IN-VIVO OBSERVATIONS OF THE INTRAMURAL ARTERIOLES AND VENULES IN BEATING CANINE HEARTS

1. To evaluate the effects of cardiac contraction on intramyocardial ( midwall) microvessels, we measured the phasic diameter change of left ventricular intramural arterioles and venules using a novel needle-pro be videomicroscope with a CCD camera and compared it with the diameter change in subepicardial and subendocardial vessels. 2. The phasic dia meter of the intramural arterioles decreased from 130 +/- 79 mu m in e nd-diastole to 118 +/- 72 mu m (mean +/- s.D.) in end-systole by cardi ac contraction (10 +/- 6%, P< 0.001, n = 21). 3. The phasic diameter i n the intramural venules was almost unchanged from end-diastole to end -systole (85 +/- 44 vs. 86 +/- 42 mu m, respectively, 2 +/- 6%, n. s., n = 14). 4. Compared with intramural vessels, the diameters of subend ocardial arterioles and venules decreased by a similar extent (arterio les: 10 +/- 8%, P <0.001; venules: 12+/-10%, P< 0.001) from end-diasto le to end-systole, respectively, whereas the diameter of the subepicar dial arterioles changed little during the cardiac cycle, and subepicar dial venule diameter increased by 9 +/- 8% (P < 0.01) from end-diastol e to end-systole. These findings are consistent with our previous repo rt. 5. We suggest that the almost uniform distribution of the cardiac contractility effect and arteriolar transmural pressure between the su bendocardium and the midmyocardium, which together constitute the syst olic vascular compressive force, accounts for the similarity in the ar teriolar diameter changes in both myocardial layers. The smaller intra vascular pressure drop from deep to superficial myocardium relative to the larger intramyocardial pressure drop explains the difference in t he phasic venular diameter changes across the myocardium.