Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind crossover trial was conducted in 10 asthmatic patients for comparison of fenoterol with salbutamol, in 12 other asthmatic patients for comparison of reproterol with salbutamol, and in 15 other asthmatic patients for comparison of terbutaline with salbutamol. The following doses were given: 1.25 mg fenoterol, 2.5 mg reproterol, 2.5 mg terbutaline and 1.25 mg salbutamol. 5 drops of each of the inhalation solutions (in 2 ml of saline) were aerosolized by a powered machine and inhaled for 15 min. FEV1 was measured before, and 15 and 45 min after inhalation. Immediately before FEV1 the following parameters for side effects were also determined: 1. heartbeats per min, systolic and diastolic blood pressure; 2. minute ventilation, arterial PCO2 and oxygen consumption; 3. arterial SO2, PO2 and the alveolar-arterial O2-gradient (AaDO2). To estimate the selectivity of each of the 3 betastimulators the ratio (formula: see text) was established for each parameter and compared to that obtained with salbutamol. In further steps the ratio of all parameters for side effects was shown, then only that of the 3 most important side effects tachycardia, hypocapnia (PaCO2) and hypoxemia (PaO2). The following order of selectivity was found: 1. salbutamol, 2. fenoterol, 3. terbutaline, 4. reproterol.
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PMID:[The bronchospasmolytics salbutamol, fenoterol, terbutaline and reproterol. Their effects and side effects in asthmatics after inhalation with an electric nebulizer]. 67 13

It has been postulated that a coronary vasoconstriction during hypocapnia might be opposed by a compensating coronary vasodilatation due to impaired myocardial oxygen supply. The present study was performed first to examine whether a maximal decline in coronary sinus (CS) oxygen content was reached during hypocapnia. During hypercapnia a myocardial "over perfusion" has been demonstrated. The second purpose of the present study was to examine whether a myocardial "over perfusion" is essential to maintain a sufficient myocardial tissue oxygen supply during hypercapnia. Closed-chest dogs were anesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Nitrogen gas and carbon dioxide could both be added to the inspiratory gas to create arterial hypoxemia (arterial SO2 65%) and hypercapnia, respectively. Arterial hypoxemia during hypocapnia increased myocardial blood flow (MBF) by 50%, while CS SO2 decreased significantly. The decrease in CS SO2 demonstrates a reserve capacity of myocardial oxygen extraction during hypocapnia, thereby ruling out any major coronary vasoconstriction during hypocapnia. Hypercapnia during normoxemia increased MBF, myocardial oxygen delivery, and CS SO2 substantially, but this was not observed when hypercapnia was created during arterial hypoxemia. From the present results we conclude that hypocapnia does not cause any major coronary vasoconstriction, while hypercapnia results in a myocardial "over perfusion," which is a luxury perfusion not essential to maintain sufficient myocardial oxygen supply during hypercapnia.
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PMID:Myocardial oxygen supply during hypocapnia and hypercapnia in the dog. 309 94

Variations of arterial PCO2 and pH are known to influence myocardial blood flow (MBF) in that hypercapnia results in a coronary vasodilatation, while hypocapnia possibly decreases MBF. The present study was performed to examine if hypocapnia and hypercapnia might influence the sensitivity to exogenous administration of adenosine. Aminophylline, an adenosine receptor blocking agent, was administered to rule out the effect of endogenously liberated adenosine during variations of PCO2 and pH. In the last part of the study, it was examined whether verapamil, a calcium-channel blocker, might influence the MBF response to variations in PCO2 and pH. Closed-chest dogs were anaesthetized with pentobarbital, and hypocapnia induced by hyperventilation. Carbon dioxide was added to the inspiratory gas to create normocapnia and hypercapnia. In the control group hypocapnia did not significantly reduce MBF although a decrease in coronary sinus (CS) SO2 indicated a coronary vasoconstriction. During continuous adenosine infusion (7.5 +/- 0.3 mg/kg/h) which increased MBF 116% during normocapnia, creating hypocapnia caused a 40% decrease in MBF. Hypercapnia seemed to potentiate the vasodilating effect of adenosine. During administration of aminophylline hypocapnia did not cause any decrease in MBF, while hypercapnia increased MBF by 39%, and these results are in harmony with the results obtained in the control group without aminophylline. Verapamil did not result in any altered MBF response to hypocapnia and hypercapnia when compared to the unblocked control group. These observations do not support the idea of any major influence of the Ca2+ fluxes blocked by verapamil as the cause of MBF changes during variations in PCO2 and pH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine modifies canine myocardial blood flow response to hypocapnia and hypercapnia, while aminophylline and verapamil do not. 312 Mar 3