To elucidate the hemodynamic effects of prazosin, an antihypertensive agent, in congestive heart failure, we studied 10 patients with ischemic cardiomyopathy and severe ventricular dysfunction. After an oral dose of 2 to 7 mg, heart rate was unchanged (P greater than 0.05). One hour after prazosin administration, mean arterial pressure declined from 95 to 78 mm Hg (P less than 0.001); left ventricular filling pressure declined from 30 to 18 mm Hg (P less than 0.001), cardiac index increased from 2.1 to 2.9 liters per minutes per square meter (P less than 0.001), and systemic vascular resistance fell from 2074 to 1156 dynes sec cm-5 (P less than 0.001). In both forearms vascular resistance and venous tone were reduced (86 to 48 mm Hg per ml per 100 g per minute, and 59 to 18 mm Hg per ml, respectively [P less than 0.001]). All responses persisted for a least six hours (P less than 0.01). Prazosin benefits severe congestive heart failure by inducing a sustained fall of both cardiac preload and impedance.
2. Powell WJ Jr, DiBona DR, Flores J, Leaf A: The protective effect of hyperosmotic mannitol in myocardial ischemia and necrosis. Circulation 54: 603, 1976 graphic end-diastolic dimension fell (5.7 to 5.4 cm, P < 0.001) while shortening fraction increased (27.6 to 30.2%, P < 0.005). Treadmill exercise duration increased from 209 to 317 seconds (P < 0.001). Symptoms diminished throughout the duration of follow-up (mean 94 days) with improvement in NYHA functional class (3.7 to 2.2, P < 0.001). Thus, prazosin possesses sustained nitroprusside-like balanced dilator actions on the systemic arterial and venous systems and is effective in the ambulatory management of chronic severe heart failure.agent are related to its equal relaxation of the vascular smooth muscle of both the peripheral resistance and the capacitance vessels.23 As the result of this balanced dilator action on the systemic venous and arterial beds, ventricular preload reduction is accompanied by decline in aortic impedance, thereby leading to relief of pulmonary congestion simultaneously with enhancement of cardiac output. However, attempts to continue the benefits of such balanced ventricular unloading therapy in ambulatory patients with chronic heart failure have been difficult because of the lack of an oral vasodilator drug with both arteriolar and venous relaxing properties. Thus the nitrates, which principally cause venodilation, are capable of reducing ventricular preload and pulmonary congestion3' 13,14,16,19,[23][24][25][26] but lack consistent effects on systemic impedance and therefore produce minimal alterations of cardiac output
The hemodynamic benefits of combining administration of dopamine with nitroprusside (NP) were evaluated in nine patients with chronic congestive heart failure due to ischemic, idiopathic myocardial or valvular cardiac disease. NP alone (68 microng/min) produced decline in left ventricular end-diastolic pressure (LVEDP) from 25.4 to 14.1 mm Hg (p less than 0.01) but modest increase in cardiac index (CI) from 2.41 to 3.02 L/min/m2 (P less than 0.05). Dopamine alone (6 microng/kg/min) caused an elevation of CI to 3.36 (P less than 0.01) but without decrease of LVEDP. Simultaneous infusion of the two agents resulted in favorable alterations in both hemodynamic variables: LVEDP decreased to 15.7 (P less than 0.01) and CI increased to 3.52 (P less than 0.01). It is concluded that dopamine substantially enhances the effectiveness of nitroprusside therapy in congestive heart failure by providing concomitantly the principal beneficial actions of the vasodilator and dopamine used separately. Thus combined dopamine with NP treatment considerably raises low CI while markedly reducing elevated LVEDP and provides a potentially efficacious pharmacologic modality for the treatment of severe congestive heart failure due to left ventricular dysfunction.
The effects of oral prazosin on the peripheral circulation were evaluated in 10 subjects, including 7 patients with chronic congestive failure due to coronary heart disease. To achieve this purpose the actions of 30 to 50 micrograms/kg body weight prazosin were assessed on both the forearm arteriolar and venous beds simultaneously with the use of the limb plethysmographic technique. Prazosin produced marked decline of forearm venous tone (FVT) from 44.5 +/- 12.3 to 14.3 +/- 3.1 mm Hg/ml (p less than 0.01) concomitant with marked decrease in forearm vascular resistance (FVR) from 70.2 +/- 11.4 to 48.4 +/- 4.9 mm Hg/ml/100 gm/min (p less than 0.05) which persisted for at least 60 mins without change in heart rate. These findings, demonstrating that prazosin induces systemic venodilation and peripheral arteriolodilation, indicate potential benefits of the oral drug for relief of pulmonary congestion and elevations of cardiac output in patients with chronic congestive heart failure.
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