Microcirculation, endothelium, and lymphatics最新文献

The present article summarizes the author's perennial research on the flow of red blood cells in microvessels, the major determinant of rheological properties of blood in the microcirculation. Two main patterns of blood flow structure in microvessels, in the smallest arteries and veins and in the capillaries are described. The red cell concentration (hematocrit) in the blood flowing in microvessels undergoes regular alterations with changes of blood flow rate and vessel diameter in the microvascular beds. Further, the red blood cell concentration and flow velocity gradients are found in the cross-section of microvessels that should considerably affect the blood rheological properties in the microcirculation. In addition, radial displacements and blood velocity fluctuations of red cells in the flow are discovered in the larger microvessels during ischemic decrease of blood flow rate. The main factor disturbing the normal blood flow structure, and hence the normal rheological properties of blood, is the intravascular aggregation of red blood cells, which is to be diagnosed and eliminated in patients with blood rheological disturbances.

The small blood vessels were examined in 31 premenopausal and 31 postmenopausal women. In each group there were 14 non-smokers and 17 smokers of age groups 35-45 and 45-59. The women underwent full gynecological examination. Blood pressure was normal in each. The small blood vessels were examined by capillaroscopy of conjunctivae and nailfolds, by oscillometry of the radial artery, skin thermometry of the wrist and terminal phalanx, and by capillary fragility. When all abnormalities in non-smokers were compared with those in smokers in the menopausal groups, a significant difference was found, (Table 4), to the disadvantage of the smokers.

A normotensive (1.0 microgram per 100 g b.w.) or hypotensive (10.0 micrograms per 100 g b.w.) dose of serotonin (5-HT) was administered endoportally while changes in microcirculation at the inlet and outlet regions of hepatic lobules were measured on-line using quantitative in vivo microscopy. The number of sinusoids with decreased (cellular) flow also was counted to index intralobular perfusion in video recordings of microvasculature examined off-line. The normotensive and hypotensive doses of 5-HT elicited decreases in intralobular perfusion within periportal and centrivenous sinusoids. Hypoperfusion was accompanied by a transient decrease in volumetric flowrate (Q) at the outlet of centrivenous sinusoids in 40% of normotensive and in 100% of hypotensive rats. At the inlet of periportal sinusoids, Q was depressed in 75% of hypotensive and in 27% of normotensive rats. The remainder of these segments had either an increase or no change in Q at the inlet and outlet. These results suggested that during conditions of 5-HT induced (lobular) hypoperfusion: (a) Q at the inlet is maintained in 73% of normotensive rats by redistribution of intralobular blood flow, and decreased in all but 25% of hypotensive rats as a function of transient reductions in total hepatic (arterial) and/or portal (venous) blood flow(s), and (b) Q at the outlet is depressed in 40% of normotensive rats by apparent increases in flow redistribution and resistance to flow generated during sinusoidal constriction, whereas in all hypotensive rats this mechanism is aggravated by decreased total hepatic (arterial) and/or portal (venous) inflow(s). Therefore, although the initial time course for microvascular responses tended to be similar for normo- and hypo-tensive doses of 5-HT, quantitative differences in regional flow distribution and Q emphasize (a) the importance of intra- and extra-hepatic determinants in the regulation of blood flow within hepatic (unit) lobules, and (b) the presence of microvascular heterogeneity within these lobular units.

The aim of this study was to determine the gastric microcirculatory alterations occurring during reperfusion after a period of ischemia and the possible role of oxyradicals in the microcirculatory disturbance. An in vivo microscopy technique was used to observe the superficial mucosal blood flow during reperfusion. After reperfusion, mucosal blood flow resumed quickly and then slowed with eventual cessation of flow. Thirty minutes of ischemia followed by reperfusion resulted in cessation of flow in 50 +/- 4% and 81 +/- 8%, of the capillaries in the microscopic field at 15 and 30 min, respectively, after reperfusion. During this mucosal microcirculatory change, numerous white thrombi were observed flowing in the mucosal microvessels. In rats pretreated with allopurinol to inhibit oxyradical formation, blood flow was maintained to a significant and markedly greater extent. Study of the submucosal microvasculature after reperfusion revealed a marked delay in transit of a fluorescein-albumin bolus from terminal submucosal arterioles through the mucosal microvasculature and back to submucosal collecting venules. Submucosal vascular diameter change could not explain the altered mucosal blood flow. These findings indicate that there is marked slowing and cessation (in many microvessels) of gastric mucosal blood flow during reperfusion after a period of ischemia, and that the obstruction to flow occurs in the mucosal microvessels. The results of the study with allopurinol suggest that oxygen-derived free radicals generated by xanthine oxidase may play a major role in the genesis of this gastric mucosal microcirculatory disturbance.