1. ^*From Divison of Neurosurgery, University of Texas Medical Branch, Galveston, U.S.A.
2. ^†From Neurosurgical Pathophysiology, Johannes Gutenberg University of Mainz, Mainz, Germany); Laboratory of origin: Institute for Neurosurgical Pathophysiology, Johannes Gutenberg University of Mainz, Langenbeckstr. 1, 55101 Mainz, Germany.

Correspondence: Oliver Kempski, University of Mainz, Germany; e-mail: oliver.kempski@uni-mainz.de.

Received 18 September 2003; Accepted 5 December 2003.

Abstract

The reaction of cerebral capillaries to ischemia is unclear. Based on Hossmann's observation of postischemic "delayed hypoperfusion," we hypothesized that capillary flow is decreased during reperfusion because of increased precapillary flow resistance. To test this hypothesis, we measured cerebral capillary erythrocyte velocity and diameter changes by intravital microscopy in gerbils. A cranial window was prepared over the frontoparietal cortex in 26 gerbils anesthetized with halothane. The animals underwent either a sham operation or fifteen minutes of bilateral carotid artery occlusion causing global cerebral ischemia. Capillary flow velocities were measured by frame-to-frame tracking of fluorescein isothiocyanate labeled erythrocytes in 1800 capillaries after 1-hour reperfusion. Capillary flow velocities were decreased compared to control (0.25 0.27mm/s vs. 0.76 0.45 mm/s; P < 0.001). Precapillary arteriole diameters in reperfused animals were reduced to 76.3 6.9% compared to baseline (P < 0.05). Capillary diameters in reperfused animals (2.87 0.97 m) were reduced (P < 0.001) compared to control (4.08 1.19 m). Similar reductions of precapillary (24%) and capillary vessel diameters (30%) and absolute capillary flow heterogeneity indicate that delayed (capillary) hypoperfusion occurs as a consequence of increased precapillary arteriole tone during reperfusion.