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)

The effects of tryptophan hydroxylase inhibition with p-chlorophenylalanine (PCPA; 100 mg/kg iv) on ventilatory control were studied in awake goats. Ventilation, CO2 production, and blood gases were measured 16-24 h after PCPA at rest and during mild exercise in normoxia and at rest in hypoxia and hypercapnia. PCPA increased ventilation 36% at rest, predominantly through an effect on respiratory frequency, and decreased arterial PCO2 (PaCO2) 6.5 Torr. Ventilatory gain in exercise (delta VI/deltaVCO2) was increased 20% by PCPA thereby maintaining PaCO2 at its new resting value. Hypoxia (fractional inspired O2 concentration = 0.12) had little effect on ventilation or PaCO2 at rest, either on control or on PCPA test days. Ventilatory sensitivity to CO2 at rest (delta VI/delta PaCO2) was unaffected by PCPA. Bilateral carotid body denervation (CBX) was performed in the animals, and experiments were repeated 3 mo after the first administration of PCPA. CBX alone decreased ventilation 29% and increased PaCO2 9.4 Torr. Administration of PCPA increased ventilation 35%, decreased PaCO2 by 10.2 Torr at rest, and increased ventilatory gain in exercise 26%. Thus carotid bodies are not necessary for the ventilatory response to PCPA. Furthermore, the primary neural pathways associated with exercise or hypercapnia are not specifically affected by inhibition of serotonin metabolism via PCPA.
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PMID:Effects of p-chlorophenylalanine on ventilatory control in goats. 621 79

This study characterized in rhesus monkeys the effects of selected adenosine agonists on ventilation during normal atmospheric conditions and during conditions of hypercapnia, hypoxia and hyperoxia. In seated, unanesthetized monkeys prepared with a head plethysmograph, ventilation during exposure to air, CO2 (3, 4 and 5%) mixed in air (hypercapnia), 10% O2 mixed in N2 (hypoxia) and 100% O2 (hyperoxia) was measured during cumulative dosing with each drug. The nonselective (A1/A2) agonist, 5'-N-ethylcarboxamidadenosine (NECA), the peripherally active, A2-selective agonist, CGS 21680 [2-(carboxyethylphenylamino)adenosine-5'-carboxamide], and the A1-selective agonists, N6-cyclohexyladenosine and N6-cyclopentyladenosine, increased respiratory frequency (f), but had no significant effect on minute volume (VE) during exposure to air. The relative potencies for increasing f corresponded closely with their potencies for binding at A2 receptors. NECA and CGS 21680 increased f in a dose-dependent manner during exposure to 3% CO2, but proportional increases in f were less pronounced as the concentration of CO2 increased. NECA and CGS 21680 also increased f during hypoxia, but neither had a significant effect on f during subsequent hyperoxia. The highest dose of CHA and CPA decreased f below control values during exposure to 5% CO2 and decreased f and VE during hyperoxia. In contrast, the adenosine antagonist, caffeine, and the selective phosphodiesterase inhibitor, rolipram, increased f and VE under all conditions. During hypercapnia, the magnitude of the increases in f was similar at each concentration of CO2 studied. Caffeine and rolipram increased f and VE during hypoxia, and f and VE remained elevated during hyperoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of adenosine agonists on ventilation during hypercapnia, hypoxia and hyperoxia in rhesus monkeys. 849 37