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.

Adult↗

PubMed1974

The cardiovascular effects of morphine. The peripheral capacitance and resistance vessels in human subjects.

To evaluate the effects of morphine on the peripheral venous and arterial beds, 69 normal subjects were evaluated before and after the intravenous administration of 15 mg morphine. Venous tone was determined by three independent techniques in 22 subjects. The venous pressure measured in a hand vein during temporary circulatory arrest (isolated hand vein technique) fell from 20.2+/-1.4 to 13.4+/-0.9 mm Hg (P < 0.01) 10 min after morphine, indicating that a significant venodilation had occurred. With the acute occlusion technique, morphine induced a reduction in forearm venous tone from 12.8+/-1.1 to 7.9+/-2.3 mm Hg/ml/100 ml (P < 0.01). Although forearm venous volume at a pressure of 30 mm Hg (VV[30]) was increased from 2.26+/-0.17 to 2.55+/-0.26 ml/100 ml, measured by the equilibration technique, the change was not significant (P > 0.1). Of note is that the initial reaction to morphine was a pronounced venoconstriction, demonstrated during the first 1-2 min after the drug. (Isolated hand vein pressure increased to 37.2+/-5.4 mm Hg, P < 0.01). This rapidly subsided, and by 5 min a venodilation was evident. Morphine did not attenuate the venoconstrictor response to a single deep breath, mental arithmetic, or the application of ice to the forehead when measured by either the isolated hand vein technique or the equilibration technique. To evaluate the effects of morphine on the peripheral resistance vessels in 47 normal subjects, forearm blood flow was measured plethysmographically before and 10-15 min after the intravenous administration of 15 mg of morphine. Although mean systemic arterial pressure was unchanged, forearm blood flow increased from 2.92+/-0.28 to 3.96+/-0.46 ml/min/100 ml (P < 0.01), and calculated vascular resistance fell from 42.4+/-5.2 to 31.6+/-3.2 mm Hg/ml/min/100 ml (P < 0.01). When subjects were tilted to the 45 degrees head-up position, morphine did not block the increase in total peripheral vascular resistance that occurs; however, it did significantly attenuate the forearm arteriolar constrictor response (before morphine, + 25.7+/-5.4; after morphine, + 13.7+/-5.3 mm Hg/ml/min/100 ml, P < 0.05). However, morphine did not block the post-Valsalva overshoot of blood pressure, nor did it block the increase in forearm vascular resistance produced by the application of ice to the forehead. Similarly, morphine did not block the arteriolar or venoconstrictor effects of intra-arterially administered norepinephrine. Morphine infused into the brachial artery in doses up to 200 mug/min produced no changes in ipsilateral forearm VV[30], forearm blood flow, or calculated forearm resistance. Intra-arterial promethazine, atropine, and propranolol did not block the forearm arteriolar dilator response to intravenous morphine; however, intra-arterial phentolamine abolished the response. These data suggest that in human subjects, morphine induces a peripheral venous and arteriolar dilation by a reflex reduction in sympathetic alpha adrenergic tone. Morphine does not appear to act as a peripheral alpha adrenergic blocking agent but seems to attenuate the sympathetic efferent discharge at a central nervous system level.

Adult↗

PubMed1974