MYOCARDIAL PROTECTION BY ETHYL-ISOPROPYL AMILORIDE, A SPECIFIC NA+-H+ EXCHANGE INHIBITOR, FOLLOWING HEMORRHAGIC SHOCK

被引:0
作者
Soliman, Mona [1 ]
Al-Drees, Abdul-Majid [1 ]
机构
[1] King Khalid Univ Hosp, Coll Med, Dept Physiol, Riyadh 11461, Saudi Arabia
关键词
Hemorrhage; Rat; Isolated heart; Contractility; Ethyl-Isopropyl Amiloride; Langendorff; HEART-FAILURE; RAT-HEART; SODIUM; CALCIUM; ISCHEMIA; CELLS; CARE; NA+; PH;
D O I
暂无
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Hemorrhagic shock and resuscitation is well known to result in myocardial dysfunction and injury. Stimulation of the Na+-H+ exchanger plays an important role in the pathway of myocardial injury. The purpose of the present study was to examine the protective effects of blocking the cardiac Na+-H+ exchange, using 100 mM ethyl-isopropyl amiloride (EIPA), a specific Na+-H+ exchanger blocker, on myocardial contractile function on ex vivo resuscitation of isolated rat heart following one hour of hemorrhagic shock. Methodology: Sprague- Dawley rats were assigned to hemorrhage, hemorrhage + EIPA, sham hemorrhage and sham hemorrhage + EIPA groups. Rats were hemorrhaged for one hour. Hearts were harvested and ex vivo treated and resuscitated by perfused in the Langendorff System. Myocardial function was determined. Results: The results showed that inhibition of the Na+-H+ exchanger using EIPA improved the post-resuscitation myocardial contractile function. Conclusion: Blocking the Na+-H+ exchanger using 100mM EIPA following 60 minutes of hemorrhagic shock improved myocardial function.
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收藏
页码:289 / 292
页数:4
相关论文
共 17 条
[1]   INTRACELLULAR PH AND CA2+ HOMEOSTASIS IN THE PH PARADOX OF REPERFUSION INJURY TO NEONATAL RAT CARDIAC MYOCYTES [J].
BOND, JM ;
CHACON, E ;
HERMAN, B ;
LEMASTERS, JJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1993, 265 (01) :C129-C137
[2]   Hypertonic resuscitation modulates the inflammatory response in patients with traumatic hemorrhagic shock [J].
Bulger, Eileen M. ;
Cuschieri, Joseph ;
Warner, Keir ;
Maier, Ronald V. .
ANNALS OF SURGERY, 2007, 245 (04) :635-641
[3]  
Catania R. A., 1999, Annals Academy of Medicine Singapore, V28, P120
[4]   INVIVO MYOCYTE SODIUM ACTIVITY AND CONCENTRATION DURING HEMORRHAGIC-SHOCK [J].
CHIAO, JJC ;
MINEI, JP ;
SHIRES, GT ;
SHIRES, GT .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (03) :R684-R689
[5]   Towards improving prehospital trauma care [J].
Coats, TJ ;
Goode, A .
LANCET, 2001, 357 (9274) :2070-2070
[6]   Intensive care unit management of the trauma patient [J].
Deitch, Edwin A. ;
Dayal, Saraswati D. .
CRITICAL CARE MEDICINE, 2006, 34 (09) :2294-2301
[7]   CALCIUM-CHANNEL BLOCKADE IN CANINE HEMORRHAGIC-SHOCK [J].
HORTON, JW .
AMERICAN JOURNAL OF PHYSIOLOGY, 1989, 257 (05) :R1012-R1019
[8]   ELECTROGENIC SODIUM-CALCIUM EXCHANGE IN CULTURED EMBRYONIC CHICK HEART-CELLS [J].
JACOB, R ;
LIEBERMAN, M ;
LIU, S .
JOURNAL OF PHYSIOLOGY-LONDON, 1987, 387 :567-588
[9]   Therapeutic potential of Na-H exchange inhibitors for the treatment of heart failure [J].
Karmazyn, M .
EXPERT OPINION ON INVESTIGATIONAL DRUGS, 2001, 10 (05) :835-843
[10]   Mechanisms of protection of the ischemic and reperfused myocardium by sodium-hydrogen exchange inhibition [J].
Karmazyn, M .
JOURNAL OF THROMBOSIS AND THROMBOLYSIS, 1999, 8 (01) :33-38