Ultrastructural, morphometric and X-ray microanalytical studies of ischemia and reperfusion-induced myocardial injury using ionic lanthanum as a probe for indicating membrane permeability changes

1994 ◽  
Vol 27 (1) ◽  
pp. 15-25
Author(s):  
Shinji Koba ◽  
Hiroshi Suzuki ◽  
Noburu Konno ◽  
Youichi Takeyama ◽  
Takashi Katagiri

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.





2002 ◽  
Vol 25 (11) ◽  
pp. 1539-1549 ◽  
Author(s):  
L. Van Der Weerd ◽  
M. M. A. E. Claessens ◽  
C. Efdé ◽  
H. Van As


1988 ◽  
Vol 66 (12) ◽  
pp. 1518-1523 ◽  
Author(s):  
M. Renuka Prasad ◽  
Ronald Clement ◽  
Hajime Otani ◽  
Randall Jones ◽  
Dipak K. Das ◽  
...  

The increase of cellular fatty acids appears to be one of the causes of the myocardial injury during ischemia and reperfusion. This study was designed to examine whether a hypolipidemic drug such as clofibrate can reduce the myocardial injury during ischemia and reperfusion. Clofibrate was fed to experimental pigs for 9 days. Isolated in situ hearts from both experimental and control pigs were subjected to 60 min of regional ischemia induced by occluding the left anterior descending coronary artery, followed by 60 min of global ischemia by hypothermic cardioplegic arrest and 60 min of reperfusion. The clofibrate feeding resulted in the better cardiac performance as judged by increased coronary blood flow, improved left ventricular function, and reduced myocardial injury as judged by creatine kinase release. Although the clofibrate-fed animals contained higher levels of thiobarbituric reactive materials, the free fatty acid levels of plasma and myocardium were much lower compared with control animals. The clofibrate feeding was also associated with increased peroxisomal catalase and (β-oxidation of fatty acids. These results suggest that decreased levels of free fatty acids in the plasma and the myocardium and increased catalase activity induced by antilipolytic therapy appear to provide beneficial effects to the myocardium during ischemia and reperfusion.



Nature ◽  
1977 ◽  
Vol 270 (5636) ◽  
pp. 391-396 ◽  
Author(s):  
Charles F. Stevens




Blood ◽  
1965 ◽  
Vol 26 (3) ◽  
pp. 367-382 ◽  
Author(s):  
JAMES H. JANDL

Abstract The normal survival of red cells requires maintained regulation of cell size and shape. This regulation is to a large extent dependent upon membrane permeability and the active transport of cations. Agents such as C' that affect permeability markedly by creating large holes in the membrane lead to rapid cell death. Most hemolytic disorders thus far studied involve lesser increases in membrane permeability and hemolysis occurs more gradually by the sequence of colloid osmotic swelling, loss of cell surface, and spherocytosis. With very mild permeability changes, as in hereditary spherocytosis, the cell may compensate for an increased leak-rate for cations by increased active transport. This compensation requires increased glycolysis and optimal metabolic conditions, however, and the cell rapidly decompensates during glucose deprivation or metabolic stress. The interaction between reticuloendothelial tissues and red cells provides such a stress for leaky cells and hastens their destruction.



2013 ◽  
pp. 34-48
Author(s):  
Richard D. Keynes ◽  
David J. Aidley ◽  
Christopher L.-H. Huang


1988 ◽  
Vol 4 (1) ◽  
pp. 31-37 ◽  
Author(s):  
Steven W. Werns ◽  
Benedict R. Lucchesi


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