The association of increased plasma MB CPK activity and irreversible ischemic myocardial injury in the dog.

Abstract

SUMMARY To evaluate the concordance between elevated plasma MB CPK and irreversible myocardial ischemic injury, coronary occlusion was induced for 10 minutes to 48 hours in 21 open chest dogs and 13 conscious animals. Results of plasma CPK and MB CPK assayed in samples obtained serially for 24 hours were compared to microscopic changes in hearts from the same animals examined 48 hours after occlusion. Twelve of the 34 dogs died within two hours after coronary occlusion. Among the surviving 22 dogs, one failed to exhibit gross or electrocardiographic evidence of ischemia and was therefore excluded. Twelve had coronary occlusion maintained for 30 THE DIAGNOSIS of acute myocardial infarction often depends upon the demonstration of elevated plasma enzyme activity.' Enzymatic estimation of infarct size depends on several premises, one of which is that release of enzyme from the ischemic heart reflects cell death rather than reversible injury.2 However, it is possible that release of myocardial enzymes into the circulation may not reflect necrosis but may occur even when ischemic cells are not irreversibly damaged. Elevated activity of MB CPK in plasma, an isoenzyme of creatine phosphokinase, has been found to be a sensitive index of myocardial injury.3`6 In man, the MB CPK isoenzyme is confined almost exclusively to myocardium and is virtually absent from skeletal muscle,7 although this point is controversial.8 9 In dogs, MB CPK appears to be found in the gastrointestinal tract as well as the heart.8Despite substantial circumstantial evidence, it is not clear whether release of MB CPK from the ischemic heart is tantamount to myocardial cell death. This issue deserves consideration particularly because under some experimental conditions, such as exposure of myocardium to calcium-free media, enzyme is released from the heart in the absence of irreversible contractile failure.10 Furthermore, although changes in activity of enzymes in plasma such as glutamic oxaloacetic transaminase (GOT) have been associated with experimental myocardial ischemic injury for many years, release resulting from ischemia insufficient to produce cell death has not been completely excluded." Many experimental studies concerned with these issues employed open chest animal preparations in which release of enzyme from traumatized skeletal muscle may have occurred.The recent recognition of MB CPK as a marker of myocardium in contrast to skeletal muscle4 and the development of techniques permitting quantitative estimation of MB CPK activity in plasma samples" encouraged us to examine minutes or longer and in 11 of these peak plasma MB CPK activity exceeded the normal range (mean ± 2 SD) and baseline values by at least 100%. Necrosis was present in the hearts from each manifested by nuclear pyknosis, eosinophilia, shrinkage of cytoplasm, and leukocytic infiltration. In the remaining nine dogs with occlusion for less than 30 minutes, peak plasma MB CPK activity was not elevated and necrosis was not detected. The close concordance between plasma MB CP...

Attenuation of dysfunction in the postischemic 'stunned' myocardium by dimethylthiourea.

“…TTC staining confirmed the absence of infarction in all animals. This finding is consistent with previous studies2' 14,15 showing that the myocardial injury associated with a 15 min coronary occlusion in the dog is completely reversible.…”

Avaliação comparativa do valor prognóstico de quatro marcadores bioquímicos de lesão miocárdica pós intervenções percutâneas utilizando stents coronarianos

“…The pathophysiology involved in this process has not yet been completely clarified. Ishikawa et al 13 , however, in experimental studies with dogs, reported that coronary occlusion longer than 20 minutes was associated with enzyme release (total CK and CK-MB) and produced histopathologic evidence of myocardial necrosis (ie, irreversible damage), an observation with relevant diagnostic and therapeutic implications [14][15][16] . In addition, when the combined events were decomposed, we observed that the patients with an elevation in the CK-MB activity after stent implantation had a greater tendency towards mortality (10.6% x 0.6%; P = 0.10) and additional revascularization procedures (30% x 12%; P = 0.14) in one year.…”

Quantification of cerebral infarct size by creatine kinase BB isoenzyme.

“…This assumption is based on the observation in cardiac muscle that CK release is an indicator of irreversible damage. 21 The total CKBB per gram of tissue was calculated by taking the measurement of CK in international units in whole brain and the final concentration of purified CKBB obtained in our isolation procedures. …”

“…In several of our animals, there was a secondary rise in CKBB which appeared at various intervals for a variable length of time. If one accepts the premise that a rise in CKBB represents ongoing tissue destruction as occurs in the myocardium, 21 then this secondary rise may represent ongoing destruction from secondary mechanisms, or a further breakdown of the blood brain barrier. It may also explain why with larger infarctions, our method tended to underestimate the actual measured value as shown in figure 6.…”