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L Opie

Publications and source records attributed to L Opie.

18 recordsLinked to original sources
PubMed2001

Taking HIV to court.

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Acquired Immunodeficiency Syndrome↗
PubMed1998

Role of cyclic nucleotide phosphodiesterases in ischemic preconditioning.

Several signal transduction pathways have been implicated in the mechanism of protection induced by ischemic preconditioning (PC). For example, stimulation of a variety of G-protein coupled receptors results in stimulation of protein kinase C (PKC) which has been suggested to act as common denominator in eliciting protection. PC also significantly attenuated cAMP accumulation during sustained ischemia, suggesting involvement of an anti-adrenergic mechanism. The aim of this study was to evaluate the beta-adrenergic signal transduction pathway (as evidenced by changes in tissue cAMP and cAMP- and cGMP-phosphodiesterase) during the PC protocol as well as during sustained ischemia. Isolated perfused rat hearts were preconditioned by 3 x 5 min global ischemia (PC1,2,3) interspersed by 5 min reperfusion, followed by 25 min global ischemia. Tissue cAMP- and cGMP-PDE activity as well as cAMP and cGMP levels were determined at different time intervals during the PC protocol and sustained ischemia. Tissue cAMP increased with each PC ischemic event and normalized upon reperfusion, while PDE activity showed the opposite, viz a reduction during ischemia and an increase during reperfusion. Except for PC1, tissue cGMP showed similar fluctuations. Throughout 25 min sustained ischemia, cAMP- and cGMP-PDE activities were higher in PC than in nonpreconditioned hearts, associated with a significantly lesser accumulation in cAMP and higher cGMP levels in the former. Fluctuations in cyclic nucleotides during preconditioning were associated with concomitant changes in PDE activity, while the attenuated beta-adrenergic response of preconditioned hearts during sustained ischemia may partially be due to increased PDE activity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1989

Trial alert.

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Cardiovascular Agents↗
PubMed1983

Intravenous dl-carnitine fails to increase the double-product during atrial pacing in patients with effort angina. A double-blind randomized study.

Infusions of DL-carnitine are reported to improve the tolerance to atrial pacing of patients with angina pectoris. In the present study, six patients with angina of effort and triple vessel disease received two placebo and two carnitine infusions administered in a double-blind randomized fashion. Carnitine did not affect either the double product (heart rate X systolic blood pressure) at maximal pacing (ST depression: 2.3 +/- 0.2 mm, +/- SEM) or the tolerated pacing time. Intravenous carnitine, in the dose given, is of no therapeutic benefit in myocardial ischemia precipitated by tachycardia. It could be effective when free fatty acids are elevated as during catecholamine stimulation.

Angina Pectoris↗
PubMed1977

Coronary heart disease in marathon runners.

Six highly trained marathon runners developed myocardial infarction. One of the two cases of clinically diagnosed myocardial infarction was fatal, and there were four cases of angiographically-proven infarction. Two athletes had significant arterial disease of two major coronary arteries, a third had stenosis of the anterior descending and the fourth of the right coronary artery. All these athletes had warning symptoms. Three of them completed marathon races despite symptoms, one athlete running more than 20 miles after the onset of exertional discomfort to complete the 56 mile Comrades Marathon. In spite of developing chest pain, another athlete who died had continued training for three weeks, including a 40 mile run. Two other athletes also continued to train with chest pain. We conclude that the marathon runners studied were not immune to coronary heart disease, nor to coronary atherosclerosis and that high levels of physical fitness did not guarantee the absence of significant cardiovascular disease. In addition, the relationship of exercise and myocardial infarction was complex because two athletes developed myocardial infarction during marathon running in the absence of complete coronary artery occlusion. We stress that marathon runners, like other sportsmen, should be warned of the serious significance of the development of exertional symptoms. Our conclusions do not reflect on the possible value of exercise in the prevention of coronary heart disease. Rather we refute exaggerated claims that marathon running provides complete immunity from coronary heart disease.

Adult↗