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)

Rat pial arteries were observed through a closed cranial window during hypercapnic and hypoxic episodes whilst the cerebral cortex was superfused at 37 degrees C first with artificial cerebrospinal fluid (CSF) and subsequently with adenosine deaminase (ADA, 0.5-2.0 U/ml) in CSF. The results indicate that ADA attenuated hypercapnic and hypoxic dilatatory arteriolar responses by 64% and 56% respectively. Recovery was obtained by superfusing with ADA-free CSF for 1 h. We conclude that adenosine is involved in hypercapnia- and hypoxia-evoked dilation of pial arteries.
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PMID:Adenosine deaminase reduces hypoxic and hypercapnic dilatation of rat pial arterioles: evidence for mediation by adenosine. 193 88

Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.
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PMID:Adenosine in the control of the cerebral circulation. 270 69

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

Experiments were performed on isolated, nonworking rat hearts perfused at constant pressure according to the Langendorff technique to evaluate the role of adenosine in hypercapnia-evoked coronary vasodilation. Hypercapnia/acidosis resulted in increases in heart rate and coronary flow rates in conjunction with a decrease in ventricular contractile tensions. The adenosine deaminase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA, 10 microM) reduced the heart rate and enhanced CO2-evoked increases in coronary vascular flow. 5-Iodotubercidin (1 microM), an inhibitor of adenosine kinase, caused a reduction in heart rate and enhanced coronary flow rates during hypercapnic perfusion. Adenosine deaminase (1 U/ml) significantly attenuated CO2-evoked increases in coronary vascular flow. These results extend those of previous investigations implicating adenosine in the regulation of coronary flow during conditions of respiratory or metabolic acidosis.
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PMID:Further evidence for the role of adenosine in hypercapnia/acidosis-evoked coronary flow regulation. 1055 85

A 51-year-old man presented with back pain in 1997. He had a 30-year-history of occupational asbestos exposure. His chest CT showed bilateral pleural thickening and pleural effusion. The pleural effusion of the right thorax exhibited both elevated level of adenosine deaminase and increased numbers of lymphocytes. Antituberculous chemotherapy had no effect on the exudates. Progressive bilateral pleural thickening were found on chest CT, and pulmonary function tests showed severe restrictive ventilatory impairments since 1998. Thoracoscopic pleural biopsy was conducted in 2001 to exclude pleural malignant mesothelioma. No malignancy was found in pleural samples. After 3-year observation and excluding other causes, he was given a diagnosis of benign asbestos pleurisy. In 2005, fibrotic changes were found in both lower lung fields in chest CT. He suffered from respiratory failure with carbon dioxide retention, and died in 2006. The autopsy disclosed asbestos-related lung diseases. We suspected that diffuse pleural thickening could be a major cause of fatal respiratory impairment in this case.
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PMID:[Autopsy case of diffuse pleural thickening presenting respiratory impairment and benign asbestos pleurisy]. 1851 12

High tidal volume ventilation is detrimental to alveolar fluid clearance (AFC), but effects of ventilation pressure (P) on AFC are unknown. In anesthetized BALB/c mice ventilated at constant tidal volume (8 ml/kg), mean AFC rate was 12.8% at 6 cmH(2)O P, but increased to 37.3% at 18 cmH(2)O P. AFC rate declined at 22 cmH(2)O P, which also induced lung damage. Increased AFC at 18 cmH(2)O P did not result from elevated plasma catecholamines, hypercapnia, or hypocapnia, but was due to augmented Na(+) and Cl(-) absorption. PKA agonists and beta-agonists stimulated AFC at 10 cmH(2)O P by upregulating amiloride-sensitive Na(+) transport. However, at 18 cmH(2)O P, PKA agonists and beta-agonists reduced AFC. At 15 cmH(2)O P, the AFC rate was intermediate (mean 26.6%), and forskolin and beta-agonists had no effect. Comparable P dependency of AFC and beta-agonist responsiveness was found in C57BL/6 mice. The effect on AFC of increasing P to 18 cmH(2)O was blocked by adenosine deaminase or an A(2b)-adenosine receptor antagonist, and could be mimicked by adenosine in mice ventilated at 10 cmH(2)O P. Modulation of adenosine signaling also resulted in altered responsiveness to beta-agonists. These findings indicate that, in the normal mouse lung, basal AFC rates and responses to beta-agonists are impacted by ventilation pressure in an adenosine-dependent manner.
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PMID:Effect of ventilation pressure on alveolar fluid clearance and beta-agonist responses in mice. 1968 2