The diameter of the arterial and arteriolar blood vessels was measured as a function of time in the hamster skin fold window preparation. When the animals recovered from the surgical implantation, the diameters of the arterial microvessels exhibited a continuous rhythmic activity throughout the preparation for a period of 2 wk while the chamber was intact. The amplitude of the diameter changes was directly proportional to the mean vessel size. The frequency of this phenomenon was determined by power spectrum analysis implemented with a Fourier transform method and was found to decrease from a maximum of 9-15 cycles/min in 8- to 15-micron A4 arterioles to 1-3 cycles/min in 70- to 100-micron A1 small arteries. A1 and A4 vessels had relatively well-defined characteristic fundamental frequencies, whereas A2 and A3 vessels showed a power spectrum that included the frequencies present in A1 and A4 vessels. The activity was not synchronized throughout the microvasculature, and frequencies and amplitudes of diameter variations changed at branching points. Anesthesia induced by the intravenous injections of pentobarbital and chloralose-urethan invariably stopped this activity throughout the preparation. The distribution of this time-dependent activity and the nature of the effect of the anesthetics suggests that this phenomenon is due to local pacemaker activity of groups of unitary smooth muscle cells.
Arteriolar vasomotion was characterized in the skin muscle of the unanesthetized hamster skinfold window preparation and related to the specific arterioles that give rise to the different types of activity. The arterioles were classified according to the Strahler method: order 0 was assigned to capillaries and order 4 to the largest arterioles. The arterioles showed vasomotion with a specific range of frequencies that varied according to the vessel order; the highest fundamental frequency (9.1 +/- 3.9 cycles/min) was detected in the smallest order 1 arterioles and the lowest frequency (2.1 +/- 0.9 cycles/min) in order 4 vessels. Hypoxia (8, 11, and 15% O2 gas mixture inspiration) increased the frequency of vasomotion, decreased mean and effective diameters, and reduced capillary blood flow. The effects were more pronounced with an 8 and 11% O2 gas mixture. Hypoxia caused high-frequency vasomotion to shift from order 1 and 2 arterioles to the beginning of order 3 arterioles, which in this condition dominated the daughter vessels and generated the prominent activity (24 +/- 4 cycles/min, 11% O2 gas mixture). Hypertoxia (100% O2) induced differentiated arteriolar responses. The smallest vessels showed prolonged constriction, decreased mean and effective diameters, and reduced frequency of vasomotion. Capillary blood flow was restricted. Order 3 vessels did not constrict or dilate.
Increased formation of reactive oxygen species (ROS) on reperfusion after ischemia underlies ischemia-reperfusion (I/R) damage. We measured, in real time, oxygen tension in both microvessels and tissue and oxidant stress during postischemic reperfusion in the hamster cheek pouch microcirculation. We measured Po2 by using phosphorescence quenching microscopy and ROS production in the systemic blood. We evaluated the effects of a nitric oxide synthase inhibitor (NG-monomethyl-L-arginine, L-NMMA) and SOD on the oxidative stress during reperfusion. Microvascular injury was assessed by measuring diameter change, the perfused capillary length (PCL), and leukocyte adhesion. During early reperfusion, arteriolar Po2 was significantly lower than baseline, whereas capillary Po2 varied between 7 and 0 mmHg. Arterial blood flow did not regain baseline values, whereas Po2 returned to baseline in arterioles and tissue after 30 min of reperfusion. During 5 and 15 min of reperfusion, ROS increased by 72 and 89% versus baseline, respectively, and declined to baseline after 30 min of reperfusion. Pretreatment with SOD maintained ROS at normal levels, increased arteriolar diameter, blood flow, and PCL, and decreased leukocyte adhesion (P < 0.05). L-NMMA decreased ROS only within 5 min of reperfusion, which increased significantly by 72% later during reperfusion. L-NMMA worsened leukocyte adhesion (P < 0.05). In conclusion, our results show that the early reperfusion is characterized by low Po2 linked to increased production of ROS. At early reperfusion both SOD and L-NMMA decreased ROS production, whereas only SOD reduced it during later reperfusion. We suggest that low-flow hypoxia profoundly affects vascular endothelial damage during reperfusion through changes in ROS and nitric oxide production.
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