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)

Ventilatory responses to hypercapnia in experienced marijuana smokers have previously been shown to decrease, increase, or not change acutely after marijuana. In one study, minute ventilation (VE) and O2 consumption (VO2) increased but hypoxic ventilatory response did not change after smoking marijuana. We further investigated the effects of marijuana of increasing potency (0, 13, and 20 mg THC) on ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia in 11 young, healthy men who smoked marijuana regularly but refrained from any smoked substance, alcohol, caffeine, or other drugs for greater than or equal to 12 h before study. Ventilatory and P0.1 responses to hypoxia and hypercapnia were measured on 3 separate days before and 5 and 35 min (hypoxia) and 15 and 45 min (hypercapnia) after smoking. In a companion 3-day study, 12 young male habitual marijuana smokers underwent measurements of VE, VO2, and CO2 production (VCO2) before and 5 to 135 min after smoking marijuana containing 0, 15, or 27 mg THC. None of the active marijuana preparations caused significant changes in ventilatory or P0.1 responses to either hypercapnia or hypoxia or in resting VE, VO2 or VCO2. We conclude that smoking marijuana (13 to 27 mg THC) has no acute effect on central or peripheral ventilatory drive or metabolic rate in habitual marijuana smokers. These conclusions cannot be applied to infrequent users of marijuana without further study.
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PMID:Effects of smoked marijuana of varying potency on ventilatory drive and metabolic rate. 132 50

The effect of oral caffeine on resting ventilation (VE), ventilatory responsiveness to progressive hyperoxic hypercapnia (HCVR), isocapnic hypoxia (HVR), and moderate exercise (EVR) below the anaerobic threshold (AT) was examined in seven healthy adults. Ventilatory responses were measured under three conditions: control (C) and after ingestion of either 650 mg caffeine (CF) or placebo (P) in a double-blind randomized manner. None of the physiological variables of interest differed significantly for C and P conditions (P greater than 0.05). Caffeine levels during HCVR, HVR, and EVR were 69.5 +/- 11.8, 67.8 +/- 10.8, and 67.8 +/- 10.9 (SD) mumol/l, respectively (P greater than 0.05). Metabolic rate at rest and during exercise was significantly elevated during CF compared with P. An increase in VE from 7.4 +/- 2.5 (P) to 10.5 +/- 2.1 l/min (CF) (P less than 0.05) was associated with a decrease in end-tidal PCO2 from 39.1 +/- 2.7 (P) to 35.1 +/- 1.3 Torr (CF) (P less than 0.05). Caffeine increased the HCVR, HVR, and EVR slopes (mean increase: 28 +/- 8, 135 +/- 28, 14 +/- 5%, respectively) compared with P; P less than 0.05 for each response. Increases in resting ventilation, HCVR, and HVR slopes were associated with increases in tidal volume (VT), whereas the increase in EVR slope was accompanied by increases in both VT and respiratory frequency. Our results indicate that caffeine increases VE and chemosensitivity to CO2 inhalation, hypoxia, and CO2 production during exercise below the AT.
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PMID:Effect of caffeine on ventilatory responses to hypercapnia, hypoxia, and exercise in humans. 231 73

The possibility that endogenously released adenosine, a potent vasodilator, is involved in the increase in cerebral blood flow (CBF) response to hypercapnia has been investigated in an anesthetized, paralyzed rat model. The left retroglenoid vein was cannulated and cerebral venous blood flow measured with a drop counter. Animals were ventilated with a 40% oxygen, 60% nitrogen gas mixture. At 20 min intervals, at a constant rate of flow, the inspired gas mixture was altered to 10% carbon dioxide, 40% oxygen, 50% nitrogen for periods of between 30-90 sec. This brief hypercapnic challenge induced a rapid increase in CBF in the absence of any change in MABP. An involvement of adenosine in this response was demonstrated using an adenosine antagonist, caffeine, an uptake inhibitor, dipyridamole and an adenosine deaminase inhibitor, deoxycoformycin. Caffeine (10 and 20 mg/kg i.p.) 15 min prior to hypercapnic challenges significantly decreased the peak increases in CBF. Dipyridamole (0.1 mg/kg) and deoxycoformycin (0.1 microgram/kg) enhanced the peak increases in flow. These results are consistent with an important role for adenosine in coupling PCO2 to cerebral blood flow.
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PMID:An involvement of adenosine in cerebral blood flow regulation during hypercapnia. 349 49

Although the presence of fetal breathing movements (FBMs) has been suspected for almost a century, the major advances in the field were made during the last decade. Experimental animal techniques of detection include instrumentation of fetuses with electronic recording equipment. Human studies use more indirect, although no less accurate, A-mode or real-time B-scan ultrasonography in the recording of FBMs. The fetus does not make breathing movements continuously; however, there are periods of FBMs interspersed with periods of apnea. Inherent to FBMs is a diurnal variation. Hypoxia and hypoglycemia diminish FBMs, while hypercarbia and hyperglycemia have the opposite effect. Caffeine, barbiturates, and general anesthetics modify FBMs by their influence on the CNS. Preliminary studies have shown the presence of FBMs to indicate a state of fetal well-being. Possibly, in the future, testing for FBMs may become a useful clinical tool in the identification of the fetus at risk.
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PMID:Fetal breathing movements. An update for the pediatrician. 668 79

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
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PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

The respiratory effects of caffeine and paraxanthine, two xanthine adenosine antagonists with phosphodiesterase (PDE) activity, CGS 15943, a non-xanthine adenosine antagonist lacking PDE inhibitory activity, and rolipram, a non-xanthine PDE inhibitor lacking adenosine antagonist activity, were characterized in unanesthetized, seated rhesus monkeys exposed to 10% O2 balanced in N2 (hypoxia). Ventilation was measured continuously by enclosing the monkey's head in a fitted helmet and using a pressure-displacement plethysmographic technique. Respiratory frequency (f) and minute volume (VE) increased during 15-minute periods of hypoxia, and intramuscular administration of caffeine (0.3 and 1.0 mg/kg), paraxanthine (0.3 and 1.0 mg/kg) and CGS 15943 (0.03 and 0.1 mg/kg) attenuated the ventilatory response to hypoxia. In contrast, rolipram (0.003-0.03 mg/kg) did not significantly alter the ventilatory response to hypoxia. Drug effects also were characterized in monkeys exposed to air (normoxia) or 3%, 4% and 5% CO2 balanced in air (hypercapnia). Doses of caffeine, paraxanthine or CGS 15943 that attenuated the ventilatory response to hypoxia had no significant effect on f or VE during conditions of normoxia or hypercapnia. The results indicate that adenosine may play a major role in the function of peripheral, O2-sensitive mechanisms during hypoxia.
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PMID:Attenuation of hypoxia-induced increases in ventilation by adenosine antagonists in rhesus monkeys. 763 51

The effects of caffeine and several selective phosphodiesterase (PDE) inhibitors on ventilation and on schedule-controlled behavior were studied in rhesus monkeys. In seated, unanesthetized monkeys prepared with a head plethysmograph, ventilation during exposure to air (normocapnia) and to elevated levels of CO2 (3, 4 and 5%) mixed in air (hypercapnia) was measured after cumulative doses of each drug. In other monkeys, behavioral effects were studied by administering cumulative doses preceding sequential periods of fixed-ratio or fixed-interval responding. The nonselective PDE inhibitors, caffeine and 3-isobutyl-1-methylxanthine, and the type IV-selective PDE inhibitors, rolipram and Ro 20-1724, had pronounced respiratory-stimulant effects during conditions of normocapnia and hypercapnia, and their potencies in increasing ventilation corresponded with their potencies as PDE inhibitors. The type III-selective PDE inhibitor, CI-930, had only modest respiratory-stimulant effects at the highest dose studied, and the type V-selective PDE inhibitor, zaprinast, had no respiratory effect. CGS 15943, a selective adenosine antagonist lacking PDE-inhibitory effects, also had only modest respiratory-stimulant effects at the highest dose studied. In contrast to their relative potencies and efficacies in stimulating respiration, caffeine and 3-isobutyl-1-methylxanthine were less efficacious than CGS 15943 in increasing fixed-interval responding, and CI-930, rolipram and Ro 20-1724 only decreased fixed-interval responding. Zaprinast had little or no behavioral effect. The results support the interpretation that inhibition of type IV PDE plays a prominent role in the respiratory-stimulant effects of xanthines, whereas the behavioral-stimulant effects are more closely related to antagonism of adenosine receptors.
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PMID:Comparative effects of caffeine and selective phosphodiesterase inhibitors on respiration and behavior in rhesus monkeys. 768 4

This study characterized the effects of caffeine (1.0-30.0 mg/kg) and nicotine (0.1-3.0 mg/kg) administered alone and in combination on ventilation in unanesthetized rhesus monkeys. In seated monkeys prepared with a head plethysmograph, ventilation was measured during exposure to air (normocapnia), CO2 (3%, 4% and 5%) mixed in air (hypercapnia), 10% O2 mixed in N2 (hypoxia) and 100% O2 (hyperoxia). Caffeine produced marked, dose-dependent increases in ventilation during conditions of normocapnia and hypercapnia. In contrast, acute administration of nicotine had less pronounced respiratory-stimulant effects during all conditions. The joint effects of caffeine and nicotine on ventilation generally did not differ from those obtained with caffeine alone. Chronic administration of nicotine (1.0 mg/kg/day) for 4 consecutive wk via osmotic pumps significantly decreased the half-life of caffeine but had little effect on ventilation or on sensitivity to the respiratory-stimulant effects of caffeine. Two primary metabolites of caffeine, theophylline and paraxanthine, were active as respiratory stimulants and were equipotent to caffeine, and the joint effects of caffeine and its metabolites were additive. The results indicate that caffeine and nicotine stimulate respiration through different pharmacological mechanisms, in contrast to caffeine and its metabolites which exhibit a similar pharmacological profile. Moreover, significant pharmacokinetic interactions may be obtained when caffeine and nicotine are coadministered.
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PMID:Effects of caffeine on ventilation during acute and chronic nicotine administration in rhesus monkeys. 779 Oct 79

A young man underwent anaesthesia and surgery after multiple fractures. After 2 hours of anaesthesia, the patient developed hypercapnia, acidosis, hyperpyrexia and mild muscle rigidity. He was treated for malignant hyperthermia. Muscle tension studies with caffeine-halothane and muscle histology proved normal. The differential diagnosis of this abnormal metabolic response is briefly discussed.
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PMID:A hypermetabolic reaction during anaesthesia and surgery. A case report. 821 15

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


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