Compensatory subendocardial hyperkinesis in the cat is abolished during coronary insufficiency outside an acutely ischaemic region.
OBJECTIVE
The aims were to determine (1) whether acute coronary occlusion provoked uniform hyperkinesis in remote non-ischaemic myocardium, and (2) how subsequent coronary stenosis affected such hyperkinesis.


METHODS
Two pairs of ultrasonic crystals were placed in the anterior left ventricular midwall of nine pentobarbitone anaesthetised open chest cats. One pair (longitudinal) ran parallel to subendocardial fibres; the other pair (circumferential) was aligned with subepicardial and mid-myocardial fibres. Following circumflex coronary occlusion, subsequent hypoperfusion of the anterior wall was established by controlled constriction of a shunt line from the right subclavian artery to the left main coronary artery in two discrete steps.


RESULTS
Following circumflex occlusion maximum systolic shortening of segments aligned to subendocardial fibres increased from 6.7(SEM 0.9)% to 11.5(1.4)% (p less than 0.001), whereas circumferential segment shortening was unchanged, at 12.2(0.8)% v 14.1(1.1)%. During mild shunt stenosis [delta P = 42(2) mm Hg] subendocardial tissue blood flow in the anterior wall decreased by 42(10)% (p less than 0.001), and longitudinal segment shortening decreased from 11.5(1.4)% to 6.9(1.1)% (p less than 0.001). Corresponding shortening of circumferential segments did not change. During severe shunt stenosis [delta P = 52(3) mm Hg] subendocardial tissue blood flow decreased further, and shortening of longitudinal segments approached zero value (p less than 0.001).


CONCLUSIONS
Compensatory hyperkinesis of remote non-ischaemic myocardium following an acute coronary occlusion may depend mostly on augmented subendocardial contraction.
Birkeland
S
S
Department of Surgery, University of Bergen, Haukeland Hospital, Norway.
Westby
J
J
Hessevik
I
I
Grong
K
K
Hexeberg
E
E
Lekven
J
J
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002415:Cats; D003327:Coronary Disease / Q000503:physiopathology*; D004195:Disease Models, Animal; D006321:Heart / Q000503:physiopathology*; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology; D010477:Perfusion; D012039:Regional Blood Flow / Q000502:physiology