Ischemic dysfunction and impaired recovery in hypertensive hypertrophied hearts is associated with exaggerated intracellular sodium accumulation.
The primary objectives of this study were to determine if hypertrophied spontaneously hypertensive rat (SHR) hearts exhibited a greater increase in intracellular sodium (Na+i) compared with Wistar-Kyoto (WKY) control rats during low flow ischemia, and to determine whether Na+i accumulation in these hearts was associated with greater ischemic dysfunction and damage. In addition, intracellular pH and high energy phosphates were monitored to assess the relationships between changes in these variables and changes in Na+i. Interleaved 31P and 23Na spectra were acquired in perfused hearts from 8- to 10-month-old rats during low flow ischemia and reperfusion, while left ventricular pressures were monitored continuously. The majority of SHR (n = 13) exhibited an increase in Na+ similar to that for WKY and did not demonstrate exaggerated ischemic dysfunction or damage. However, a subgroup of SHR (n = 7) exhibited exaggerated Na+i accumulation during ischemia, compared with WKY, that was associated with contractile failure and a greater increase in left ventricular end diastolic pressure during ischemia, and slower recovery of developed pressure during reperfusion. Greater Na+i accumulation in this SHR subgroup preceded significantly greater depletion of high energy phosphates compared with WKY. In conclusion, increased Na+i accumulation was observed in all hypertrophied hearts with greater ischemic dysfunction compared with WKY. These results suggest that impaired Na+i handling may indeed contribute to the greater susceptibility of hypertrophied hearts to ischemic dysfunction and damage.
Golden
A L
AL
Cardiovascular Research Laboratory, University of Tennessee College of Veterinary Medicine, Knoxville.
Bright
J M
JM
Pohost
G M
GM
Pike
M M
MM
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D010710:Phosphates / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012964:Sodium / Q000378:metabolism*; D016277:Ventricular Function, Left / Q000502:physiology
D007773:Lactates; D010710:Phosphates; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D012964:Sodium