Ischaemic preconditioning--time course of renewal in the pig. 1993

S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
Max-Planck-Institute, Department of Experimental Cardiology, Bad Nauheim, Germany.

OBJECTIVE The aim was to examine whether ischaemic preconditioning can be renewed by a second cycle of brief coronary occlusions in pigs subjected to two different reperfusion intervals (1 h or 4 d). METHODS Ischaemic preconditioning was induced by a cycle of two 10 min occlusions of the left anterior descending coronary artery separated by 30 min of reperfusion. Infarction was induced with a subsequent 1 h occlusion and a 2 h reperfusion period. There were four experimental groups: in group I (n = 5), a 30 min reperfusion was interposed after the preconditioning cycle prior to the sustained occlusion; in group II (n = 5), this time frame was extended to 1 h; in group III (n = 5), the preconditioning cycle was renewed 1 h after the first cycle; in group IV (n = 5), the second cycle was performed 4 d later. Control pigs (n = 5) were subjected to 1 h coronary occlusion and 2 h reperfusion without previous short occlusions. Infarct size was measured with p-nitro blue tetrazolium and was expressed as a percent of area at risk. RESULTS The percent of the risk region infarcted was 69.9 (SEM 3.8)% for controls, 22.9 (3.5)% in group I (p < 0.001 v controls), 67.3 (5.2)% in group II, 66.3 (4.2)% in group III, and 17.9 (3.9)% in group IV (p < 0.001 v controls). Regional wall function measured with ultrasonic crystals deteriorated through the reperfusion intervals, indicating different underlying mechanisms for ischaemic preconditioning and myocardial stunning. CONCLUSIONS Ischaemic preconditioning with two 10 min occlusions reduced infarct size resulting from a 60 min coronary occlusion when that was performed 30 min after the last short occlusion. This effect was lost after 1 h. Preconditioning could be renewed by a second cycle of brief coronary occlusion and reperfusion 4 d but not 1 h after the first cycle. These results suggest the release of a mediator from an exhaustible pool.

UI MeSH Term Description Entries
D008297 Male Males
D009203 Myocardial Infarction NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION). Cardiovascular Stroke,Heart Attack,Myocardial Infarct,Cardiovascular Strokes,Heart Attacks,Infarct, Myocardial,Infarction, Myocardial,Infarctions, Myocardial,Infarcts, Myocardial,Myocardial Infarctions,Myocardial Infarcts,Stroke, Cardiovascular,Strokes, Cardiovascular
D009206 Myocardium The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow. Muscle, Cardiac,Muscle, Heart,Cardiac Muscle,Myocardia,Cardiac Muscles,Heart Muscle,Heart Muscles,Muscles, Cardiac,Muscles, Heart
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013552 Swine Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA). Phacochoerus,Pigs,Suidae,Warthogs,Wart Hogs,Hog, Wart,Hogs, Wart,Wart Hog
D013997 Time Factors Elements of limited time intervals, contributing to particular results or situations. Time Series,Factor, Time,Time Factor
D015425 Myocardial Reperfusion Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY. Coronary Reperfusion,Reperfusion, Myocardial,Coronary Reperfusions,Myocardial Reperfusions,Reperfusion, Coronary,Reperfusions, Coronary,Reperfusions, Myocardial
D017202 Myocardial Ischemia A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION). Heart Disease, Ischemic,Ischemia, Myocardial,Ischemic Heart Disease,Disease, Ischemic Heart,Diseases, Ischemic Heart,Heart Diseases, Ischemic,Ischemias, Myocardial,Ischemic Heart Diseases,Myocardial Ischemias

Related Publications

S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
March 2016, The British journal of surgery,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
June 1995, Cardiovascular research,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
January 2003, APMIS. Supplementum,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
January 2003, Neurourology and urodynamics,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
January 1994, BMJ (Clinical research ed.),
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
July 1996, Lancet (London, England),
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
February 2010, Journal of cardiothoracic and vascular anesthesia,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
January 1995, Pharmacological research,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
April 1993, Cardiovascular research,
S Sack, and M Mohri, and M Arras, and E R Schwarz, and W Schaper
December 2007, Lancet (London, England),
Copied contents to your clipboard!