The pathology of cardiac ischaemia: Cellular and molecular aspects

Lee, John A.

doi:10.1002/path.1711750203

Cited by 4 publications

(1 citation statement)

References 42 publications

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“…An important role in this process is played by CI-channels and K+,2Cl--symport. The decrease of the cell volume is accompanied by opposite processes: entry of CI-, Na +, and K § into the cytoplasm via Na+,K +, 2Cl--uniport and Na § via Na+/H+-exchange [7,10,13].A decrease in the coronary blood flow modulates activity of proteolytic and lipolytic enzymes, induces accumulation of metabolic products in the ischemic region, and activates Na+/H+-exchange [2,8,9,15]. These changes may form the basis for an increase in the intracellular osmotic pressure and water entry into the cytoplasm [1,5,11].…”

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Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

1999

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Subtotal 30-min ischemia leads to myoglobin release and increases water content in the heart. Reperfusion partially restores the developed pressure. Addition of furosemide (a Na +, K+,2CI --symport blocker) or NMA (inhibitor of Na § to perfusate decreases myocardial water content, reduces myoglobin loss, and completely restores myocardial contractile function. The low-rate perfusion of isolated heart and its reperfusion with solutions containing DIOA (inhibitor of K+,C1--co-transport) or IAA-94 (C1-channel blocker) increases water accumulation and myoglobin release from the myocardium, and deteriorated its contractile function during reperfusion.Key Words: myocardial ischemia; edema; Na+, K+, Na+/H § K+, amiloride derivatives Similar to other cells, cardiomyocytes possess a system regulating their volume [4,6,7,10]. The volume regulation system is activated by swelling or shrinkage of cardiomyocytes [10,13,14]. An increase in the cardiomyocyte volume stimulates efflux of the osmotically active substances (osmolytes) from the cells, which decreases the amount of intracellular water. An important role in this process is played by CI-channels and K+,2Cl--symport. The decrease of the cell volume is accompanied by opposite processes: entry of CI-, Na +, and K § into the cytoplasm via Na+,K +, 2Cl--uniport and Na § via Na+/H+-exchange [7,10,13].A decrease in the coronary blood flow modulates activity of proteolytic and lipolytic enzymes, induces accumulation of metabolic products in the ischemic region, and activates Na+/H+-exchange [2,8,9,15]. These changes may form the basis for an increase in the intracellular osmotic pressure and water entry into the cytoplasm [1,5,11]. It is supposed that extreme cardiomyocyte swelling may be a cause of mechanical rupture of the sarcolemma [6,12]. Department of Biochemistry, Voronezh State Medical AcademyThe role of sarcolemmal anion-transporting mechanisms (CI-channels, K+,C1 --and K+,Na+,2C1--symport, and Na+/H+-exchange) in the development of cardiomyocyte edema and their ischemic and reperfusion damage is not clear. Our aim was to study the effects of these ion-exchange sarcolemmal systems on myocardial edema during subtotal ischemia and reperfusion. MATERIALS AND METHODSExperiments were performed on hearts perfused according to the Langendorff technique. Random-bred albino rats were decapitated under ether narcosis, the hearts were isolated and placed into cold Ringer--Lock solution. The initial solution contained (in mM): 140 NaC1, 0.5 NaH2PO 4, 5 KCI, 5 Tris-OH (pH 7.4), 11 glucose, and 2 CaCI z. The heart was perfused with oxygenated solution through cannulated aorta at the rate of 10 ml/min/g wet tissue at 37~ To stabilize the contractile activity, the heart was perfused with initial solution for 15 min. The cardiac parameters during this period were considered as control (100%). Subtotal ischemia was modeled by reducing the perfusion 0007-4888/99/0004-0363522.00 e1999 Kluwer Academic/Plenum Publishers

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confidence: 98%

Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

1999

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Durchblutungsstörungen des Myokard

Hort¹,

Arnold²,

Frenzel³

2000

Pathologie Des Endokard, Der Kranzarterien Und Des Myokard

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The old spontaneously hypertensive rat as a model for transmyocardial laser revascularisation research

Huikeshoven¹,

Wal

Tukkie

et al. 2003

Lasers in Medical Science

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Animal models used in transmyocardial laser revascularisation (TMLR) research lack the increased fibrosis observed in patients with chronic myocardial ischaemia. This pathology has also been described in patients with chronic elevated afterload, and therefore we evaluated the spontaneously hypertensive rat (SHR) as a model for TMLR research. We compared (1) the myocardial pathology of SHR with the pathology of three TMLR patients, (2) the reaction to TMLR in SHR and human myocardium using three different lasers, and (3) myocardial hypoxia in SHR myocardium and (healthy) Wistar rat myocardium. SHR and human myocardium both showed increased fibrosis and a similar myocardial reaction to TMLR (comparable morphology of fibrotic TMLR channel scars). More hypoxic cells were observed in SHR than in Wistar control rat myocardium. The similarities between SHR and human chronic ischaemic myocardium make the SHR a suitable model for TMLR research.

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The pathology of cardiac ischaemia: Cellular and molecular aspects

Cited by 4 publications

References 42 publications

Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

Effect of sarcolemmal anion transport system blockers on the development of ischemia-induced myocardial edema and recovery of contractile function during reperfusion

Durchblutungsstörungen des Myokard

The old spontaneously hypertensive rat as a model for transmyocardial laser revascularisation research

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