Biomedical subjects
Publications and source records attributed to M J Daly.
The relationship between differential renal uptake of Tc-99m 2-3 dimercaptosuccinic acid (DMSA) and differential renal function was examined in normal and abnormal dogs by correlating Tc-99m DMSA localization with relative renal blood flow and creatining clearance. There was close correlation of fractional Tc-99m DMSA localization with relative renal function.
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1. Characterization of the beta-adrenoceptors mediating inhibition of gastric acid secretion in the conscious Heidenhain pouch dog has been investigated by determination of the effects of propranolol, (+)-propranolol, practolol and H35/25 on salbutamol and isoprenaline-induced inhibition of gastric acid secretion. 2. The gastric antisecretory effect of salbutamol was significantly blocked by propranolol and H35/25 but not by practolol or (+)-propranolol. The effect of isoprenaline was significantly blocked by propranolol and practolol but not by H35/25 or (+)-propranolol. 3. It is concluded that both beta1- and beta2-adrenoceptors can mediate inhibition of pentagastrin-induced gastric secretion in conscious dogs with a Heidenhain pouch. Salbutamol exerts its antisecretory effect through beta2-adrenoceptors, whereas isoprenaline mediates its effects primarily through beta1-adrenoceptors. 4. The results are discussed with regard to the sub-classification of beta-adrenoceptors and to the possible role of adrenoceptors in the physiological control of gastric secretion. 5. In this study it is concluded that the tachycardia induced by isoprenaline or salbutamol is mediated primarily through reflexes activated by beta2-adrenoceptor mediated vasodilatation.
Renal images of 194 normal subjects given 99mTc-dimer captosuccinic acid (DMSA) were reviewed to establish normal values an optimal imaging techniques for this new renal agent. Images were consistently of high quality. Normal renal size (posterior length) averaged 11.5 +/- 1 cm, and renal radioactivity (functioning tubular mass) was equally divided between the left and right kidney. 99mTc-DMSA appears to be an excellent renal parenchymal imaging agent.
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1 The beta-adrenoceptor agonists, (-)-isoprenaline and (+/-)-salbutamol, reduced pepsinogen secretion induced by pentagastrin in conscious dogs with Heidenhaim pouches. 2 (-)-Isoprenaline and (+/-)-salbutamol also reduced gastric acid secretion while producing a moderate tachycardia.
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1 The potencies of fifteen beta-adrenoceptor agonists of widely differing chemical structures were compared with that of (-)-isoprenaline on bronchial muscle, soleus muscle, blood pressure and heart rate in the anaesthetized cat. The beta-adrenoceptor antagonist potencies of propranolol and practolol were determined against (-)-isoprenaline in the same model. 2 (-)-Isoprenaline was the most potent agonist and its action was essentially unselective. Thus, on all four parameters the minimal effective dose was 0.003-0.01 mug/kg and maximal or near maximal responses were produced by 0.3-1 mug/kg. Trimetoquinol was also an essentially unselective agonist. 3 For thirteen of the remaining fourteen agonists, potency was similar on bronchial muscle, soleus muscle and blood pressure but significantly lower on heart rate. 4 The remaining agonist - AH 7616 (4-hydroxy-alpha1-[[(1-methyl-3,3-diphenyl-propyl)amino]-methyl]-m-xylene-alpha1, alpha3-diol, acetate) - was also significantly less potent on heart rate than on the other parameters; in addition, it was clearly less potent on soleus muscle and blood pressure than on bronchial muscle when 5-hydroxytryptamine (5-HT) was used to induce bronchospasm. However, when acetylcholine was used instead of 5-HT the potency of AH 7616 on induce bronchospasm. However, when acetylcholine was used instead of 5-HT the potency of AH 7616 on bronchial muscle, soleus muscle and blood pressure was very similar. AH 7616 may therefore possess a specific 5-HT antagonist action in addition to its beta-adrenoceptor agonist action. 5 The fifteen test agonists were longer acting than (-)-isoprenaline and this was particularly true of trimetoquinol and soterenol. 6 The beta-adrenoceptor antagonist potency of propranolol was almost identical on bronchial muscle, soleus muscle and blood pressure and very slightly lower on the heart. Practolol was 10-12 times more potent on the heart than on bronchial muscle, soleus muscle and blood pressure. 7 These findings suggest that it may not be possible to separate the bronchodilating and tremorenhancing properties of beta-adrenoceptor agonists. The results with agonists and antagonists are in accord with Lands' dual beta-adrenoceptor sub-classification.
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1 The actions of five beta-adrenoceptor antagonists, chosen because of reported differences in their selectivities, were compared using the positive chronotropic, vasodepressor and bronchodilator responses to isoprenaline in anesthetized dogs. 2 Propranolol was a potent antagonist of the isoprenaline responses in all three systems. 3 Practolol and acebutolol (M & B 17,803) blocked the positive chronotropic responses to isoprenaline to a greater extent than the vasodepressor or bronchodilator responses. 4 Butoxamine and alpha-methyl dichloroisoprenaline showed the opposite selectivity, blocking the vasodepressor and bronchodilator responses to isoprenaline to a greater extent than positive chronotropic responses. However, both drugs were considerably less potent than the other antagonists studied and their selectivities were less clear-cut than those of practolol or acebutolol. 5 All the antagonists lowered the resting heart rate and to a lesser extent the diastolic blood pressure. The effects of propranolol, practolol and acebutolol on heart rate probably result from cardiac beta-adrenoceptor blockade. With butoxamine and alpha-methyl dichloro isoprenaline, however, the effects on heart rate probably result from a direct cardiodepressant action. 6 The relevance of the results to the problem of the sub-classification of beta-adrenoceptors is discussed.
In the anaesthetized guinea-pig micro-embolism induced by barium sulphate causes marked increases in pulmonary resistance and decreases in pulmonary compliance. Bronchodilator drugs prevent these changes with salbutamol showing much greater activity on pulmonary resistance changes than compliance changes. The results are discussed with regard to the site of action in the respiratory tree and potential clinical use.
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