Studies in Clinical Shock and Hypotension. II. Hemodynamic Effects of Norepinephrine and Angiotensin*

Although vasoconstrictor drugs have been widely used for many years in the treatment of hypoten-sion and shock, their clinical value is still the sub-ject of much controversy (1). Norepinephrine has been recommended for support of the blood pressure in shock occurring in a wide variety of clinical settings (2-5), but Nickerson (6) claims that its vasoconstrictor effect is deleterious and that it increases blood pressure at the expense of a further reduction in blood flow. Studies of the hemodynamic effects of norepi-nephrine in animal shock models have given con-flicting results. The rise in blood pressure induced by norepinephrine in hemorrhagic shock in dogs has been attributed to increases in cardiac output in some studies (7-9), but others have shown in-creases only in peripheral resistance (10) or in both output and resistance (11). Circulatory ef-fects also have been shown to vary at different stages of the hemorrhagic shock procedure (12, 13). Hemodynamic responses to norepinephrine have been studied extensively in normal subjects, but observations in hypotensive patients have been limited because of the difficulties encountered in performing studies on such acutely ill individuals. Gilbert and his associates (14) reported a slight fall in cardiac output during the infusion of norepi-nephrine in four patients with septic shock, whereas one of two hypotensive patients studied by Sambhi, Weil, Udhoji, and Rosoff (15) ex-hibited an increase in cardiac output. Smulyan, Cuddy, and Eich (16) found that norepinephrine increased the cardiac output in three of six patients