2001Chineae Journal of Organ TransplantationRequires access

Heat shock preconditioning enhances myocardial recovery in isolated rabbit heartafter long-term preservation by induction of heat shock protein 72

Yang Don

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Abstract

ObjectiveHeat shock preconditioning model was used to investigate whether preconditioning can improve the myocardial recovery following long term cold arrest and its possible mechanims and molecular basis. MethodsTwenty healthy rabbits were randomly divided into two groups equally: group Ⅰas control group and group Ⅱ as heat shock pretreatment group. Before storage, the hearts were perfused with K H solution for 35?min, then arrested with STS (4?℃) and immersed in STS (4?℃) for storage for 6?h. The hearts were re perfused with 37?℃ K H solution for 25?min. Before storage and at the end of reperfusion, heart rate (HR), coronary flow (CF), left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were measured. The post storage recovery of cardiac function was expressed as a percentage of prestorage control values. The contents of HSP72, NO, CK MB, LDH, SOD, LPO in myocardial tissues were measured at the end of reperfusion. Myocardial water content was also measured at the same time. Results The myocardial recovery in the group Ⅱ was more satisfactory than in the group Ⅰ and correlated with the content of HSP72 in myocardial tissues (r= 0.95). The content of NO in myocardial tissue in the group Ⅱ was obviously higher than in the group Ⅰ. Conclusions Heat shock preconditioning could obviously improve the myocardial recovery in the heart after long term cold storage for 6?h, reduce the enzymes release and the ischemia/reperfusion injury. HSP72 was responsible for the molecular basis of heat shock preconditioning.The protective effect of HSP72 might be induced by endothelia protection.

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ObjectiveHeat shock preconditioning model was used to investigate whether preconditioning can improve the myocardial recovery following long term cold arrest and its possible mechanims and molecular basis. MethodsTwenty healthy rabbits were randomly divided into two groups equally: group Ⅰas control group and group Ⅱ as heat shock pretreatment group. Before storage, the hearts were perfused with K H solution for 35?min, then arrested with STS (4?℃) and immersed in STS (4?℃) for storage for 6?h. The hearts were re perfused with 37?℃ K H solution for 25?min. Before storage and at the end of reperfusion, heart rate (HR), coronary flow (CF), left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were measured. The post storage recovery of cardiac function was expressed as a percentage of prestorage control values. The contents of HSP72, NO, CK MB, LDH, SOD, LPO in myocardial tissues were measured at the end of reperfusion. Myocardial water content was also measured at the same time. Results The myocardial recovery in the group Ⅱ was more satisfactory than in the group Ⅰ and correlated with the content of HSP72 in myocardial tissues (r= 0.95). The content of NO in myocardial tissue in the group Ⅱ was obviously higher than in the group Ⅰ. Conclusions Heat shock preconditioning could obviously improve the myocardial recovery in the heart after long term cold storage for 6?h, reduce the enzymes release and the ischemia/reperfusion injury. HSP72 was responsible for the molecular basis of heat shock preconditioning.The protective effect of HSP72 might be induced by endothelia protection.

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Available abstract

ObjectiveHeat shock preconditioning model was used to investigate whether preconditioning can improve the myocardial recovery following long term cold arrest and its possible mechanims and molecular basis. MethodsTwenty healthy rabbits were randomly divided into two groups equally: group Ⅰas control group and group Ⅱ as heat shock pretreatment group. Before storage, the hearts were perfused with K H solution for 35?min, then arrested with STS (4?℃) and immersed in STS (4?℃) for storage for 6?h. The hearts were re perfused with 37?℃ K H solution for 25?min. Before storage and at the end of reperfusion, heart rate (HR), coronary flow (CF), left ventricular systolic pressure (LVSP) and left ventricular end diastolic pressure (LVEDP) were measured. The post storage recovery of cardiac function was expressed as a percentage of prestorage control values. The contents of HSP72, NO, CK MB, LDH, SOD, LPO in myocardial tissues were measured at the end of reperfusion. Myocardial water content was also measured at the same time. Results The myocardial recovery in the group Ⅱ was more satisfactory than in the group Ⅰ and correlated with the content of HSP72 in myocardial tissues (r= 0.95). The content of NO in myocardial tissue in the group Ⅱ was obviously higher than in the group Ⅰ. Conclusions Heat shock preconditioning could obviously improve the myocardial recovery in the heart after long term cold storage for 6?h, reduce the enzymes release and the ischemia/reperfusion injury. HSP72 was responsible for the molecular basis of heat shock preconditioning.The protective effect of HSP72 might be induced by endothelia protection.

Key concepts: Preload, Shock (circulatory), Heat shock protein, Cardiology, Internal medicine, Viaspan, Cold storage, Ischemic preconditioning

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Heat shock preconditioning enhances myocardial recovery in isolated rabbit heartafter long-term preservation by induction of heat shock protein 72 — Research Paper | ScholarLens