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Capillary diameter changes were studied in the tenuissimus muscle of 29 urethan-anesthetized New Zealand White rabbits. Capillaries were visualized with transillumination bright-field microscopy (saltwater lens, x 50; resolution approximately 0.3 microns). Median capillary diameter during the control period was 4.4 microns (range 3.2-6.9 microns). Complete aortic occlusion resulted in a reduction of median femoral arterial pressure to 17 mmHg (range 4-22 mmHg). During 2 min of occlusion, capillary diameter decreased by 6%, with greater change on the arteriolar side of the capillary than on the venular side. During reactive hyperemia after release of the occluder, capillary diameter maximally increased by 12% compared with the control period, with a larger response at the arteriolar end of the capillary than at the venular end. Median capillary resistance was estimated to increase by 27% during occlusion and to decrease by 36% during peak reactive hyperemia. The observed diameter changes are compatible with the idea that capillaries change their diameter relative to changes in transmural pressure.

A method is presented to assess in vivo in transparent tissues the leukocyte subtypes that roll in microvessels. In nine rabbits anesthetized with ketamine-xylazine, leukocyte nuclei were stained in situ with acridine yellow (3 mg/kg i.v. for 5 min). Intravital fluorescence video microscopy in 24 mesenteric venules (17-29 microns, median 21) indicated labeling of all rolling leukocytes. On the basis of the shape of their nucleus, 67-100% (median 89) could be classified unequivocally (13-366 cells analyzed, median 77) as polymorphonuclear (PMN, i.e., granulocytes) or monomorphonuclear (lymphocytes and monocytes). Of these classified cells, 94-100% were PMNs (median 100, including 1 stray value of 69%). This PMN percentage was independent of the level of leukocyte rolling (2-36/min, median 14), vessel diameter, flow velocity (0.5-2.5 mm/s), or duration of the experiment (< 6 h). The dye had no significant influence on hemodynamic parameters, systemic leukocyte counts (1.5-7.8 x 10(9)/l), or in vitro differentiation pattern (27-38% granulocytes, 0-2% monocytes, 61-71% lymphocytes). In conclusion, our method demonstrated that the leukocytes that roll in postcapillary venules of the exteriorized rabbit mesentery are almost exclusively granulocytes.

Intravital bright-field videomicroscopy was used to investigate whether leukocyte rolling can be observed under normal physiological conditions. We studied skin venules in trained conscious rats and anesthetized rats and mice without touching the skin itself. Leukocyte rolling was spontaneously present in all hindpaw venules of Lewis rats (diam 8-27 microns) and also in all mouse ear venules (Swiss, 13-38 microns; BALB/c, 12-56 microns). Rolling levels (in leukocytes/min, median and range) were 8 (3-15) in conscious rats, 9 (3-19) in anesthetized rats, 30 (5-160) in anesthetized Swiss mice, and 10 (3-22) in anesthetized BALB/c mice. These levels appeared to be independent of time. Noninvasive mechanical stimulation induced an average increase of 32%. Fluorescent labeling of leukocytes in vivo with acridine orange had no influence. In Swiss mice, the rolling velocity was < 50 microns/s for > 75% of the leukocytes (median 31 microns/s); this parameter did not correlate with reduced velocity (17-68 s-1) and hence wall shear rate. Our finding that leukocyte rolling is spontaneously present in skin venules of anesthetized and conscious animals suggests a constant vigilance of the host defense mechanisms in the skin.

In the mesentery of the anesthetized rabbit, the thromboembolic reaction after wall puncture lasts six times longer in arterioles than in venules, a difference that cannot be explained by fluid dynamic conditions before puncture. In the present study, it was investigated whether this difference in response between arterioles and venules results from a different degree of stenosis by the thrombus and/or a difference in velocity changes resulting in a different pressure drop over the thrombus. Arteriolar and venular mean red blood cell velocity and vessel diameter were measured before puncture and after this injury in the stenosed vessel segment and upstream. Thrombi with similar heights were formed in arterioles and venules and induced similar degrees of stenosis. A surface area reduction less than 55% induced only a small and similar decrease in volume flow (less than 10%) in arterioles and venules. Reduced velocity, a measure of wall shear rate, increased similarly in both vessel types for similar degrees of stenosis. In conclusion, changes in fluid dynamic factors, as induced by thrombus formation, cannot be held responsible for the difference in thromboembolic reaction between arterioles and venules.