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A C Catron

Publications and source records attributed to A C Catron.

3 recordsLinked to original sources

Norepinephrine-induced pulmonary petechiae in the rat: an experimental model with potential implications for sudden infant death syndrome.

Autonomic nervous system abnormalities have been implicated in infants dying of or considered at high risk of sudden infant death syndrome (SIDS). In a rat model, norepinephrine (0.02 mg/kg) caused systemic hypertension and numerous pulmonary petechiae, the latter a common finding in SIDS. Petechiae were not seen below the diaphragm. The animals were killed by tracheal occlusion 5 min after the intravenous administration of norepinephrine. The number of pulmonary petechiae was greatly reduced by alpha-adrenergic blockade (phentolamine) and dopaminergic blockade (haloperidol) but not by beta-adrenergic blockade (timolol). A significantly greater reduction of peak mean systemic arterial pressure occurred after alpha-adrenergic blockade than with other blocking agents. It is conceivable that hypoxia-induced endogenous catecholamine release contributes to the pathogenesis of pulmonary petechiae found at necropsy of SIDS victims.

Animals↗

Maternal nicotine administration and fetal brain stem damage: a rat model with implications for sudden infant death syndrome.

Several recent studies have established maternal smoking as a significant risk factor for sudden infant death syndrome (SIDS). To test our hypothesis that nicotine, a component of cigarette smoke, may exert an injurious effect on the fetal brain stem, we administered nicotine in drinking water to Sprague-Dawley rats prior to and throughout the first 20 days of gestation. The nicotine dose and schedule of consumption in this experiment paralleled that of human usage. Fetuses from nicotine-treated mothers had significantly more dead cells in a standard section of the medulla than controls, but little difference was observed in the postnatal respiratory responses of treated and control animals to the inhalation of various gas mixtures. The birth weights of nicotine-exposed fetuses were significantly less than those of controls. Although the degree of fetal brain stem injury produced by nicotine in this experiment is small, it is our concern that maternal smoking might cause a more severe lesion in the human fetus and thereby increase the risk of SIDS by contributing to aberrant postnatal respiratory responses to noxious stimuli.

Animals↗