Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kainic acid, topically applied to the ventral surface of the medulla immediately caudal to the trapezoid body in the urethane/chloralose anaesthetised rat, led to a depression of ventilation and a sustained rise in blood pressure; ventilatory responses to hypercapnia (10% carbon dioxide) and hypoxia (11% oxygen) were slightly depressed. Widespread application of kainic acid to an area at and slightly rostral to the rootlets of the hypoglossal nerve produced a stimulation of ventilation and an unsustained rise in blood pressure. Apnea ensued 12-28 min after application. Ventilatory responses to hypercapnia and hypoxia were markedly attenuated; more discrete bilateral application revealed two regions, one immediately rostral and lateral to the hypoglossal rootlets and the other over the point of exit of the hypoglossal nerve rootlets, which specifically contributed to the diminution of the chemosensory responses. These results raise questions about the medullary circuitry which mediates the chemoreflex regulation of breathing.
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PMID:Kainic acid on the rat ventral medullary surface depresses hypoxic and hypercapnic ventilatory responses. 211 62

Sites of central CO2 chemosensitivity were investigated in isolated brain stems from Rana catesbeiana tadpoles and frogs. Respiratory neurograms were made from cranial nerve (CN) 7 and spinal nerve 2. Superfusion of the brain stem with hypercapnic artificial cerebrospinal fluid elicited increased fictive lung ventilation. The effect of focal perfusion of hypercapnic artificial cerebrospinal fluid on discrete areas of the ventral medulla was assessed. Sites of chemosensitivity, which are active continuously throughout development, were identified adjacent to CN 5 and CN 10 on the ventral surface of the medulla. In early- and middle-stage tadpoles and frogs, unilateral stimulation within either site was sufficient to elicit the hypercapnic response, but simultaneous stimulation within both sites was required in late-stage tadpoles. The chemosensitive sites were individually disrupted by unilateral application of 1 mg/ml protease, and the sensitivity to bath application or focal perfusion of hypercapnia was reassessed. Protease lesions at CN 10 abolished the entire hypercapnic response, but lesions at CN 5 affected only the hypercapnic response originating from the CN 5 site. Neurons within the chemosensitive sites were also destroyed by unilateral application of 1 mM kainic acid, and the sensitivity to bath or focal application of hypercapnia was reassessed. Kainic acid lesions within either site abolished the hypercapnic response. Using a vital dye, we determined that kainic acid destroyed neurons by only within 100 microm of the ventral medullary surface. Thus, regardless of developmental stage, neurons necessary for CO2 sensitivity are located in the ventral medulla adjacent to CN 5 and 10.
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PMID:Ontogeny of central CO2 chemoreception: chemosensitivity in the ventral medulla of developing bullfrogs. 1461 6