Mechanisms of action of morphine in the treatment of experimental pulmonary edema

The Cardiovascular Effects of Morphine THE PERIPHERAL CAPACITANCE AND RESISTANCE VESSELS IN HUMAN SUBJECTS

“…Morphine is one of the most useful drugs available for treating patients with acute pulmonary edema (1)(2)(3)(4) and…”

“…Morphine might alter any portion of the reflex arc from peripheral mechanoreceptor perception of hypotension through central nervous system integration to the usual effector responses of tachycardia, peripheral arteriolar constriction, and possibly venoconstriction. It has been suggested by animal studies that morphine does produce a venodilation that leads to a peripheral pooling of blood, and that this is the mechanism by which morphine improves pulmonary edema (2,16,18). Further, numerous studies have been done on the effects of morphine on the peripheral resistance vessels; however, considerable conflict still exists regarding the direction, magnitude, and mechanism of the response (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19).…”

Effects of morphine on coronary and left ventricular dynamics in conscious dogs.

“…was given, which exerted a mild respira- (5,23,24), it is thought to exert little effect on the normal circulation, as reflected by alterations in heart rate, arterial pressure, cardiac output, and systemic vascular resistance (1, 3, 4). Except for a transient in- 5 The average ±.SEM changes from control are shown for LV end-diastolic diameter, dP/dt/P, late diastolic arterial pressure, coronary flow, and resistance after small doses of morphine, i.e., 0.25 mg/kg every 15 min (6 dogs).…”

“…The beneficial effects of morphine in the therapy of acute pulmonary edema are attributed to its sedative action and to a reduction in venous return due to peripheral venous pooling (5,23,24). A reduction in venous return due to venous pooling would tend to reduce cardiac preload, i.e., end-diastolic size.…”

Harmful impact of morphine use in acute heart failure

“…The use of opiates in the treatment of heart failure dates back to the 1960s, and opiates were considered one of the most important agents for treatment of heart failure in the 1970s (2,3). The most reasonable argument for use of morphine in treating acute heart failure is that it possesses some vasodilatory properties, which have been reported in several studies performed between the 1960s and 1980s (4)(5)(6), suggesting that morphine is beneficial in acute heart failure by decreasing venous tone and increasing peripheral venous pooling, leading to decreased cardiac filling pressures. Achieving decreased filling pressure is an important goal of therapy in the early phase of acute heart failure; therefore, morphine could prove beneficial in this regard.…”