The contribution of local factors to the elevated venous tone of congestive heart failure.

Since the concept of an elevated venous tone in congestive heart failure (CHF) has been recently questioned, the venous volume of the elevated calf at a venous pressure of 30 mm Hg (VV[30]) was determined in 18 normal volunteers (N) and 10 CHF patients with a mercury-in-rubber strain gauge plethysmograph. CHF patients had a significantly lower VV[30] at rest and after intra-arterial phentolamine (2 mg) than normal subjects, suggesting that in these patients a state of peripheral venoconstriction existed (rest-N: 4.63+/-0.17, CHF: 1.7+/-0.23 ml/100 ml, P < 0.01; pre- and postphentolamine-N: 4.85+/-0.21 to 4.95+/-0.31, CHF: 2.26+/-0.29 to 2.68+/-0.38 ml/100 ml, P < 0.01). Of note is that alpha adrenergic blockade failed to increase VV[30] significantly in N, but did increase it in CHF (P < 0.05), suggesting that part of the decreased VV[30] in CHF in due to an augmented sympathoadrenal discharge. When sodium nitrite (30 mg) was given as a single intra-arterial injection before or after phentolamine or when given in four successive doses at 3-min intervals, the VV[30] of CHF patients was never increased to more than 3.62+/-0.42 ml/100 ml and was always less than N (P < 0.01). Importantly, VV[30] in CHF after these interventions was even significantly less than that of N before intervention (P < 0.05), suggesting that factors other than local active smooth muscle venoconstriction were operative in CHF to lower VV[30]. It is suggested that perhaps clinically undetectable edema and an elevated tissue pressure may account for these differences.