Activity of endogenous myocardial lipases during incubation at acid pH

Weglicki, William B.; Owens, K.; Ruth, Robin C.; Sonnenblick, Edmund H.

doi:10.1093/cvr/8.2.237

Cited by 11 publications

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“…These structural characteristics (transitions) result in a change in membrane fluidity from the liquid-crystalline state to the solid gel state [31][32][33][34] yielding a "leaky" membranous state. A cascade of damaging events may follow including: activation and leakage of lysosomal and lipoprotein hydrolases, 35,36 activation of calcium-dependent phospholipases 37,38 and the release of free fatty acids, 39 activation of the apoptotic cascade [40][41][42][43][44] and disruption of the cytoskeletal matrix. [45][46][47] Along with the generation of free radicals, the oxidative stressors attendant to hypothermia may result in the onset of apoptosis or gene regulated cell death.…”

Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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Section: A Long Cold Journeymentioning

confidence: 99%

Cryopreservation

Baust¹,

2009

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“…omal enzymes occurs in the heart during early and late ischemia.I, 2,[10][11][12][13][14] In recent years, aprotinin (a naturally occurring protease inhibitor) has been routinely given in many institutions in patients undergoing cardiac operations, particularly those with an increased risk of blood loss. The effect of the drug on perioperative blood loss in cardiac surgery is established.P"?…”

mentioning

confidence: 99%

Aprotinin improves myocardial recovery after ischemia and reperfusion:

Gurevitch¹,

Barak²,

Hochhauser³

et al. 1994

The Journal of Thoracic and Cardiovascular Surgery

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Aprotinin improves myocardial recovery after ischemia and reperfusion Effects of the drug on isolated rat heartsThe effects of aprotinin, a protease inhibitor, on the ischemic and nonischemic isolated rat heart was investigated with the use of the modified Langendorlf model. During phase I of the study, hearts were perfused with either low-dose aprotinin (10 5 Kill/L), high-dose aprotinin (10 6 KIU /L), or normal saline solution added to modified Krebs-Henseleit solution. No statistically significant differences in contraction amplitude, contractility, coronary flow, and wet/dry heart weight ratio were observed among the three groups of hearts. In phase II, hearts were exposed to a 40-minute period of global ischemia at 31 0 C. Ischemic arrest was induced by warm cardioplegia. Before ischemia and during cardioplegia, hearts were perfused with either aprotinin 10 6 KIU/L (n = 10) or normal saline solution (n = 10) for .30 minutes. On reperfusion, recovery of hearts treated with aprotinin was significantly better than that of control hearts, as reflected by better contractility (analysis of variance, p = 0.011), higher coronary flow (p < 0.025), and lower creatine kinase levels (p <0.05). No statistically significant differences in contraction amplitude were observed between the two groups. When the effect of ischemia within each group of hearts was analyzed, the preserving effect of aprotinin was even more pronounced. In the control group, ischemia caused a decrease in contractility (p < 0.025) and a decrease in oxygen consumption (p = 0.006); by contrast, in the aprotinin group the preischemic values were maintained. Accordingly, we conclude that aprotinin at concentrations up to 10 6 KIU /L has no deleterious effect on normally perfused hearts and has a significant protective effect on the ischemic heart when used in high doses in the preischemic period. (J THoRAe CARDIOVASC SURG 1994;108:109-18)

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A Paradigm Shift in Cryopreservation: Molecular-Based Advances to Improve Outcome

Baust

Cryogenic Engineering

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Activity of endogenous myocardial lipases during incubation at acid pH

Cited by 11 publications

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Cryopreservation

Cryopreservation

Aprotinin improves myocardial recovery after ischemia and reperfusion:

A Paradigm Shift in Cryopreservation: Molecular-Based Advances to Improve Outcome

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