Refrigerated platelets stored in whole blood up to 5 days adhere to thrombi formed during hemorrhagic hypotension in rats.

Essentials In vivo function of platelets stored at various conditions was studied in normo- and hypotension. Refrigerated platelets stored up to 5 days performed as well as those stored at room temperature. Platelet adhesion and thrombus formation were higher in ruptured vessels of hemorrhaged animals. In vivo data suggest that refrigerated platelets are hemostatically effective during hypotension. SUMMARY: Background There is renewed interest in the therapeutic use of cold-stored platelets for bleeding patients. However, critical information is absent or partially available in vitro. Therefore, thrombus formation and platelet adhesion were studied in vivo, in situ, using bleeding and thrombosis models in instrumented rats, and confocal intravital videomicroscopy. Objectives We tested the hypothesis that refrigerated (4 °C) platelets (stored for 24 h or 5 days) participated in thrombus formation as well as platelets stored at room temperature (RT, 22 °C). This hypothesis was tested in normovolemia and hemorrhagic hypotension. Methods & Results After fluorescently-labeled platelet infusion, endothelial injury and vessel rupture were laser-induced in cremaster microvessels and platelet adhesion in > 230 developing thrombi was evaluated. Blood samples were collected for biochemistry and coagulation assays while multiple systemic physiologic parameters were recorded. Hemorrhagic hypotension study animals were subjected to 40% hemorrhage, leading to hypotension and hemodilution, during in vivo platelet adhesion assessments. The fluorescence intensity associated with labeled platelet adherence provided a quantitative index of adhesion. Cold-stored platelets performed as well as those stored at RT in normovolemic animals. During hypotension, cold-stored platelets still performed as well as RT-stored platelets, whereas platelet adhesion and thrombus formation were increased relative to normovolemic animals, in bleeding model experiments. Conclusions We found the methodology suitable for evaluating platelet function in vivo after different storage conditions in fully monitored animals. Refrigerated platelets (stored up to 5 days) participated as well as RT-stored platelets in thrombi formed after hemorrhage, suggesting that refrigerated platelets are effective during hypotensive situations.

Effects of hypertonic saline solution on mesenteric microcirculation.

We evaluated systemic and microvascular effects of hypertonic NaCl solution on normovolemic and hemorrhaged animals. Forty-three Wistar rats (186 +/- 4 g, mean +/- SEM) were anesthetized with pentobarbital and cannulated for mean arterial pressure (MAP), heart rate (HR), and mean pulse pressure (MPP) monitoring and blood withdrawal. Diameters of 126 arterioles and 88 venules of the exteriorized mesentery were studied by using intravital microscopy. Microvascular blood flow was calculated from diameter and red blood cell velocity measurements. The protocol consisted of 15 min control, 30 min hypotension (MAP = 52.9 +/- 0.9 mmHg, hemorrhaged vol. = 17.1 +/- 0.7 mL/kg) and 60 min post-infusion of either normal (0.9%) or hypertonic saline (7.5%, 4 mL/kg). Normovolemic animals showed no systemic or microvascular effects of hypertonic saline. Hemorrhagic hypotension resulted in HR fall that was not changed after infusions. Hypertonic infusion reversed MPP decrease during hypotension but only partially restored MAP and microvascular blood flow. Venules did not change diameter during protocols. During hypotension, 24% of arterioles displayed vasomotion (38% of the rats) with low- and high-frequency components present in 74% and 87% of arterioles, respectively. Arterioles with vasomotion during hypotension had larger control diameters (28.9 +/- 2.0 microm) and contracted more (30.8 +/- 4.1%) than arterioles without vasomotion (18.7 +/- 1.2 microm and 8.1 +/- 1.5%, respectively). Mean arteriolar diameter did not change after infusions. After hypertonic solution, the number of vessels showing vasomotion increased 80%, frequency of vasomotion was unchanged, and amplitude increased. These findings may help to explain some of the mechanisms underlying resuscitation effects of hypertonic infusions during hemorrhagic hypotension.

Vasomotion in rat mesentery during hemorrhagic hypotension.

Although vasomotion has been considered a feature of the microvascular bed under physiological conditions, it has also been observed following hypotension in several tissues. In this work, 158 mesenteric microvessels of 36 rats were investigated quantitatively in normovolemic and hemorrhaged animals, focussing on diameter changes, particularly vasomotion incidence and characteristics. The femoral arteries of Wistar rats (body weight BW = 188 +/- 23 g, mean +/- SD) anesthetized with pentobarbital were cannulated for arterial pressure (AP) monitoring and blood withdrawal. The protocol consisted of 15 min control and 30 min of hemorrhagic hypotension (AP = 52 +/- 5 mmHg, hemorrhaged vol. = 17 +/- 4 ml/kg BW). During control normovolemic conditions, analysis of mesenteric microcirculation using intravital videomicroscopy revealed neither arteriolar nor venular vasomotion. During hemorrhagic hypotension (HH) microvascular blood flow reduced to 25% of control. While venules did not show diameter changes during HH, arterioles contracted to 85 +/- 20% of control and arteriolar vasomotion appeared in 42% of the animals and 27% of the arterioles. The amplitude of arteriolar diameter change during HH relative to mean diameter and to control diameter averaged 65 +/- 24% (range: 32-129%) and 41 +/- 10% (range: 25-62%), respectively. Vasomotion analysis showed two major frequency components: 1.7 +/- 0.8 and 7.0 +/- 5.2 cycles/min. Arterioles showing vasomotion had a mean control diameter larger than the remaining arterioles and showed the largest constriction during HH. We conclude that hemorrhagic hypotension does not change venular diameter but induces arteriolar constriction and vasomotion in rat mesentery. This activity is expressed as slow waves with high amplitude and fast waves with low amplitude, and is dependent on vessel size.

Determination of macromolecular exchange and PO2 in the microcirculation: a simple system for in vivo fluorescence and phosphorescence videomicroscopy.

We have developed a system with two epi-illumination sources, a DC-regulated lamp for transillumination and mechanical switches for rapid shift of illumination and detection of defined areas (250-750 microm(2)) by fluorescence and phosphorescence videomicroscopy. The system permits investigation of standard microvascular parameters, vascular permeability as well as intra- and extravascular PO2 by phosphorescence quenching of Pd-meso-tetra (4-carboxyphenyl) porphine (PORPH). A Pechan prism was used to position a defined region over the photomultiplier and TV camera. In order to validate the system for in vivo use, in vitro tests were performed with probes at concentrations that can be found in microvascular studies. Extensive in vitro evaluations were performed by filling glass capillaries with solutions of various concentrations of FITC-dextran (diluted in blood and in saline) mixed with different amounts of PORPH. Fluorescence intensity and phosphorescence decay were determined for each mixture. FITC-dextran solutions without PORPH and PORPH solutions without FITC-dextran were used as references. Phosphorescence decay curves were relatively unaffected by the presence of FITC-dextran at all concentrations tested (0.1 microg/ml to 5 mg/ml). Likewise, fluorescence determinations were performed in the presence of PORPH (0.05 to 0.5 mg/ml). The system was successfully used to study macromolecular extravasation and PO2 in the rat mesentery circulation under controlled conditions and during ischemia-reperfusion.

Determination of macromolecular exchange and PO2 in the microcirculation: a simple system for in vivo fluorescence and phosphorescence videomicroscopy

We have developed a system with two epi-illumination sources, a DC-regulated lamp for transillumination and mechanical switches for rapid shift of illumination and detection of defined areas (250-750 æm²) by fluorescence and phosphorescence videomicroscopy. The system permits investigation of standard microvascular parameters, vascular permeability as well as intra- and extravascular PO2 by phosphorescence quenching of Pd-meso-tetra (4-carboxyphenyl) porphine (PORPH). A Pechan prism was used to position a defined region over the photomultiplier and TV camera. In order to validate the system for in vivo use, in vitro tests were performed with probes at concentrations that can be found in microvascular studies. Extensive in vitro evaluations were performed by filling glass capillaries with solutions of various concentrations of FITC-dextran (diluted in blood and in saline) mixed with different amounts of PORPH. Fluorescence intensity and phosphorescence decay were determined for each mixture. FITC-dextran solutions without PORPH and PORPH solutions without FITC-dextran were used as references. Phosphorescence decay curves were relatively unaffected by the presence of FITC-dextran at all concentrations tested (0.1 æg/ml to 5 mg/ml). Likewise, fluorescence determinations were performed in the presence of PORPH (0.05 to 0.5 mg/ml). The system was successfully used to study macromolecular extravasation and PO2 in the rat mesentery circulation under controlled conditions and during ischemia-reperfusion

pO2 measurements in arteriolar networks.

Previous studies from our laboratory have shown that the average arteriolar pO2 in the hamster skinfold preparation is lower than arterial systemic pO2. In the present work we tested the hypothesis that there is a longitudinal gradient of pO2 along precapillary vessels. Experiments were performed in Syrian golden hamsters bearing a dorsal skin chamber. The oxygen-dependent quenching of phosphorescence of palladium-porphyrin complexes was used to measure intravascular pO2 in the microcirculation. Arterioles were classified in four orders according to their position in the network, first-order vessels being the entrance points. Simultaneous determinations of diameter (D), red blood cell velocity, and systemic blood gases were also made. There was a significant fall of pO2 between vessels of different orders. First-order arterioles (mean D = 64 microns) had pO2 of 51.8 +/- 9.8 mm Hg (mean +/- SD) which was equivalent to approximately equal to 73% of the arterial systemic pO2. Within the arteriolar network, further decreases of intravascular pO2 were measured, leading to a pO2 of 34.0 +/- 7.9 mm Hg in terminal arterioles (mean D = 7.7 microns). In some vessels pO2 was measured in different positions of the same arteriole. The average longitudinal arteriolar oxygen saturation gradient was 3.4 +/- 0.4 delta %/mm (range 0.8-7.2). A significant and positive correlation was found between pO2 and microhemodynamic parameters when arterioles were grouped according to their order. This relation was not significant for venules which showed a mean pO2 of 30.8 +/- 10.8 mm Hg. Tissue pO2 averaged 24.6 +/- 5.8 mm Hg. We conclude that: (1) There is an oxygen loss in arterial vessels larger than 100 micrograms in diameter, (2) arteriolar pO2 in this preparation depends on the position of the vessel within the network, (3) a substantial portion of oxygen delivery to the hamster skin is provided by the arteriolar network, and (4) only a small pO2 gradient exists between terminal arterioles and venules, suggesting that the contribution of the capillary network to tissue oxygenation is relatively small.

Inhibition of angiogenesis and metastases of the Lewis-lung cell carcinoma by the quinoline-3-carboxamide, Linomide.

Linomide has antitumor effects when administered in vivo but not in vitro. Recent data indicate that at least part of this effect can be attributed to anti-angiogenic properties. The aim of the present investigation was to study the anti-angiogenic effects of Linomide on early tumor-induced angiogenesis in vivo, using a newly developed skinfold chamber technique in the mouse, and to relate this to the effect of Linomide on the number of metastases that develop from a s.c. implanted tumor. Tumor spheroids of Lewis lung cell carcinoma (LLC) with a diameter of about 800 microns were implanted in dorsal skinfold chambers inserted on CB6/Fl mice. Tumor cells were pre-labelled with a fluorescent vital dye (CMTMR), which allowed the estimation of the growth of the implanted tumor spheroids. Linomide, given orally from day 7 to day 11, reduced the incidence of lung metastasis arising from LLC tumors at day 21 in a dose-dependent manner, a 55% reduction being found at a dose of 50 mg/kg/day (N = l9 for the controls and N = 10 for treatment groups). In the dorsal skinfold chamber, the vascular network in Linomide treated animals (100 mg/kg/day, N = 22) was more heterogenous, large areas within the tumor being completely avascular; in addition, capillary density at the tumor site was reduced by 34% 6 days after implantation and by 39% after 14 days. In the control group (N = 16), tumor volume doubling time was not significantly different in the early avascular part of the observation period as compared to the later vascular phase; this indicates that the growth of these micro-tumors in the early avascular phase is not angiogenesis dependent. However, in the Linomide treated animals, tumor volume doubling time was significantly prolonged by 42% during the later part of the observation period. Taken together, the data indicate that the prolongation of the tumor doubling time is due to the anti-angiogenic activity of Linomide.

Quantitative angiogenesis in a syngeneic tumor spheroid model.

The aim of this work was to develop a system for noninvasive, in vivo, and in situ study of tumor angiogenesis in awake mice. Tumor spheroids were prepared from Lewis lung carcinoma cells prelabeled with methylrhodamine. A transparent chamber consisting of two titanium frames was implanted into the dorsal skin of CB6 mice. One layer of the skin was removed in a 15-mm area and covered with a coverslip. A few days later, the coverslip was removed and one to three tumor spheroids (diameters, 500-900 microns) were placed over the upper tissue layer. The selected fields were recorded under trans- and epi-illumination using video microscopy. Separate fluorescence filter sets were used to visualize the FITC-labeled plasma and the rhodamine-labeled tumor spheroids. The dual labeling technique allowed precise identification of the tumors and the study of tumor and microvessel growth for up to 14 days. The tumor area and morphometric parameters of tumor vessels were measured from recorded images. After implantation, tumor cells formed well-defined tumor foci. Venular and capillary dilation and tortuosity were observed in the surrounding tissue 1-2 days after implantation, followed by the appearance of buds and sprouts. After that, vascular networks developed around and within the spheroid. During the first week, angiogenesis was very intense: at Day 6, vascular density and tumor area reached 81 and 19% of their respective maximum values. Vascular densities at Days 3, 6, 10, and 14 were 106 +/- 59, 147 +/- 62, 183 +/- 108, and 173 +/- 38 cm-1, respectively. Tumor volume increased exponentially, with a doubling time of 2 days. Similar results were obtained in nude mice. The model allows detailed repeated observations of angiogenesis and permits quantitative evaluation of tumor growth and angiogenesis in vivo. It is applicable for mechanistic studies as well as therapeutic and pharmacokinetic studies of angiostatic and cytotoxic anti-tumor agents.

Systemic and subcutaneous microvascular oxygen tension in conscious Syrian golden hamsters.

Arteriolar and venular oxygen tension distribution was studied in the subcutaneous connective tissue of the chamber window preparation in conscious Syrian golden hamsters as a function of the systemic PO2, PCO2, pH, arterial pressure and hematocrit, microvascular red blood cell (RBC) velocity, vessel diameter, and blood flow in the same microvessels. PO2 was measured with the phosphorescence decay technique using Pd-meso-tetra(4-carboxyphenyl)porphyrin (30 mg/kg body wt iv). Systemic arterial and venous PO2s were 71.6 +/- 13.1 and 28.4 +/- 5.1 mmHg, while oxygen tension was 45.1 +/- 13.3 mmHg in arterioles and 30.1 +/- 10.7 mmHg in venules. The relatively low arteriolar PO2 and the small arteriolar-venular PO2 gradient indicate that some blood oxygen exits directly to the tissue or is shunted before reaching the capillaries. RBC velocity was the strongest correlate of microvascular PO2 (arterial correlation coefficient = 0.503 and venous correlation coefficient = 0.560, P < 0.001). Microvascular PO2 was also correlated with blood flow, vessel diameter, blood pH, and PCO2 but not with systemic PO2. Arterial oxygen tension was only significantly related to PCO2, pH, and hematocrit. These findings suggest that oxygen delivery to the tissue improves with increasing blood flow velocity and that microvascular PO2 is a locally regulated parameter in the absence of major systemic perturbations.

Noninvasive measurement of microvascular and interstitial oxygen profiles in a human tumor in SCID mice.

Simultaneous measurements of intravascular and interstitial oxygen partial pressure (PO2) in any tissue have not previously been reported, despite the importance of oxygen in health and in disease. This is due to the limitations of current techniques, both invasive and noninvasive. We have optically measured microscopic profiles of PO2 with high spatial resolution in subcutaneous tissue and transplanted tumors in mice by combining an oxygen-dependent phosphorescence quenching method and a transparent tissue preparation. The strengths of our approach include the ability to follow PO2 in the same location for several weeks and to relate these measurements to local blood flow and vascular architecture. Our results show that (i) PO2 values in blood vessels in well-vascularized regions of a human colon adenocarcinoma xenograft are comparable to those in surrounding arterioles and venules, (ii) carbogen (95% O2/5% CO2) breathing increases microvascular PO2 in tumors, and (iii) in unanesthetized and anesthetized mice PO2 drops to hypoxic values at < 200 microns from isolated vessels but drops by < 5 mmHg (1 mmHg = 133 Pa) in highly vascularized tumor regions. Our method should permit noninvasive evaluations of oxygen-modifying agents and offer further mechanistic information about tumor pathophysiology in tissue preparations where the surface of the tissue can be observed.

Morphometric analysis of the anastomosing arteriolar network in cat sartorius muscle.

Topological and geometrical characteristics of the anastomotic arteriolar network in cat sartorius muscle were studied. The vessels were dilated and filled with gelatin-ink solution and the muscle cleared with methylsalicylate. The analysis was done on 11 muscles and included 2297 vascular segments and 772 vascular loops classified according to their position within the network. On average, each muscle had 644 transverse arterioles arising from the anastomotic vessels. The length of vascular segments close to feeding arteries was greater than those located in the central region, while the number of transverse arterioles per unit length of arcade vessel showed an opposite tendency. Most vessel orders had similar diameters, except for the segments at the periphery of the muscle, which were significantly larger. No correlation was found between vessel length and diameter. Vascular loops located in the central part of the network were smaller, as assessed by area, perimeter, number of segments, segment length and number of branches. The variability of the parameters between muscles was smaller than variability within each muscle. We concluded that, in addition to the parameters previously reported, quantitative descriptions of anastomotic networks may be enhanced by considering certain topological aspects of microvessels. The separation of segments and loops according to the position in the network may reveal differences between muscles of different sizes and functions which would not be detected if the vessels were considered as a single group.

The quinoline-3-carboxamide linomide inhibits angiogenesis in vivo.

Linomide (Roquinimex) has antitumor activity when given in vivo (but not when applied in vitro) that has been attributed to immune host mechanisms. Recent studies, however, suggest that Linomide may also possess antiangiogenic properties. The aim of the present study was to evaluate the antiangiogenic effect of Linomide using an intravital microscopic technique. Syngeneic pancreatic islets were isolated and implanted into the dorsal skinfold chamber of Syrian golden hamsters. This model allows detailed repeated in vivo observations and quantitative analysis of revascularization of pancreatic islet grafts. The neovascularization process of the islets is a highly reproducible phenomenon that is completed within about 2 weeks, resulting in a microvascular network very similar to that of islets in situ. The plasma concentration profile of Linomide following a single oral dose of the compound was determined. The elimination of Linomide was fast, the half-life being 2.6 +/- 0.2 h. Due to the short half-life, the hamsters were given Linomide twice a day. One group of animals (n = 9) was force-fed Linomide (100 mg/kg per day) from the day of implantation throughout the 2-week observation period, and the results were compared with those obtained in a nontreated control group (n = 7). At days 6, 10, and 14 after implantation, the neo-vasculature of the islets was examined. In the control group, 91% +/- 4% (mean +/- SEM) of the islets showed the first signs of angiogenesis at day 6, whereas in the Linomide-treated group the corresponding value was 48% +/- 12%. At days 10 and 14, the "take-rate" in the control group increased to 94% +/- 3% for day 0 and to 94% +/- 4% (n = 6) for day 14, whereas in the treated group the corresponding take-rate was 67% +/- 11% and 72% +/- 12%, respectively. The functional capillary density in the control group at days 6, 10, and 14 was 223 +/- 17,348 +/- 29, and 495 +/- 29 cm-1, respectively, and that in the Linomide treated group was 91 +/- 28, 181 +/- 43, and 229 +/- 47 cm-1, respectively. These results demonstrate that Linomide suppresses the neovascularization of the islet grafts by both delaying the onset of and reducing the percentage of islets displaying angiogenesis as well as by decreasing the rate of proliferation of capillary endothelium of the revascularized islets.

Microvessel PO2 measurements by phosphorescence decay method.

A system is described for the in vivo noninvasive measurement of intravascular PO2 at the microscopic level. Under special circumstances the method can also be used to measure interstitial PO2. The PO2 determination is based on the O2-dependent quenching of phosphorescence of palladium-porphyrins bound to albumin. This compound was injected intravenously in the dosage of 30 mg/kg body wt and dissolved in saline to a concentration of 15 mg/ml. The phosphorescence emission was excited by epi-illumination with a strobe xenon arc and measured by a photomultiplier in a well-defined tissue area as small as 15 x 30 microns. A selected portion of the phosphorescence decay was fitted by a single exponential, and the Stern-Volmer equation was used to calculate PO2. Calibration was performed in vitro using saline and blood and was in agreement with previous reports. In vivo observations were made in normal tissue regions from the unanesthetized hamster transparent skin fold chamber preparation. The method allows PO2 determinations, in the range of 0-80 mmHg, in microvessels with diameters of 15-100 microns. Simultaneous transillumination of the tissue also allows measurement of vessel diameter and red blood cell velocity in the same vessels.

Nailfold capillaroscopy in non-insulin dependent diabetes mellitus: blood flow velocity during rest and post-occlusive reactive hyperaemia.

Direct intravital microscopic examinations of nailfold capillaries were made in two groups of subjects: 15 healthy volunteers (C) and 16 non-insulin dependent (D II) diabetic patients. In the diabetic group, the disease duration was less than 1 year (n = 4), between 1 and 10 years (n = 8) and between 10 and 18 years (n = 4). Capillary morphology was evaluated and the distribution of morphological patterns was significantly different between the two groups (P less than 0.001). The number of enlarged capillaries was increased in the D II group compared to the C group and capillaries with nodular apical elongations were only found in diabetics. Capillary blood flow velocity (CBFV) was measured during rest and after release of 60 s arterial occlusion. To assess autoregulatory capacity we determined peak CBFV post occlusion and time to reach it in single capillaries. Mean resting CBFV was not statistically different in the two groups but mean peak CBFV post occlusion was significantly lower (C: 1.49 +/- 0.14 mm s-1; mean +/- SE; D II: 0.93 +/- 0.13 mm s-1, P less than 0.05) and mean time to reach it significantly prolonged (C: 8.9 +/- 0.6 s; D II: 18.0 +/- 1.9 s; P less than 0.05) in diabetics compared to controls. Thus skin microvascular autoregulatory responses are disturbed in these patients. The impairments of the reactive hyperaemia response could not be correlated to either metabolic control or duration of the disease.

Shape and orientation of arterial loops in cat sartorius muscle.

A method is described to quantify the shape and orientation of vascular loops (arcades). Shape is characterized by an ellipticity factor, calculated from area and perimeter values. Orientation is measured as the angle formed by the great axis of the loop with the muscle fibers. These parameters were calculated for 772 arteriolar loops of the cat sartorius muscle. The results show that, on the average, the ellipticity factor is a linear function of the number of segments. The observed values change in the opposite direction from the expected values for regular polygons. Simple calculations are presented to rectify this discrepancy. Most loops are oriented parallel to the muscle fibers.

Microcirculatory responses in cat sartorius muscle to hemorrhagic hypotension.

The purpose of this study was to examine changes in the microcirculation that might explain the rise in vascular resistance during hemorrhagic hypotension. Diameter and red blood cell velocity of microcirculatory vessels in exteriorized cat sartorius muscles were studied during 4 h of hemorrhagic hypotension at 60 mmHg. During hypotension, vascular resistance of the muscles rose approximately 70% while calculated volume flow in arterioles and venules fell to about the same degree. Average red blood cell velocity for all capillaries showed a comparable decline. Red blood cell flow stopped in approximately 60% of capillaries, but the extent of stoppage varied greatly among capillary fields. Arterioles larger than 45 microns constricted 9-29%, with the largest arterioles showing the greatest constriction. Arterioles smaller than 45 microns dilated 34-56%, with the smallest arterioles showing the greatest dilation. Venular diameter did not change with hemorrhage. The predominance of arteriolar dilation, especially in the later stages of hypotension, should lead to a fall in vascular resistance of the muscle. This effect may be offset by constriction of arteries outside the microcirculatory field observed and blockage of capillaries or venules by formed elements.

A new scheme for hierarchical classification of anastomosing vessels.

A new scheme is presented for hierarchical classification of vessels in anastomosing networks. The scheme is based on topological information, i.e. on patterns of vessel interconnection, not on vessel dimensions. As an illustration, this ordering scheme is applied to the anastomosing arteriolar network in cat sartorius muscle. Vascular segments are classified and the frequency distribution of segment length is determined for each order. In addition, vascular loops are classified, and the area, perimeter, and number of segments per loop are determined.

Nailfold capillaroscopy in diabetes mellitus: morphological abnormalities and relationship with microangiopathy.

The morphology and density of nailfold capillaries were evaluated in patients with Type I and Type II diabetes mellitus and in healthy controls, using videocapillaroscopy. A protocol of well-defined capillary patterns was used. Diabetic patients had more tortuous and enlarged capillaries than controls. Nodular apical elongation was found only in diabetics and was more frequent in patients with a longer history of disease. Type II diabetic patients with chronic clinical complications had a higher frequency of enlarged capillaries and nodular apical elongation. Glycemic control was without influence. Capillary density did not differ among the groups.

Nailford capillaroscopy in diabetes mellitus: morphological abnormalities and relationship with microangiopathy

the morphology and density of nailfold capillaries were evaluated in patients with Type I and Type II diabetes mellitus and in healthy controls, using videocapillaroscopy. A protocol of well-defined capillary patterns was used. Diabetic patients had more tortuous and enlarged capillaries than controls. Nodular apical elongation was found only in diabetics and was more frequent in patients with a longer history of disease. Type II diabetic patientes with chronic clinical complications had a higher frequency of enlarged capillaries and nodular apical elongation. Glycemic control was without influence. Capillary densitu did not differ among the groups