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-probe videomicroscope with a CCD camera and compared it with the diameter change in subepicardial and subendocardial vessels. 2. The phasic diameter of the intramural arterioles decreased from 130 +/- 79 ìm in end-diastole to 118 +/- 72 micron (mean +/- S.D.) in end-systole by cardiac contraction (10 +/- 6 %, P < 0.001, n = 21). 3. The phasic diameter in the intramural venules was almost unchanged from end-diastole to end-systole (85 +/- 44 vs. 86 +/- 42 micron, respectively, 2 +/- 6 %, n. s., n = 14). 4. Compared with intramural vessels, the diameters of subendocardial arterioles and venules decreased by a similar extent (arterioles: 10 +/- 8 %, P < 0. 001; venules: 12 +/- 10 %, P < 0.001) from end-diastole to end-systole, respectively, whereas the diameter of the subepicardial arterioles changed little during the cardiac cycle, and subepicardial venule diameter increased by 9 +/- 8 % (P < 0.01) from end-diastole to end-systole. These findings are consistent with our previous report. 5. We suggest that the almost uniform distribution of the cardiac contractility effect and arteriolar transmural pressure between the subendocardium and the midmyocardium, which together constitute the systolic vascular compressive force, accounts for the similarity in the arteriolar diameter changes in both myocardial layers. The smaller intravascular pressure drop from deep to superficial myocardium relative to the larger intramyocardial pressure drop explains the difference in the phasic venular diameter changes across the myocardium.