PubMed · 13465415
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J JASIENSKI, M POLITOWSKI. 1957-06-17. [Capillary circulation].. https://pubmed.ncbi.nlm.nih.gov/13465415/
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BACKGROUND: Many theories regarding the pathophysiology leading to ovarian hyperstimulation syndrome (OHSS) have been proposed and tested. Increased erythrocyte aggregation is associated with capillary slow flow and tissue hypoxaemia. We performed this study in order to assess the degree of erythrocyte aggregation in the peripheral blood of individuals with OHSS and undergoing controlled ovarian stimulation (COH). METHODS: Twenty women with severe OHSS, 20 women undergoing COH under IVF protocol, and 20 healthy matched controls were recruited for this prospective study. Blood samples were drawn for determination of erythrocyte aggregation as well as haematological indices. The percentage of slide covered by the cells ('erythrocyte percentage': EP) was determined using a simple slide test and image analysis. Lower EP values correspond to higher degrees of aggregation. RESULTS: The respective measures of EP were 59.2 +/- 3.0, 42.0 +/- 3.0 and 35.0 +/- 2.4% micro m for the controls, women with COH and OHSS (P < 0.01 between controls and the two stimulation groups). CONCLUSIONS: The degree of erythrocyte aggregation is enhanced in the peripheral venous blood of patients with both COH and OHSS. This finding, known to cause capillary leak, may contribute to the pathophysiology of the OHSS.
c-kit receptor tyrosine kinase is a marker of progenitor cells, which differentiate into blood and/or vascular endothelial cells, and has an important role in the amplification/mobilization of progenitor cells. c-kit is expressed in mature endothelial cells, but its role there is unclear. Stem cell factor, a c-kit ligand, dose-dependently promoted survival, migration, and capillary tube formation of human umbilical vein endothelial cells. These effects mimicked those of vascular endothelial growth factor, except that stem cell factor did not sufficiently support proliferation of these cells. After exposing cells to this factor, Akt, Erk1/2, and c-kit were immediately (</=5 min) and dose-dependently tyrosinephosphorylated. STI-571, a c-kit inhibitor, dose-dependently attenuated these phosphorylations and inhibited stem cell factor-promoted survival and capillary tube formation over the same dose range. Wortmannin and LY294002, inhibitors of phosphoinositide 3-kinase, and PD98059, an inhibitor of MEK, abrogated survival and capillary tube formation, indicating that Akt and Erk1/2 should promote survival and capillary tube formation of these endothelial cells at a locus downstream to stem cell factor/c-kit signaling. Akt was more strongly phosphorylated, whereas Erk1/2 and p38 were more weakly phosphorylated with stem cell factor than with vascular endothelial growth factor. Phospholipase Cgamma was phosphorylated only with the latter, indicating that stem cell factor/c-kit signaling is somewhat different.
BACKGROUND: Hypoplastic left heart syndrome is a condition characterized by a constellation of morphological malformations affecting the left side of the heart. We studied the capillary network, and quantified the capillarization of the ventricular myocardium, which, if different from normal, may have implications for the success of surgical reconstruction. METHODS: The capillaries were detected by immunohistochemistry using a monoclonal antibody (von Willebrand's factor) against the endothelium. Hearts with hypoplastic left heart syndrome have higher mean and maximal diffusion distances from any arbitrary point to the nearest capillary than normal hearts. RESULTS: There was no significant difference in the heterogeneity of capillary distribution between the hearts with hypoplastic left heart syndrome and the control heart. Increase in distance was found in both the right and left ventricles. CONCLUSIONS: Hearts with hypoplastic left heart syndrome show a reduction in the capillarization of both the right and left ventricles compared with age-matched controls. We believe this may be an inherent abnormality of hypoplastic left heart syndrome that may have implications for ventricular development.