On-line detection of reversible myocardial ischemic injury by measurement of myocardial electrical impedance.
The metabolic and physiological alterations associated with changes in myocardial tissue electrical resistivity during ischemia were characterized to assess the feasibility of using such resistivity as an on-line indicator of the onset of ischemic injury. Twelve anesthetized dogs underwent rapid cardiac extirpation; 5 served as untreated controls, and 7 were pretreated with metoprolol tartrate. Beta blockade was used to alter the time course of ischemic injury as demonstrated previously in studies using this experimental model. In vitro measurement of myocardial resistivity, the detection of ischemic contracture, and serial measurements of tissue adenosine triphosphate (ATP) and lactate were obtained from totally ischemic left ventricles at 37 degrees C. Myocardial resistivity began to increase significantly before onset of ischemic contracture in the untreated control group (resistivity at 42.3 +/- 3.1 minutes, contracture at 53.8 +/- 3.7 minutes; p less than 0.025) as well as the metoprolol group (resistivity at 50.7 +/- 1.5 minutes, contracture at 70.0 +/- 3.5 minutes; p less than 0.005). As expected, ischemic contracture was delayed in the beta-blocked group compared with controls (p less than 0.01). Similarly, the onset of myocardial resistivity increase was delayed in the beta-blocked group (p less than 0.025). ATP and lactate levels at the onset of myocardial resistivity increase were consistent with severe but reversible injury. Resistivity changes during ischemia correlated linearly with simultaneous ATP depletion and lactate accumulation (r = 0.88 to 0.98; p less than 0.05). Furthermore, during global ischemia studied in 3 anesthetized dogs in vivo, the onset of myocardial resistivity increase occurred after 20 minutes. Finally, 6 anesthetized dogs underwent 60 minutes of in vivo regional ischemia by coronary artery occlusion, followed by 60 minutes of reperfusion. Myocardial resistivity in the ischemic region increased immediately and steadily after coronary occlusion, followed by a rapid decrease during subsequent reperfusion. These data show that myocardial resistivity may be useful for identifying severe but still reversible ischemic injury in on-line fashion during regional and global myocardial ischemia.
Ellenby
M I
MI
Department of Surgery, Duke University Medical Center, Durham, NC 27710.
Small
K W
KW
Wells
R M
RM
Hoyt
D J
DJ
Lowe
J E
JE
D000255:Adenosine Triphosphate / Q000032:analysis; D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology*; D004285:Dogs; D004553:Electric Conductivity; D004566:Electrodes; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D066298:In Vitro Techniques; D007773:Lactates / Q000032:analysis; D008790:Metoprolol / Q000494:pharmacology; D008991:Monitoring, Physiologic / Q000295:instrumentation / Q000379:methods*; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000032:analysis; D013997:Time Factors
D007773:Lactates; D000255:Adenosine Triphosphate; D008790:Metoprolol