypertension in 69% of the rabbits studied 1–40 hours postoperatively (acutely) but in only 25% of those studied 3–30 days after surgery (chronically). In the majority of the chronic SAD rabbits, increased total peripheral resistance (TPR) was the basis of the hypertension. All SAD rabbits had increased heart rates. Acutely, most high-cardiac output hypertensive rabbits had increased splanchnic resistance with normal blood flow, whereas all of them had low or normal renal resistance with high blood flow. Flows were increased in other major regions. Acutely, in the few high-TPR hypertensive rabbits, resistance was significantly increased in splanchnic tissue, liver, and carcass but not in the kidneys. Chronically, renal resistance was elevated in both types of hypertension. Chronic high-TPR rabbits had increased resistance in all major regions, but, unlike the acute high-TPR group, increased carcass resistance was located in bone rather than skeletal muscle. In the few chronic high-cardiac output hypertensive rabbits, TPR was reduced and regional blood flows were high with the exception of that to the kidneys and liver. Skin received a larger percent of cardiac output in chronic hypertensive rabbits than it did in acute hypertensive rabbits regardless of the hemodynamic basis of the hypertension.

Regional and Systemic Hemodynamic Patterns in Rabbits with Neurogenic Hypertension