Biomedical subjects
D Yellon
Publications and source records attributed to D Yellon.
Does ischemic preconditioning occur in patients?
Ischemic preconditioning offers powerful protection from ischemic necrosis in a wide range of animal species, but does it occur in humans? Support for preconditioning in humans comes from several sources: studies showing increased tolerance to repetitive balloon inflations during angioplasty, some (but not all) studies suggesting that preinfarction angina confers an early beneficial effect, studies showing that patients can develop sudden tolerance to repetitive exercise- or pacing-induced ischemia, cardiothoracic studies of intermittent aortic cross-clamping showing better preservation of myocardial adenosine triphosphate and in vitro studies of isolated human trabecular muscle and isolated human ventricular myocytes that demonstrate a biology consistent with preconditioning. In the future, preconditioning or "preconditioning mimetic" agents have the potential to be applied to a wide array of cardiovascular disorders and might result in better preservation of the heart in instances of cardiopulmonary bypass, heart transplantation, angina and myocardial infarction.
Spinal cord stimulation or ischaemic preconditioning?
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ATP-dependent potassium channel openers and preconditioning.
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Sympathetically induced myocardial ischaemia causes the heart to release plasma kinin.
A recently developed highly sensitive radioimmunoassay method for detecting plasma kinin was used to re-evaluate the results of previous studies, in which plasma kinin had been measured with a bioassay method. To clarify the mechanism of plasma kinin release in global myocardial ischaemia the left main coronary artery was cannulated using a Griggs type autoperfusing cannula after pentobarbital anaesthesia in open chest dogs. The animals were divided into a non-coronary constricted group (n = 4) and a moderately coronary constricted group (n = 7). Cardiac sympathetic nerve stimulation (10 V, 4 Hz, 2 ms duration) was given to both groups. Haemodynamic recordings and blood samples were taken before and after coronary constriction as well as after sympathetic nerve stimulation. The arterial and coronary sinus plasma kinin concentrations were determined with the new radioimmunoassay method. After sympathetic nerve stimulation apparent myocardial ischaemia occurred and the plasma kinin concentration in coronary sinus blood increased significantly in the constricted group. In the non-constricted group, however, myocardial ischaemia did not appear and no significant change in coronary sinus plasma kinin concentrations was seen. These findings show that there was a pronounced release of plasma kinin from the heart when apparent myocardial ischaemia occurred.