[Phenomena of pharmacological rebound observed in the isolated ductus deferens of the guinea pig with certain anti-beta substances].
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Biomedical subjects
Publications and source records attributed to G Rolla.
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The current treatment of airway obstruction using beta-agonists and theophylline is designed to increase intracellular level of cAMP. Experimental data show that cGMP and cAMP induce functionally additive relaxation of airways. Nitrates relax smooth muscle through the activation of guanylate cyclase. We wondered whether an additive effect of nitroglycerin (NTG) on beta2-agonist-induced bronchodilatation was present in asthmatic patients. To this aim we evaluated the acute bronchodilating effect of inhaled salbutamol (200 mu g MDI) in 10 asthmatics, pre-treated with inhaled NTG or placebo, in a double-blind cross-over design. FEV1 after NTG was higher than that obtained after placebo (2197 +/- 175 vs. 1981 +/- 155 ml, P <0.001). Mean FEV1 obtained 5 min after salbutamol was higher when patients were pre-treated with NTG than placebo (2694 +/- 217 vs 2440 +/- 228 ml respectively, P <0.001). The bronchodilatation due to salbutamol was identical whether NTG or placebo was inhaled first, respectively at 458 +/- 68 and 497 +/- 44 ml after 5 min. After 15 min FEV1 was higher than baseline, but no significant difference was still present between the value observed after pre-treatment with NTG or placebo (2554 +/- 235 and 2551 +/- 205 ml respectively). In conclusion, in asthmatics nebulized NTG produces a moderate and short-lasting bronchodilatation, which is additive with that produced by salbutamol.
The effect of lung surgery on respiratory function has been investigated in 40 patients considering separately the three main procedures (pneumonectomy, lobectomy and thoracotomy alone) to ascertain if the resected lung and the volume removal can influence this function in the immediate postoperative period. The patients were submitted to spirometry and arterial gas analysis preoperatively and during 9 days postoperation; the tests controlled were VC, FEV1, TV and RR. No significant difference has been noticed among various surgical procedures.
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Impaired arterial oxygenation, ranging from an increased alveolar-arterial oxygen gradient to severe hypoxaemia, is commonly reported in patients with advanced liver disease. Hepatopulmonary syndrome is defined by the clinical triad of liver disease, alveolar-arterial oxygen gradient of >15 mmHg, evidence of intrapulmonary vascular dilatations. Three methods are available for detecting intrapulmonary vascular dilatations: contrast-enhanced echocardiography, technetium 99m-labelled macroaggregated albumin scanning and pulmonary arteriography. A recent hypothesis that assigns to nitric oxide the crucial role as mediator of abnormal pulmonary vasodilatation and oxygen is discussed; the measurement of nitric oxide in the exhaled air may represent a possible marker of gas exchange abnormalities in liver disease. The therapeutic options to relieve the hepatopulmonary syndrome are discussed. While no pharmacological treatment has proved to be clinically useful, liver transplantation was reported to cure the response to transplantation is discussed. The response of hypoxaemia to 100% oxygen breathing appears to be the most important prognostic factor of perioperative death rate.
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