Nimodipine reduces morbidity, mortality after disruption of cerebral blood flow.

Nimodipine is a 1,4 dihydropyridine with Ca++ channel blocking properties. It is more lipophilic than most calcium channel blockers, and thus has a greater volume of distribution within the brain. Many actions of nimodipine have been proposed from work done in animal models following induction of complete or partial cerebral ischemia for varying lengths of time. However, these experimental results have not been sufficiently documented in patient populations, and there exists conflicting data as to nimodipine's mechanism of action in the cerebral ischemic patient. Regardless of the exact mechanisms of action, studies suggest that nimodipine may significantly reduce morbidity and mortality in patients following disruption of cerebral blood flow.

Low temperature worsens mammalian oxygen toxicity.

Oxygen toxicity was assessed in mice exposed to 5 ATA of oxygen. Central nervous system toxicity was measured as the latent period before convulsions, and lung damage estimated by wet and dry weight measurements. Our results confirmed previous findings that hyperbaric oxygen induces hypothermia in animals, and this effect is profound in mice exposed to 5 ATA of oxygen at ambient temperatures of 15 degrees C and 5 degrees C. However, even marked hypothermia had very little effect on the latent times to convulsions in mice. Unexpectedly, the combination of hypothermia and hyperbaric oxygen produced much more severe lung damage than either treatment alone, with a 2.7-fold increase in weight in the 5 degrees C group (average rectal temperature of 16.1 degrees C). These results indicate that hyperoxic-induced hypothermia cannot be considered a protective mechanism against oxygen toxicity and indeed hypothermia can markedly potentiate hyperbaric oxygen toxicity.

Endogenous opioids are not involved in the pathology induced by hyperbaric oxygen treatment.

In mice, oxygen at hyperbaric pressures (515 kPa; 5 ATA) induces convulsions and lung damage (edema and hemorrhage). Morphine treatment (15 mg X kg-1, i.p.) significantly protects against the development of this pathology. The protection is abolished by naloxone (1 mg X kg-1, i.p.). Electric footshock, which induces diverse opioid effects, affords no protection against hyperbaric oxygen damage. Possible mechanisms of the morphine action are discussed.