HEAT-SHOCK IMPROVES ISCHEMIC TOLERANCE OF HYPERTROPHIED RAT HEARTS

被引:27
作者
CORNELUSSEN, R [1 ]
SPIERING, W [1 ]
WEBERS, JHG [1 ]
DEBRUIN, LG [1 ]
RENEMAN, RS [1 ]
VANDERVUSSE, GJ [1 ]
SNOECKX, LHEH [1 ]
机构
[1] UNIV LIMBURG, CARDIOVASC RES INST MAASTRICHT, DEPT PHYSIOL, 6200 MD MAASTRICHT, NETHERLANDS
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 1994年 / 267卷 / 05期
关键词
CARDIAC HYPERTROPHY; REGIONAL MYOCARDIAL FLOW; CATALASE; ARRHYTHMIAS;
D O I
10.1152/ajpheart.1994.267.5.H1941
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The postischemic recovery of hypertrophied hearts was studied 24 h after total body hyperthermia. To this end, anesthetized aortic-banded and sham-operated rats were subjected to heat shock (AoB(HS) and Sham(HS), respectively). Cardiac hypertrophy was induced 8 wk earlier. In isolated ejecting hearts, functional recovery after 45 min of global ischemia was poor and moderate in nonheated (control) hypertrophied (AoB(C)) and nonheated (control) nonhypertrophied (Shame) hearts, respectively. Heat shock significantly improved postischemic recovery in both AoB(HS) and Sham(HS) hearts. This improvement of functional recovery was associated with a significant reduction of the duration of arrhythmias. In addition, coronary flow was significantly higher in both types of heat-shocked hearts than in the corresponding control hearts during the preischemic as well as the postischemic period. Postischemic endocardial flow, assessed using radioactive microspheres, was significantly improved in AoB(HS) hearts. Compared with the corresponding control hearts, the native endogenous catalase activity was not changed in AoB(HS) hearts but was significantly increased in Sham(HS) hearts. The present findings suggest that the postischemic functional improvement after total body hyperthermia can be explained by increased and more homogeneous myocardial perfusion, which may also reduce the duration of postischemic arrhythmias. This effect is especially beneficial for the hypertrophied heart, which is known to be extremely vulnerable to the ischemic insult probably caused by subendocardial underperfusion.
引用
收藏
页码:H1941 / H1947
页数:7
相关论文
共 31 条
[11]   EFFECT OF ENDOTHELIN ON TOTAL AND REGIONAL CORONARY RESISTANCE AND ON MYOCARDIAL-CONTRACTILITY [J].
DOMENECH, R ;
MACHO, P ;
GONZALEZ, R ;
HUIDOBROTORO, JP .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1991, 192 (03) :409-416
[12]   DIFFERENTIAL EXPRESSION OF HSP70-STRESS PROTEINS IN HUMAN ENDOTHELIAL-CELLS EXPOSED TO HEAT-SHOCK AND HYDROGEN-PEROXIDE [J].
JORNOT, L ;
MIRAULT, ME ;
JUNOD, AF .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1991, 5 (03) :265-275
[13]   ACQUISITION AND DECAY OF HEAT-SHOCK-ENHANCED POSTISCHEMIC VENTRICULAR RECOVERY [J].
KARMAZYN, M ;
MAILER, K ;
CURRIE, RW .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 259 (02) :H424-H431
[14]   MECHANICAL DEFORMATION OF VESSEL WALL AND SHEAR-STRESS DETERMINE THE BASAL RELEASE OF ENDOTHELIUM-DERIVED RELAXING FACTOR IN THE INTACT RABBIT CORONARY VASCULAR BED [J].
LAMONTAGNE, D ;
POHL, U ;
BUSSE, R .
CIRCULATION RESEARCH, 1992, 70 (01) :123-130
[15]   CYTOKINES INDUCE STRESS PROTEIN-FORMATION IN CULTURED CARDIAC MYOCYTES [J].
LOWFRIEDRICH, I ;
WEISENSEE, D ;
MITROU, P ;
SCHOEPPE, W .
BASIC RESEARCH IN CARDIOLOGY, 1992, 87 (01) :12-18
[16]  
LOWRY OH, 1951, J BIOL CHEM, V193, P265
[17]   REPERFUSION-INDUCED ARRHYTHMIAS - MECHANISMS AND PREVENTION [J].
MANNING, AS ;
HEARSE, DJ .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1984, 16 (06) :497-518
[18]   ATTENUATION BY HEAT-STRESS OF A SUBMAXIMAL CALCIUM PARADOX IN THE RABBIT HEART [J].
MARBER, MS ;
WALKER, JM ;
LATCHMAN, DS ;
YELLON, DM .
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1993, 25 (09) :1119-1126
[19]   BLOOD-FLOW DISTRIBUTION IN THE LEFT-VENTRICULAR FREE WALL IN OPEN-CHEST DOGS [J].
PRINZEN, FW ;
VANDERVUSSE, GJ ;
RENEMAN, RS .
BASIC RESEARCH IN CARDIOLOGY, 1981, 76 (04) :431-437
[20]  
RABINOV M, 1991, J THORAC CARDIOV SUR, V102, P695