Maximization of skin capillaries during intravital video-microscopy in essential hypertension: comparison between venous congestion, reactive hyperaemia and core heat load tests. (1/62)

Intravital capillary video-microscopy is a dynamic method for studying skin capillaries. The technique of direct intravital microscopy (without dyes) depends on the presence of red blood cells inside capillaries for their identification. The aim of the present study was to compare different techniques to try to establish the best method for maximizing the number of visible perfused capillaries during intravital capillary microscopy. We compared the effects of venous congestion with those of post-occlusive reactive hyperaemia (Study 1). We also investigated venous congestion followed first by post-occlusive reactive hyperaemia and then by a core heat load test (Study 2). Finally we investigated venous congestion followed by post-occlusive reactive hyperaemia combined with venous congestion (Study 3). In Study 1, capillary density increased with venous congestion from a baseline value of 74+/-2 (mean+/-S.E.M.) per field to 82+/-3 per field (P<0.0001; analysis of variance). With reactive hyperaemia, there was an apparent decrease in visible capillary density to 69+/-2 per field. In Study 2, baseline capillary density was 69+/-4 per field, and this increased significantly with venous congestion to 74+/-4 per field (P=0.01). With both reactive hyperaemia and core heat load, the apparent density was 62+/-4 per field. In Study 3 the baseline density was 70+/-2 per field, and this increased significantly with venous congestion to 80+/-3 per field (P<0.0001). With reactive hyperaemia combined with venous congestion, the density was 81+/-3 per field (P=0.328 compared with venous congestion alone). The results show that venous congestion at 60 mmHg for 2 min is the most effective method for visualization of the maximal number of perfused skin capillaries during intravital video-microscopy.  (+info)

Quantitation of microcirculatory abnormalities in patients with primary Raynaud's phenomenon and systemic sclerosis by video capillaroscopy. (2/62)

OBJECTIVE: : To assess nailfold capillary density and dimensions in patients with primary Raynaud's phenomenon (PRP), limited cutaneous systemic sclerosis (LSSc) and diffuse cutaneous SSc (DSSc), and healthy control subjects. METHODS: : Using the technique of nailfold video capillaroscopy, capillary density and dimensions were averaged from all visible capillaries in a 3 mm length of the nailfold from right and left ring fingers of each subject. Twenty healthy control subjects, 15 patients with PRP, 13 patients with DSSc and 21 patients with LSSc were examined. Intra-observer and inter-observer variability were calculated in 18 and 23 patients, respectively. RESULTS: : There were significant trends for capillary density to fall and for all dimensions to rise across the four groups (P < 0. 0001 for density and all dimensions, order healthy controls, PRP, DSSc and LSSc). Intra- and inter-observer reproducibility studies showed that although there was good correlation between and within observers, the limits of agreement were between +/-25-50% indicating lack of reproducibility. CONCLUSIONS: : Microcirculatory abnormalities can be quantified using the technique of video capillaroscopy and were most marked in patients with LSSc.  (+info)

C-peptide inhibits leukocyte-endothelium interaction in the microcirculation during acute endothelial dysfunction. (3/62)

C-peptide is a cleavage product that comes from processing proinsulin to insulin that induces nitric oxide (NO) -mediated vasodilation. NO modulates leukocyte-endothelium interaction. We hypothesized that C-peptide might inhibit leukocyte-endothelium interaction via increased release of endothelial NO. Using intravital microscopy of the rat mesentery, we measured leukocyte-endothelium interactions after administration of C-peptide to the rat. Superfusion of the rat mesentery with either thrombin or L-NAME consistently and significantly increased the number of rolling, adhering, and transmigrated leukocytes. C-peptide significantly attenuated either thrombin- or L-NAME-induced leukocyte-endothelium interactions in rat mesenteric venules. A control scrambled sequence of C-peptide characterized by the same amino acid composition in a randomized sequence failed to inhibit leukocyte-endothelium interactions. These effects of C-peptide were associated with decreased surface expression of the cell adhesion molecules P-selectin and ICAM-1 on the microvascular endothelium. Endothelial nitric oxide synthase (eNOS) mRNA levels were increased in rats injected with C-peptide. This enhanced eNOS expression was associated with a marked increase in basal NO release from the aorta of C-peptide-treated rats. We conclude that C-peptide is a potent inhibitor of leukocyte-endothelium interaction and that this effect is specifically related to inhibition of endothelial cell adhesion molecules via maintenance of NO release from the vascular endothelium.  (+info)

Capillaroscopy and the measurement of capillary pressure. (4/62)

Capillaries play a critical role in cardiovascular function as the point of exchange of nutrients and waste products between the tissues and circulation. Studies of capillary function in man are limited by access to the vascular bed. However, skin capillaries can readily be studied by the technique of capillaroscopy which enables the investigator to assess morphology, density and blood flow velocity. It is also possible to estimate capillary pressure by direct cannulation using glass micropipettes. This review will describe the techniques used to make these assessments and will outline some of the changes that are seen in health and disease.  (+info)

Differentiation between primary and secondary Raynaud's phenomenon: a prospective study comparing nailfold capillaroscopy using an ophthalmoscope or stereomicroscope. (5/62)

BACKGROUND: Nailfold capillary microscopy is a routine procedure in the investigation of patients with Raynaud's phenomenon (RP). As a standard method, nailfold capillary morphology is inspected with a stereomicroscope to look for capillary abnormalities such as giant loops, avascular areas, and bushy capillaries, which have all been found to be associated with certain connective tissue diseases. AIM: To investigate prospectively whether nailfold capillary inspection using an ophthalmoscope is of equivalent diagnostic value to standard nailfold capillary microscopy. METHOD: All the fingers of 26 patients with RP were examined in a blinded fashion and compared with the final diagnosis one month later. RESULTS: All giant loops, large avascular areas, and bushy capillaries were identified by both methods. The correlation for moderate avascular areas and crossed capillaries was 0.93 and 0.955 respectively. The correlation for minor abnormalities that do not contribute to the differentiation between primary and secondary RP was 0.837 and 0.861 respectively. All patients were classified identically by the two methods. CONCLUSION: For the evaluation of patients with RP, nailfold capillary morphology can reliably be assessed with an ophthalmoscope.  (+info)

Rarefaction of skin capillaries in patients with anginal chest pain and normal coronary arteriograms. (6/62)

AIMS: Patients with arterial hypertension often have a reduction in capillary density (rarefaction) and a reduction in coronary flow reserve because of functional and structural alterations of the coronary microcirculation. Patients with chest pain and normal coronary arteriograms may have coronary microvascular dysfunction, but it is not known whether capillary rarefaction plays a role in the pathogenesis of this syndrome. The aim of this study was to compare capillary density in hypertensive and normotensive subjects with anginal chest pain and normal coronary arteriograms vs asymptomatic hypertensives and healthy controls. METHODS AND RESULTS: We studied 49 patients with typical anginal chest pain, positive exercise testing and normal coronary arteriograms; 22 were hypertensive and 27 were normotensive. We used intra-vital video-microscopy to examine the skin of the dorsum of the middle finger of the non-dominant hand before and after maximization of perfused capillaries with venous congestion. Mean capillary density was significantly lower in patients with chest pain and normal coronary arteriograms independent of their blood pressure level, compared to normotensive healthy controls. Differences were found both at baseline [51+/-2 (hypertensive) and 52+/-2 (normotensive) vs 65+/-2 (controls) per 0.56 mm(2) respectively], (P<0.0001) and after maximization [57+/-3 (hypertensive) and 59+/-2 (normotensive) versus 75+/-3 (controls) respectively] (P<0.0001). CONCLUSIONS: Skin capillary density is significantly lower in patients with chest pain and normal coronary arteriograms compared to normotensive controls. The pathophysiological importance of capillary rarefaction in patients with chest pain and normal coronary arteriograms remains unknown. Further studies are needed to determine whether the abnormality is associated with myocardial flow disturbances such that the findings can be extended to the heart.  (+info)

Impaired skin capillary recruitment in essential hypertension is caused by both functional and structural capillary rarefaction. (7/62)

Capillary rarefaction occurs in many tissues in patients with essential hypertension and may contribute to an increased vascular resistance and impaired muscle metabolism. Rarefaction may be caused by a structural (anatomic) absence of capillaries, functional nonperfusion, or both. The aim of this study was to assess the extent of structural versus functional capillary rarefaction in the skin of subjects with essential hypertension. We examined skin capillary density with video microscopy before and during maximization of the number of perfused capillaries by venous congestion (structural capillary number) and before and during postocclusive reactive hyperemia (capillary recruitment, which may have a structural and/or functional basis). The study group was composed of 26 patients with never-treated essential hypertension and 26 normotensive control subjects. In both groups, intermittently perfused capillaries in the resting state were an important functional reserve for recruitment during postocclusive hyperemia. Recruitment of perfused capillaries during postocclusive reactive hyperemia was decreased in the hypertensive subjects compared with normotensive control subjects (47.9+/-6.8 versus 55.3+/-8.2 capillaries/mm(2), respectively; P<0.01). During venous occlusion, maximal capillary density was significantly lower in the hypertensive subjects than in the control subjects (52.5+/-6.6 versus 57.2+/-8.6 capillaries/mm(2), respectively; P<0.05), suggesting structural rarefaction. However, in the hypertensive subjects compared with the normotensive subjects, a smaller proportion of the maximal number of capillaries was perfused during postocclusive hyperemia (91.6+/-7.5% versus 97.2+/-2.7%, respectively; P<0.05), suggesting an additional functional impairment of capillary recruitment. If the difference in capillary numbers during venous congestion ( approximately 4.6 capillaries/mm(2)) truly reflects the structural difference between the normotensive and hypertensive subjects, then, at most, 62% (4.6/7.4x100%) of the difference in capillary numbers during postocclusive hyperemia ( approximately 7.4 capillaries/mm(2)) can be explained by structural defects, and at least 38% can be explained by functional defects. In conclusion, in patients with essential hypertension, recruitment of perfused capillaries is impaired, which can be explained by both functional and structural rarefaction.  (+info)

Penumbral microcirculatory changes associated with peri-infarct depolarizations in the rat. (8/62)

BACKGROUND AND PURPOSE: This study was designed to investigate the influence of peri-infarct depolarization elicited by occlusion of the middle cerebral artery on the dynamics of the microcirculation. METHODS: The microcirculation in the frontoparietal cortex of 9 rats was visualized in real time through a closed cranial window with the use of laser-scanning confocal fluorescence microscopy combined with intravenous fluorescein isothiocyanate (FITC)-dextran and FITC-labeled erythrocytes. The direct current potential/electrocorticogram was continuously monitored. Intraluminal focal ischemia was induced for 2 hours in 6 rats anesthetized with halothane and mechanically ventilated. Reperfusion was monitored for 1 hour. Three rats underwent sham operation. Brains were removed 24 hours after occlusion and processed for histology. RESULTS: In control conditions, the velocity of fluorescent erythrocytes through capillaries was 0.51+/-0.19 mm/s (mean+/-SD), and the diameter of the arterioles studied was 33+/-12 microm. Under ischemia, erythrocyte velocity through capillaries was significantly decreased to 0.33+/-0.14 mm/s, while arteriole diameter did not change significantly. During spontaneous peri-infarct depolarizations, arteriole diameter was significantly increased (119+/-23% of baseline), while capillary erythrocyte velocity was further decreased by 14+/-34%. The direction of arteriolar blood flow episodically and transiently reversed during approximately half of the peri-infarct depolarizations. The decrease in capillary erythrocyte velocity was more pronounced (23+/-37%) in these cases. After reperfusion, the microcirculatory variables rapidly returned to baseline. All rats in the ischemic group had infarcts 24 hours after occlusion. CONCLUSIONS: Peri-infarct depolarization has an adverse influence on penumbral microcirculation, reducing capillary perfusion by erythrocytes, despite dilatation of arterioles. These findings suggest that a steal phenomenon contributes to the deleterious effect of these depolarizations.  (+info)