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Biomedical subjects

A H Watt

Publications and source records attributed to A H Watt.

At least 37 records · Page 2Linked to original sources
PubMed1987

Intravenous infusion of adenosine but not inosine stimulates respiration in man.

The effects on respiration of intravenous infusions of the endogenous nucleoside adenosine and its deaminated metabolite, inosine, administered in random order, single-blind, were compared in six healthy volunteers. The infusion rate of each nucleoside was initially 3.1 mg min-1 and was increased stepwise every 2 min, as tolerated, up to a possible maximum of 23.4 mg ml-1. The maximum dose rates received by all subjects were 8.5 mg min-1 for adenosine and 16.8 mg min-1 for inosine. Adenosine infusion at rates of 6.1 mg min-1 and above caused a significant increase in minute ventilation, principally due to an increase in tidal volume, with an associated significant fall in end-tidal Pco2. Mean inspiratory flow rate increased and expiratory duration decreased during adenosine infusion, but there was no change in inspiratory duration. Adenosine infusion also caused a significant increase in heart rate and a slight, but significant increase in systolic blood pressure. Infusion of inosine at dose rates up to 16.8 mg min-1 produced no pharmacological effects. This study shows that adenosine by infusion produces sustained respiratory stimulation in man and demonstrates that it does not depend on prior conversion of adenosine to inosine or related metabolites and that it is not secondary to systemic hypotension.

Adenosine↗
PubMed1987

Adenosine-induced respiratory stimulation in man depends on site of infusion. Evidence for an action on the carotid body?

Adenosine is an endogenous nucleoside which stimulates respiration in man and other mammals. In animals adenosine appears to initiate respiratory stimulation within the carotid body, but whether this is the site of action in man is not known. We administered adenosine by intra-aortic infusion to 12 subjects undergoing cardiac catheterisation. When adenosine was infused at three sites proximal to the carotid circulation, minute ventilation was significantly higher than baseline values or those during adenosine infusion at a more distal site. These results support the hypothesis that adenosine-induced respiratory stimulation in man is mediated in the carotid body.

Adenosine↗
PubMed1987

Adenosine causes transient dilatation of coronary arteries in man.

We investigated the effects of i.v. adenosine on coronary blood flow in 10 normal subjects undergoing investigation for chest pain. Coronary flow transiently doubled after greater than or equal to 3.5 mg adenosine without increase in perfusion pressure, systolic load or inotropic state at a constant, paced heart rate. The data provide direct evidence that adenosine dilates coronary arteries in man. The transience of the effect suggests a possible role for adenosine in repeated estimations of coronary flow reserve.

Adenosine↗
PubMed1987

A comparison of the effects of oral nadolol and topical timolol on intraocular pressure, blood pressure, and heart rate.

We compared the effects of oral nadolol 20 mg once daily and topical timolol 0.25% twice daily on the intraocular pressures of 22 glaucoma suspects, in a 12 week double-masked crossover study. Both nadolol and timolol reduced intraocular pressure (p less than 0.001). The reductions in intraocular pressure did not differ significantly after two weeks and four weeks of treatment. Nine of these subjects underwent treadmill exercise tests in order to compare the effects of nadolol and timolol on the cardiovascular system. The effects of the two treatments on blood pressure were comparable, but nadolol caused a significantly greater reduction in heart rate than timolol at rest (p less than 0.05). Nadolol reduces intraocular pressure effectively and may prove a useful alternative treatment for chronic simple glaucoma.

Administration, Oral↗
PubMed1987

Left main coronary artery occlusion with preserved left ventricular function: a report of three cases.

Three patients with angina pectoris are reported in whom occlusion of the left main coronary artery was found at coronary arteriography. In these three patients left ventricular function was well preserved. In all three the right coronary artery was dominant and there were prominent epicardial and septal collateral vessels to the territories normally supplied by the left anterior descending and circumflex arteries. It seems reasonable to suggest that this coronary artery anatomy and collateral vessel formation accounted for the preservation of the left ventricular myocardium in these patients.

Collateral Circulation↗
PubMed1986

Comparison of respiratory effects of intravenous adenosine in neonatal and adult rabbits.

We administered adenosine by repeated intravenous bolus doses to 34 neonatal rabbits in a dose of 120 micrograms X kg-1 (which we had previously found to stimulate respiration in adult rabbits). In 13 neonatal animals adenosine produced transient respiratory depression. In 15 neonatal animals the change in respiration in response to adenosine did not reach statistical significance. In two animals a transient increase in respiration occurred in response to adenosine. In the neonatal group as a whole intravenous adenosine significantly depressed ventilation. In eleven of the animals studied as neonates, respiratory responses to adenosine were again studied in adulthood. In 10 animals respiratory stimulation occurred in response to adenosine. In the adult group adenosine significantly increased ventilation, in contrast to its effects in the neonatal group. The respiratory effects of intravenous adenosine have not been previously described in neonatal animals. Respiratory stimulation produced by intravenous adenosine in adult rabbits contrasts with the respiratory depression commonly seen in neonatal rabbits in this study. It is suggested that altered responses to adenosine may be involved in the difference between the ventilatory response to hypoxia in adult and neonatal animals.

Adenosine↗
PubMed1986

Plasma amiodarone concentrations during intravenous infusion.

Amiodarone is a useful antiarrhythmic agent whose pharmacokinetics are incompletely characterised. In order to optimise efficacy of an antiarrhythmic drug, information regarding plasma concentrations achieved during use of the drug is necessary. We report plasma amiodarone and desethylamiodarone concentrations in eight patients following intravenous infusion at a rate of 175 mg h-1 for the first 2 h, followed by infusion at a rate of 50 mg h-1 for a further 46 h a regimen very similar to that recommended by the manufacturers. In at least three of eight patients plasma concentrations were below the suggested therapeutic range of 1.0-2.5 mg l-1 from 3 to 16 h after the infusion was started. Our data suggests that larger doses of intravenous amiodarone than those previously recommended may be necessary to obtain optimal benefit from the drug.

Aged↗
PubMed1986

Transient bradycardia and subsequent sinus tachycardia produced by intravenous adenosine in healthy adult subjects.

Adenosine was administered in increasing intravenous bolus doses to nine healthy volunteers. A transient decrease in heart rate was observed which occurred about 20 s after injection. This was due to a reduction in sinus rate and/or transient block of conduction through the atrioventricular node, and lasted less than 10 s. An increase in sinus rate which followed any transient bradycardia was also observed. The maximum bradycardia and maximum tachycardia were each significantly related to the logarithm of adenosine dose.

Adenosine↗
PubMed1986

Intravenous adenosine in the treatment of supraventricular tachycardia: a dose-ranging study and interaction with dipyridamole.

Increasing doses of adenosine were given by rapid intravenous bolus to seven patients with spontaneous supraventricular tachycardia. Adenosine restored sinus rhythm in 10 of 14 episodes of narrow complex tachycardia. In those patients in whom adenosine produced only transient ventricular slowing the underlying rhythm was atrial flutter. Transient dyspnoea occurred in all patients. In two patients taking dipyridamole the mean dose of adenosine which produced an electrophysiologic effect (restoration of sinus rhythm or ventricular slowing to under 100 beats min-1) was 1.0 +/- 0.52 mg, whereas in other patients the mean dose was 8.8 +/- 2.6 mg, suggesting potentiation of the action of adenosine by dipyridamole.

Adenosine↗
PubMed1985

Sick sinus syndrome: an adenosine-mediated disease.

It is suggested that adenosine is a mediator of the paroxysmal bradycardias and tachycardias characterising the sick sinus syndrome. Increased sensitivity to adenosine could account for the arrhythmias, which might therefore be suppressed by an adenosine antagonist such as theophylline.

Adenosine↗