PubMed · 14389380
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V V STAVSKAIA. 1955. [Methods of capillary function tests].. https://pubmed.ncbi.nlm.nih.gov/14389380/
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A computer model was developed to provide a theoretical framework for interpreting the dynamics of muscle capillary O(2) exchange in health and disease. We examined the effects of different muscle oxygen uptake (V O(2m)) and CvO(2) profiles on muscle blood flow (Q (m)) kinetics (Q (m)=V O(2m)/[CaO(2)-CvO(2)]). Further, we simulated V O(2m) and Q (m) responses to predict the CvO(2) profile and the underlying dynamics of capillary O(2) exchange (CvO(2)=CaO(2)-V O(2m)/Q (m)). Exponential equations describing V O(2m), CvO(2) and Q (m) responses in vivo were used in the simulations. The results indicated that Q (m) kinetics were relatively insensitive to CvO(2) parameters, but directly associated with V O(2m) kinetics. The biphasic Q (m) response produced a substantial fall in CvO(2) within the first 15-20s of the exercise transition (phase 1 of Q (m)). These results revealed that the main determinant of CvO(2) (or O(2) extraction) kinetics was the dynamic interaction of Q (m) and V O(2m) kinetics during phase 1 of Q (m).
Previous work has shown that endothelial cell (EC)-derived matrix metalloproteinases (MMPs) regulate regression of capillary tubes in vitro in a plasmin- and MMP-1 dependent manner. Here we report that a number of serine proteases can activate MMP-1 and cause capillary tube regression; namely plasma kallikrein, trypsin, neutrophil elastase, cathepsin G, tryptase and chymase. Plasma prekallikrein failed to induce regression without coactivators such as high molecular weight kininogen (HMWK) or coagulation Factor XII. The addition of trypsin, the neutrophil serine proteases (neutrophil elastase and cathepsin G) and the mast cell serine proteases (tryptase and chymase) each caused MMP-1 activation and collagen type I proteolysis, capillary tubular network collapse, regression and EC apoptosis. Capillary tube collapse is accompanied by collagen gel contraction, which is strongly related to the wound contraction that occurs during regression of granulation tissue in vivo. We also report that proMMP-10 protein expression is markedly induced in ECs undergoing capillary tube morphogenesis. Addition of each of the serine proteases described above led to activation of proMMP-10, which also correlated with MMP-1 activation and capillary tube regression. Treatment of ECs with MMP-1 or MMP-10 siRNA markedly delayed capillary tube regression, whereas gelatinase A (MMP-2), gelatinase B (MMP-9) and stromelysin-1 (MMP-3) siRNA-treated cells behaved in a similar manner to controls and regressed normally. Increased expression of MMP-1 or MMP-10 in ECs using recombinant adenoviral delivery markedly accelerated serine protease-induced capillary tube regression. ECs expressing increased levels of MMP-10 activated MMP-1 to a greater degree than control ECs. Thus, MMP-10-induced activation of MMP-1 correlated with tube regression and gel contraction. In summary, our work demonstrates that MMP-1 zymogen activation is mediated by multiple serine proteases and MMP-10, and that these events are central to EC-mediated collagen degradation and capillary tube regression in 3D collagen matrices.
BACKGROUND: The treatment of capillary vascular malformations by pulsed dye laser results in fading of these disfiguring lesions in the majority of patients. In only a minority, however, is full clearance of the lesion achieved. It is believed that the capillary composition of a capillary vascular malformation is an important determinant of whether it will respond to further laser treatment. Moreover, by determining the type, size, and depth of the ectatic capillaries within a capillary vascular malformation, it may be possible to target these vessels with specific laser parameters. METHODS: The noninvasive technique of depth measurement videomicroscopy was used to delineate the capillary structure of 22 previously untreated capillary vascular malformations and examine how this structure changes after five treatments with a 0.45-msec pulse duration using a 585-nm pulsed dye laser. RESULTS: After one and five treatments, there was a statistically significant lightening (p < 0.02 and p < 0.001, respectively) of the lesions, as seen on Munsell Color Chart testing. Before any laser treatment, the majority (59 percent) of capillary vascular malformations displayed a superficial type 1 or mixed capillary pattern, whereas after five laser treatments, the majority displayed a deep type 2 pattern (81 percent). After five laser treatments, there was a statistically significant increase in the depth of the remaining capillaries within the lesion compared with normal skin (p < 0.02) and a statistically significant reduction in the vessel diameters (p < 0.001). CONCLUSIONS: The authors found that vessels with a diameter greater than 50 mum were adequately treated, whereas those smaller than 50 microm appeared resistant to laser treatment. These data would suggest that pulse durations longer than 0.45 msec are not required to treat large ectatic capillary vascular malformation vessels. The authors suggest that the failure to treat very-small-diameter vessels is attributable to thermal dissipation from the target vessels, whose thermal relaxation time is much shorter than the pulse duration of the laser used.