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Perfusion, Vol. 8, No. 1, 113-118 (1993)
DOI: 10.1177/026765919300800115

Ischaemia/reperfusion in the posthypoxaemic re-oxygenated myocardium: haemodynamic study in the isolated perfused rat heart

Antonio Corno

Istituto Scientifico San Raffaele, Istituto per le Malattie Cardiovascolari e Respiratorie and Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, Milan

Roberto Motterlini

Istituto Scientifico San Raffaele, Istituto per le Malattie Cardiovascolari e Respiratorie and Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, Milan

Laura Brenna

Istituto Scientifico San Raffaele, Istituto per le Malattie Cardiovascolari e Respiratorie and Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, Milan

Francesco Santoro

Istituto Scientifico San Raffaele, Istituto per le Malattie Cardiovascolari e Respiratorie and Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, Milan

Michele Samaja

Istituto Scientifico San Raffaele, Istituto per le Malattie Cardiovascolari e Respiratorie and Dipartimento di Scienze e Tecnologie Biomediche, Università degli Studi di Milano, Milan

In order to study the haemodynamics of reperfusion injury in the post hypoxaemic heart, we exposed buffer-perfused isolated rat hearts to either: (1) 20-minute low-flow ischaemia or (2) 20-minute hypoxaemia followed by re-oxygenation and further ischaemia/reperfusion. In group 2, the myocardial contractility recovered less (p <0.002) than in group 1. This model therefore represents with sufficient reliability the clinical situation where hypoxaemic hearts are re-oxgenated before ischaemia/reperfusion and receive more severe injury than hearts exposed to ischaemia/reperfusion only. To locate the major site of the injury, further data were obtained (1) with infusion of superoxide dismutase and catalase during hypoxaemia and in the first five minutes of re-oxygenation, and (2) by eliminating re-oxygenation. It appears that the major determinant of reperfusion injury in hypoxaemic hearts is to be looked for in the events underlying hypoxaemia or re-oxygenation, and is mediated by oxygen- derived free radicals.


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