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PubMed1980

Ethanol-sedative hypnotic interactions: in vitro studies on Na-K-activated adenosine triphosphatase.

The combined in vitro effects of ethanol wih methaqualone, phenobarbital, pyrazole or disulfiram were studied using rat brain microsomal NA-K-ATPase. Methaqualone and phenobarbital, either alone or in combination with ethanol, showed a dose-dependent inhibition of Na-K-ATPase activity. Kinetic studies showed that the inhibitory effects were competitive with the respect to K+ and uncompetitive with respect to MgATP for phenobarbital either alone or in combination with ethanol. Methaqualone showed a noncompetitive type of inhibition with respect to K+, whereas a mixed type of inhibition was seen in combinations with ethanol. Furthermore, methaqualone either alone or in combination with ethanol also showed an uncompetitive type of inhibition with respect to MgATP. The dose-dependent inhibition of brain Na-K-ATPase activity by disulfiram was independent of K+ and additive in combination with ethanol. Pyrazole showed no effect on brain Na-K-ATPase activity. The inhibitions by phenobarbital and methaqualone, either alone or in combination with ethanol, were significantly greater at low K+ (1 mM) and high Na+ (100-200 mM). A greater inhibition by these drugs was also obtained when Na+ is low (5 mM) and K+ is high (15 mM). The inhibition by these drugs appears to depend on K+ and Na/K ratio in the reaction medium. The combined effects of ethanol and the other CNS depressants on brains Na-K-ATPase may be important to their interaction toxicities.

Animals↗
PubMed1975

Clinical implications of warfarin interactions with five sedatives.

The intensity, uniformity and time course of anticoagulant interference by phenobarbital, secobarbital, glutethimide, chloral hydrate and methaqualone were systematically investigated in 16 patients receiving coumarin therapy. Each subject received an individualized fixed daily dose of warfarin and served as his own pre- and postsedative treatment control. Prothrombin times were measured four times weekly during five long-term experiments. Anticoagulant inhibition was observed during the administration of phenobarbital, secobarbital and glutethimide; there was no significant change in prothrombin test results during the trials of chloral hydrate and methaqualone. Barbiturates and glutethimide should not be administered to patients receiving coumarin drugs. The concurrent use of drugs from these groups is decreasing according to a survey of 200 hospital medical records. Chloral hydrate and methaqualone interact pharmacologically with orally administered anticoagulant agents, but the effect is not clinically significant. It is concluded that chloral hydrate and methaqualone may be administered safely without additional caution in prothrombin test monitoring during oral anticoagulant therapy.

Administration, Oral↗
PubMed1979

Toxic interactions of ethanol with other central depressants: antagonism by naloxone to narcosis and lethality.

The effects of naloxone on narcosis and/or lethality induced by diazepam, lithium, methaqualone and phenobarbital either alone or in combination with ethanol were studied in mice. Interaction toxicities between ethanol and the various psychotropic drugs were dose-dependent and so was the degree of antagonism by naloxone. Treatment with phenobarbital (10 mg/kg) or methaqualone (50 mg/kg) or lithium (4 meq/kg) prolonged the narcosis induced by ethanol (5 g/kg) by 45, 269 and 107% respectively. Naloxone (10 mg/kg) shortened the ethanol (5 g/kg) induced narcosis by 38%. Naloxone (10 mg/kg) also shortened narcosis induced by ethanol (5 g/kg) in combination with phenobarbital (10 mg/kg) or methaqualone (50 mg/kg) or lithium (2meq/kg) by 31, 12 and 38% respectively. At 10 mg/kg of naloxone, the LD50 due to methaqualone was increased from 240 mg/kg to 416 mg/kg, and the LD50 due to ethanol was increased from 9.2 g/kg to 10.8 g/kg. Multiple injections of naloxone significantly (p less than 0.01) protected against the lethality of phenobarbital but not that of lithium. These findings provide further evidence of naloxone antagonism towards various CNS depressants.

Animals↗