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Biomedical subjects

G Looney

Publications and source records attributed to G Looney.

6 recordsLinked to original sources
PubMed1990

Hepatobiliary effects of morphine are mediated in the brain.

Morphine slows hepatobiliary elimination of sulfobromophthalein in rodents, raising dye levels in plasma and liver. Earlier studies showed these effects to be independent of other opiate effects such as bile duct spasm, hypothermia or blood gas changes resulting from respiratory depression. Because opiate receptors are distributed throughout the body, within the central nervous system and at peripheral sites including the gastrointestinal tract, experiments were performed to ascertain whether central or peripheral sites mediate the hepatobiliary effects of morphine. Sulfobromophthalein was administered intravenously to mice and its levels were measured in plasma and liver. Tail-flick latency indicated centrally mediated analgesia. Inhibited intestinal transit of India ink reflected an opiate effect with a significant peripheral component. When injected into a cerebral ventricle morphine was much more potent in producing analgesia and raising sulfobromophthalein levels than when administered intravenously or intraperitoneally. An intravenous dose of naloxone that reversed morphine analgesia also prevented sulfobromophthalein elevation but did not prevent gut slowing. Naltrexone injected in a cerebral ventricle also reversed analgesia and sulfobromophthalein elevation but not intestinal slowing. The polar opiate agonist N-methylmorphine did not cause analgesia or raise sulfobromophthalein levels at peripheral intraperitoneal doses to 100 mg/kg. When given in a central ventricle at 4 x 10(-3) mg/kg, this agent produced analgesia and raised sulfobromophthalein but did not slow intestinal transit. After spinal cord transection, intravenous morphine did not retard the tail-flick response or affect sulfobromophthalein disposition, but peripherally mediated intestinal transit was slowed as it was in intact mice. These experiments demonstrate parallel opiate effects on analgesia and on BSP disposition but not on intestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Efficacy of bomb shelters: with lessons from the Hamburg firestorm.

Shelters for protection against the effects of nuclear weapons are often stated to be useless, largely because of firestorms. Recent models purport to show that nuclear weapons are more likely to cause firestorms than previously thought. These controversial models are based on uncertain assumptions, which are difficult or impossible to test. Regardless of the predictive validity of fire models, conclusions about the ability of shelters to protect their occupants against firestorms, if they occur, are based primarily on historical experience. A review of the original data from the Hamburg firestorm shows that almost all persons in adequate shelters survived, contradicting a currently prevailing belief that all died. The results of the strategic bombing during World War II and of nuclear weapons tests show that a considerable level of population protection can be achieved through attention to proper shelter design.

Burns↗
PubMed1985

Sodium valproate and brainstem energetics.

The effect of the anticonvulsant sodium valproate on cerebral brainstem energy metabolism has been investigated. Stupor and coma were produced in mice by the intraperitoneal injection of sodium valproate at a dose of 600 mg/kg. Glucose, glycogen, ATP, and phosphocreatine were measured in small tissue samples from the ascending reticular activating system. Levels of all metabolites were either normal or elevated in precoma and comatose mice as compared to controls. These data are consistent with the concept that sodium valproate does not have a primary action through depletion of high energy phosphates.

Adenosine Triphosphate↗