Recovery of the Heart after Normothermic Ischemia: Part II: Myocardial Function during Postischemic Reperfusion

Mulch, J; Schaper, Jutta; Gottwik, Martin; Fw, Hehrlein

doi:10.1055/s-0028-1096235

Thorac cardiovasc Surg

1979

DOI: 10.1055/s-0028-1096235

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Recovery of the Heart after Normothermic Ischemia: Part II: Myocardial Function during Postischemic Reperfusion

J Mulch¹,

Jutta Schaper²,

Martin Gottwik³

et al.

Abstract: Contraction and relaxation of the canine myocardium were examined during normothermic ischemia in an isolated heart model. Decrease in the development of tension depends on the duration of ischemia. Deficient functional recovery was observed after ischemic periods extending beyond 30 minutes, in spite of reperfusion periods of over 1 hour. A decrease in compliance was observed during the anoxic period, but a persistent defect of relaxation occurred only after 60 minutes of ischemia. After this period there was… Show more

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1988

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Cited by 3 publications

References 13 publications

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Avoidance of reperfusion injury after cardioplegia.

Brown¹,

Morritt²,

Hammo³

1982

Thorax

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Myocardial damage incurred by ischaemia appears during and seems to be accelerated by reperfusion, which restores recoverable cells and disrupts badly damaged ones. Vicious cycles of oedema, calcium accumulation, acidosis, oxygen toxicity, fibrillation and air and platelet emboli contribute to the reperfusion injury. The philosophy of cool low-pressure reperfusion gradually restoring temperature and pressure to normal is here contrasted experimentally with that of immediate normothermic, normotensive perfusion after 90 minutes of ischaemic cool, cardioplegic arrest. The preparation was a canine heart which was treated according to the usual clinical protocol except that one group was reperfused at normal temperature and pressure, and the other group started reperfusion cool and at a low pressure and over the next 10 minutes pressure and temperature were restored to normal. Isovolumic ventricular function studies were done before ischaemia and after recovery and showed statistically significant differences between the groups in favour of the immediate restoration of normal temperature and pressure of perfusion. Contractile velocity and systolic pressure showed very highly significant (p = < 0 005) differences, wall stress significant (p = < 0 025) and compliance not significant differences between the groups. Reperfusion with optimal conditions may prevent "vicious cycle" changes in ischaemically damaged but recoverable myocardium. We have shown that a step in this direction is reperfusion with blood at normal temperature and pressure rather than initially at lowered temperature and pressure.Myocardial damage appearing during reperfusion has been well-known from the earliest experience of cardioplegia as now used,' 2 and is acknowledged to be more dramatic than changes found in the ischaemic phase.3 Reperfusion accentuates the difference between recoverable and dubiously recoverable myocardium, making more obvious the damage previously only detectable by electron microscopy. The characteristic appearances of reperfusion injury result,24 6 with typical deterioration of function7-9 epitomised by "stiffness" of contraction and relaxation. Not only ischaemia but any withdrawal of metabolites or essential ions is followed by reperfusion injury on restoration of blood supply.The events which follow reperfusion are of the "vicious cycle" type. Oedema impairs the distribution and adequacy of perfusion by increasing the intramyocardial pressure and widening diffusion distances. The restoration of energy supply is further delayed by depressed mitochondrial function. High reperfusion pressures worsen the oedema but

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Avoidance of reperfusion injury after cardioplegia.

Brown¹,

Morritt²,

Hammo³

1982

Thorax

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Effects of Blood and Crystalloid Cardioplegia on Cardiac Function at Organ and Cellular Levels During Hypothermic Cardiac Arrest

1988

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The present investigation was undertaken to compare the effects of cold crystalloid and blood cardioplegia on the functional recovery of the heart; on Ca++ binding and uptake, Ca++-ATPase of the sarcoplasmic reticulum (SR), and sarcolemmal (SL) ATPase; and on serum MB fraction of creatine kinase (MBCK) after one and half hours of reperfusion following one hour of ischemic cardiac arrest in dog. This study was made also to determine if the functional changes are related to the changes in biochemistry at the molecular level. The dogs were divided into three groups: sham bypass (SB), cold crystalloid cardioplegia (CC), and pump blood cardioplegia (PB). There was a decrease in the cardiac index (CI), left ventricular work index (LVWI), and mean aortic pressure (MAP) in all three groups. The index of myocardial contractility [dp/dt)/IIP) and CI were lower in the CC group as compared with the SB and PB groups. All the hemodynamic values for the PB group were similar to those of the SB group except total systemic vascular resistance (TSVR) and left ventricular end-diastolic pressure (LVEDP) which were lower in the PB group. The index of myocardial contractility and cardiac index appeared to be greater in the PB group than in the CC group. There was a decrease in the Ca++ uptake by SR from both the CC and PB groups. Ca++ binding and Ca++,-ATPase of SR from the PB group were depressed. The sarcolemmal ATPase was unaffected in both groups. The serum MBCK increased in both PB and CC groups, though the increase was smaller in the PB group. These results indicate that the functional recovery of the heart was slightly better with pump blood cardioplegia than with cold crystalloid cardioplegia. The depressed myocardial contractility and cardiac function in the CC group were associated with a decrease in the Ca++ uptake by SR. However, the decreases in the Ca++ binding, Ca++ uptake, and Ca++ ATPase by SR from the pump blood cardioplegic group were not accompanied by decreases in the cardiac contractility and cardiac function. Myocardial damage as assessed by serum MBCK was smaller in the PB group than in the CC group.

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A Paracorporeal Rat Heart Model for Ischemic and Reperfusion Studies

Hultman

Forsberg

Hansson

et al. 1982

Upsala Journal of Medical Sciences

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Paracorporeal rat hearts were supplied with blood derived from the abdominal aorta of a supporting rat. The circulatory stability and working capacity of the supporting animal was analyzed in the experimental situation in terms of PO2, SO2, PC02, HC03, pH and electrolytes, all of which were within the normal range before and during a 60 min period of paracorporeal perfusion. For evaluation of ischemic damage in this model studies were made on three groups of excised hearts. They were subjected to 10, 15 or 20 min of complete global ischemia at 37OC (ambient temperature) and reperfused for 30 min, including ECG, observations of contractility and an analysis of creatine kinase efflux in the coronary effluent. The results showed good reproducibility and the data were in accordance with reports from similar studies on Langendorff preparations. The model, which is easily set up, inexpensive and based upon pulsatile blood perfusion, should be more physiologic than the conventional Langendorff preparation.

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Recovery of the Heart after Normothermic Ischemia: Part II: Myocardial Function during Postischemic Reperfusion

Cited by 3 publications

References 13 publications

Avoidance of reperfusion injury after cardioplegia.

Avoidance of reperfusion injury after cardioplegia.

Effects of Blood and Crystalloid Cardioplegia on Cardiac Function at Organ and Cellular Levels During Hypothermic Cardiac Arrest

A Paracorporeal Rat Heart Model for Ischemic and Reperfusion Studies

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