nalorphine and Shock

Topics: Droperidol; Fentanyl; Humans; Intubation, Intratracheal; Kidney; Methods; Nalorphine; Neuroleptanalgesia; Nitrous Oxide; Preanesthetic Medication; Respiration; Respiration, Artificial; Shock; Time Factors

Electrical stimulation of the rabbit sciatic nerve resulted in the development of shock. Injection of physiological saline (1 ml, i. v.) did not change the progressive fall of the blood pressure or depression of palpitation and respiration. The animals died 135--191 min after discontinuance of the stimulation. Injection of nalorphine (0.4 mg/kg, i. v.) or naloxone (0.1 mg/kg i. v.) greatly improved the animals' condition. The blood pressure, palpitation and respiration returned to normal in 90--120 min after the injections. No lethal cases were recorded in this group of animals. It was shown in a supplementary group of animals that naloxone did not change the reserpine-produced hypotension.

Topics: Animals; Drug Evaluation, Preclinical; Electroshock; Nalorphine; Naloxone; Pain; Rabbits; Shock; Time Factors

Critical hemodynamic changes that are observed with the reduction of blood pressure in shock and the use of vasopressor agents as a temporary measure for maintaining arterial pressure so that irreparable tissue damage can be prevented are considered in this review of the use and efficacy of vasopressor agents in shock. Indications for adrenergic stimulators include severe hypotensive episodes, in which case an alpha-beta stimulator such as metaraminol or norepinephrine is the therapy of choice; hemorrhagic shock, in which administration of an alpha-beta stimulator will help maintain essential cerebral and cardiac function by shunting blood to these areas while volume is being replaced; cardiogenic shock, in which vasodilators may reduce cardiac work by reducing diastolic blood pressure but coronary blood flow will also be reduced, counteracting the effects of decreasing the cardiac load; and endotoxic shock, in which the circulating blood volume decreases and venous return and cardiac output also decrease. Prolonged use of these agents in any of these shock situations is ultimately deleterious. Vasopressor drugs are best used to treat acute hypotension that occurs in myocardial infarction; in such cses, vasopressors are used to keep the blood pressure within normal range, but only as adjunctive therapy. In hemorrhagic shock, though norepinephrine administration may increase blood pressure, the only lasting treatment is to replace the blood as rapidly as possible.

Topics: Brain; Cerebrovascular Circulation; Humans; Metaraminol; Morphine; Myocardial Infarction; Nalorphine; Norepinephrine; Shock; Shock, Cardiogenic; Shock, Hemorrhagic; Shock, Septic; Vasoconstrictor Agents

Shock must be treated by correcting the cause, for any treatment of hypotension or shock, as such, is only an adjunctive measure; but the hemodynamic manifestations also need treatment. Vasopressors are helpful and effective under the right circumstances. Unless the blood volume is normal, the use of drugs that block the sympathetic nervous system (e.g., phenoxybenxamine) can be extremely hazardous and hasten death. However, the effect of adrenergic blocking drugs in endotoxic shock and other types of toxic shock is still to be determined; use of such drugs should be considered experimental until the results have been studied more extensively. Clinically, the most common forms of vascular shock are associated with blood loss, myocardial infarction, and endotoxemia. Characteristic hemodynamics of each situation are presented tabularly, and the physicians need to understand the differences is emphasized. The pharmacology of vasopressors, relating primarily to hemodynamic considerations and the response to vasopressors when severe reduction in blood pressure is associated with the shock syndrome is discussed. Drugs that stimulate the adrenergic receptors in the heart and blood vessels, with the exception of isoproteronol, are commonly referred to as vasopressors. The adrenergic stimulators may be classified into 3 groups: alpha (phenylephrine hydrochloride), beta (epinephrine), and alpha-beta (l-norepinephrine). Because alpha stimulators do not usually increase cardiac output, alpha-beta and beta-adrenergic stimulators are generally the most useful for treating shock. Routine use of adrenergic stimulators with the exclusion of other therapies, however, is generally unwarranted.

Topics: Bacteria; Chloramphenicol; Epinephrine; Humans; Isoproterenol; Metaraminol; Methoxamine; Morphine; Myocardial Infarction; Nalorphine; Norepinephrine; Phenoxybenzamine; Phenylephrine; Shock; Shock, Septic; Streptomycin; Tetracycline; Vasoconstrictor Agents