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At least 1,351 records · Page 75Linked to original sources

PubMed2003

Effects of mud pack treatment on skin microcirculation.

OBJECTIVES: The objective of this study was to conduct a laser-Doppler flowmetry investigation of skin microcirculation changes induced by mud pack therapy. The magnitude of the changes, potential remote effects, and potential influence of mud pack thickness were studied. METHODS: Twenty female spa therapy patients aged 28-67 years (median, 51 years) participated in the study. The reason for spa therapy was lower limb venous insufficiency in 14 patients and osteoarthritis in six patients, none of whom had involvement of the shoulders. Mud pack treatment was associated with a significant elevation in skin temperature, by 1.8 +/- 0.2 and 1.0 +/- 0.2 degrees C with the 30- and 15-mm packs, respectively (P < 0.001 for both comparisons; nonsignificant difference between the two packs). Skin blood flow increased significantly, by 619 +/- 82 and 410 +/- 124 mV with the 30- and 15-mm packs, respectively (P < 0.0001 for both comparisons; nonsignificant difference between the two packs). The vasomotion score increased markedly on the treated side, by 16.7 +/- 2.8 and 13.0 +/- 1.6 with the 30- and 15-mm packs, respectively (P < 0.005 for both comparisons; no significant difference between the two packs). Furthermore, low-frequency vasomotion waves of a type not described previously were recorded. The microcirculatory changes lasted longer than did the temperature increase. No significant changes were noted in the other shoulder or in central body temperature. RESULTS: The patients were volunteers receiving spa therapy and free of diabetes mellitus, vasoactive drug treatment, and inflammatory shoulder disease. Two mud packs, 15 and 30 mm in thickness, respectively, were applied at an interval of 48 h, at the same time of day in a given patient, and at a distance from other spa treatments. The packs were centered on the deltopectoral groove. The side and order of application of the two packs were determined at random. Superficial skin blood flow was measured by laser-Doppler flowmetry (Perimed PF4001, wavelength 82 nm) and recorded by the Perisoft computer program with a 3-s time constant downstream from a broadband filter (12 MHz). CONCLUSION: These results suggest that the vascular changes induced by mud pack therapy are not fully explained by vasodilation in response to local temperature elevation. Further studies are in order to identify the other mechanisms involved.

Adult↗

PubMed2001

Phentolamine suppresses the increase in arteriolar vasomotion frequency due to systemic hypoxia in hamster skeletal muscle microcirculation.

Systemic hypoxia (8%, 11% and 15% oxygen gas mixture inspiration) has been shown to increase the frequency of arteriolar rhythmic diameter changes in hamster skeletal muscle microcirculation. The effects of phentolamine on vasomotion frequency during systemic hypoxia were studied in Syrian hamsters implanted with a plastic chamber in the dorsum skin. Phentolamine (50 microg/100 g body wt.) was injected intravenously before the 20-min exposure to 11% oxygen gas mixture. The microvessels were studied with a fluorescent microscopy technique, using fluorescein isothiocyanate bound to dextran (mol. wt. 150,000) as a tracer. Vessel diameters were measured with a shearing method. Fourier transform and autoregressive modeling were used to assess the time variant features of diameter changes. Under baseline conditions, the arterioles were characterized by rhythmic diameter changes with fundamental frequency related to vessel size. The terminal branchings were dominated by order 3 vessel activity (frequency: 0.08-0.16 Hz) spreading downstream to all daughter arterioles. Systemic hypoxia caused an increase in vasomotion frequency of order 3 arterioles up to 0.3-0.5 Hz (average: 0.40 +/- 0.06 Hz) and a significant decrease in mean diameter (-28 +/- 5%). Phentolamine completely suppressed the rhythmic changes in diameter of order 3 arterioles that dilated significantly (+ 30 +/- 4%). Therefore, the effects of systemic hypoxia on arteriolar vasomotion appear to be triggered by an increase in sympathetic nervous discharge that induces a rise in frequency up to 0.3-0.5 Hz.

Animals↗

PubMed1997

Responses in skin microcirculation to vestibular stimulation before and during motion sickness.

BACKGROUND: Observation of physiological changes during motion sickness is required to quantify the degree of sickness. The review of the literature does not show unifying results. An objective symptom of motion sickness is facial pallor. It reflects changes in skin microcirculation which have not been measured so far. METHODS: Eleven healthy volunteers susceptible to motion sickness were subjected to eccentric vertical axis rotation. The dynamics and the correspondence of the changes in skin blood flow in two segments, forehead and finger, were measured by laser Doppler flowmeter. RESULTS AND CONCLUSIONS: The difference in the microcirculatory skin blood flow across the phases of motion sickness is significant for the forehead but not for the fingertip: the established dynamics of the forehead blood flow during motion sickness will be of benefit in quantifying the degree of sickness; there is no correlation between the blood flow changes in both measured areas; the rhythmic blood flow fluctuation increases during motion sickness; there is a difference between the blood flow responses to vestibular stimulation before the appearance of motion sickness and in the course of the sickness. Laser Doppler flowmetry is a reliable method in quantifying the degree of motion sickness.

Adult↗

PubMed2001

Young Investigator's Prizewinner 2001. Direct visualization of the influence of normothermic as opposed to hypothermic cardiopulmonary bypass on the systemic microcirculation in neonatal piglets.

The direct visualization of systemic microcirculation using intravitalmicroscopy permits the classification of proinflammatory and ischemic microvascular alterations during normothermic and hypothermic cardiopulmonary bypass in neonates. We used seven newborn piglets, on average aged 9 days, and weighing 3200g, as a control group. In addition, we studied nine piglets subjected to 60 minutes of constant nonpulsatile flow using hypothermic extracorporeal circulation at 28 degrees C, and five piglets using normothermic conditions at 37 degrees C. The microvascular network of the greater omentum and the subcutaneous tissue was directly visualized using intravitalmicroscopy. We analysed interactions between leukocytes and endothelial cells, microvascular morphology, and microrheological conditions, focussing on signs of ischemic and proinflammatory alterations. During normothermic cardiopulmonary bypass, the numbers of activated leukocytes were elevated compared to hypothermic cardiopulmonary bypass (p > 0.05). Arteriolar diameter decreased during hypothermia. Capillaries were markedly dilated during normothermia. Patterns of microvascular perfusion, for both types of cardiopulmonary bypass, showed signs of ischemic damage, revealed by a reduced functional capillary density. Perfusion dependent levels of lactate were higher during normothermic cardiopulmonary bypass (p > 0.05). This new experimental approach revealed that non-pulsatile cardiopulmonary bypass, independent of temperature, induces a proinflammatory and ischemic response compared to an unaltered control group. The markedly elevated numbers of activated adherent leukocytes, the reduced capillary density, and the high lactate levels in those undergoing bypass in normothermic conditions indicate a more pronounced inflammatory stimulus and tissue hypoperfusion compared to the possible protective effect of hypothermia for children undergoing cardiopulmonary bypass.

Animals↗

PubMed2000

Effects of chronic administration of Helicobacter pylori extracts on rat gastric mucosal microcirculation in vivo.

The mechanisms by which Helicobacter pylori contributes to gastroduodenal injury are unclear. We have previously described platelet aggregation within rat gastric mucosal microcirculation following acute administration of H. pylori extracts. However, leukocyte activation was not observed. This study aimed to determine whether chronic administration of H. pylori could induce leukocyte activation. Rats were gavaged with either H. pylori or E. coli extracts or with distilled water three times daily at three-day intervals. Acridine red was used to quantitate gastric mucosal leukocyte/platelet activity using fluorescent in vivo microscopy. Further animals received additional acute H. pylori after 1 hr and recordings were made for a further 1 hr. Significant numbers of "flyers," "rollers," and adherent leukocytes were observed throughout the study in H. pylori animals. Only adherent leukocytes were observed following E. coli. Acute H. pylori induced a further significant increase in adherent leukocytes. Significant platelet thrombi were also present in H. pylori-treated animals. In conclusion, earlier studies demonstrated platelet aggregation but no leukocyte activation, which is in contrast to the current chronic studies. Platelet activation may be the initial response to H. pylori and involved in recruitment of leukocytes. These activated cells may contribute to the development of gastric mucosal damage.

Animals↗

PubMed2001

Changes of colonic mucosal microcirculation and histology in two colitis models: an experimental study using intravital microscopy and a new histological scoring system.

This study investigated capillary blood flow (CBF) and pathomorphological alterations in the mucosa of different bowel segments at different times after disease onset in rats with colitis induced by either trinitrobenzensulfonic acid (TNBS) or mitomycin-C. CBF was determined by intravital microscopy using fluorescein-labeled erythrocytes. The histological degree of inflammation was assessed by a new scoring system. Severe acute histological changes were found in the distal colon 24 hr after induction of TNBS colitis (score: 8.9+/-1.0). CBF was increased (2.9+/-0.05 vs. 2.6+/-0.04 nl/min in healthy controls). The histological alterations persisted until day 3 (8.5+/-0.9) when CBF significantly decreased (1.8+/-0.05 nl/min). After 15 days, moderate acute inflammation was still detectable histologically (5.4+/-1.3), but CBF had returned to normal values. In mitomycin-C colitis, changes developed mainly in the proximal colon: After three days, there was mild inflammation (2.8+/-1.2) with normal CBF (2.5+/-0.1 nl/min). After seven days, the inflammation had increased (4.8+/-1.1), while CBF had decreased (1.5+/-0.06 nl/min). These changes persisted for six weeks (5.3+/-0.7; 1.2+/-0.05 nl/min). These data suggest that disturbed colonic microcirculation may play an important role in the pathogenesis of inflammatory bowel disease regardless of the histopathomorphological alterations.

Animals↗

PubMed1997

Effects of mixed ETA and ETB-receptor antagonist (Ro-47-0203) on hepatic microcirculation after warm ischemia.

There is evidence that endothelin (ET) is involved in disturbances of the hepatic microcirculation after warm ischemia. In this study we investigated the influence of a mixed ETA-, ETB-receptor antagonist (Bosentan) on ischemia-reperfusion damage of the liver by means of intravital fluorescence microscopy (IVM). Clamping of the left liver lobe (= warm ischemia) was performed in 16 male Wistar rats for 70 min. The treatment group (N = 8) received 15 mg/kg Bosentan (Ro-47-0203) 1 min prior to reperfusion. Controls (N = 8) received an equivalent amount of Ringer's solution. Between 20 and 90 min after reperfusion, leukocyte-endothelial cell interactions in sinusoids and postsinusoidal venules as well as perfusion of hepatic acini were studied. Application of Bosentan improved sinusoidal blood flow, attenuated manifestations of microvascular perfusion failure, and decreased the number of rolling leukocytes in postsinusoidal venules. Our results provide further evidence that ET is involved in postischemic impairment of hepatic microhemodynamics during reperfusion.

Animals↗

PubMed1997

Effects of somatostatin (SMS) on pancreatic microcirculation.

The effect of bolus infusion of increasing somatostatin (SMS) concentrations (1, 10, 100, 200 micrograms/100 g body wt) on pancreatic microcirculation and pancreatic tissue PO2 were investigated by using in vivo epifluorescence microscopy and a polarographic PO2 measurement technique. Additionally, the microperfusion of the pancreas, liver, spleen, stomach, and duodenum was measured by a laser Doppler device. Bolus infusion of SMS caused a significant, transient, and dose-dependent decrease in pancreatic capillary RBC velocities (to 50% of baseline) and acinar capillary overall perfusion (to 20% of baseline), which was not caused by a macrocirculatory depression. This pronounced decrease in microperfusion was not paralleled by a decline in tissue PO2. Laser Doppler measurements revealed that pancreatic and gastric microperfusion were reduced only at maximal SMS concentrations, considering that microperfusion of the liver, spleen, and duodenum was not altered. Therefore, we found further evidence that circulatory adjustment might occur during SMS inhibited secretory activity of the exocrine pancreas.

Animals↗

PubMed2002

Changes in lymph microcirculation during pathological stress.

Stress caused by immobilization and acoustic stimulation produces considerable changes in lymph microcirculation. These changes manifested in dilation of microvessels, enhanced phasic contractile activity and its abnormal pattern, accelerated lymph flow, and recruitment of new lymphangions in drainage functions.

Animals↗

PubMed2003

In vivo assessment of angioarchitecture and microcirculation in experimental liver cancer: a new model in rats.

The rising incidence of unresectable hepatocellular malignancies remains a therapeutic challenge. Little is known about the mechanisms of angiogenesis and immunological aspects of liver tumor vessels. The aim of this study was to investigate hepatic and tumor microcirculation and leukocyte-endothelium interaction by means of intravital microscopy in a rat model of hepatocellular carcinoma. Off-line analysis showed that the angioarchitecture as well as blood flow velocity in liver cancer is heterogeneous. The leukocyte-endothelium interaction is significantly reduced compared to normal liver tissue. The data suggest that the main mechanism is a reduced expression of adhesion molecules demonstrating an effective immune escape mechanism of this tumor. The model represents a useful experimental tool to explore angiogenesis inhibition or immunological therapeutic strategies in experimental liver cancer.

Animals↗

PubMed2003

Effect of N-acetylcysteine on microcirculation of mucosa in rat ileum in a model of intestinal inflammation.

Oxygen radicals are formed by the endothelium and blood cells and have specific functions in various organs systems. On the level of the microcirculation, oxygen radicals take part in the regulation of the leukocyte-endothelial interaction. The involvement of oxygen radicals has previously been found in conditions such as sepsis, ischemia-reperfusion, and inflammation. Indomethacin is a clinically applied nonsteroidal antiphlogistic, and in previous studies in the rat, it has been found to induce an inflammatory reaction in the small intestine characterized by edema and reddening of the intestinal epithelium, ulceration, and dysregulation in the intestinal-epithelial barrier function. In the present study, we investigated the effect of N-acetylcysteine on erythrocyte velocity and the arteriolar diameter of the main arteriole in single villi, thus providing insight in the perfusion of the mucosa in indomethacin-induced intestinal inflammation. N-Acetylcysteine is known to inactivate superoxide and its precursors. Therefore, we used N-acetylcysteine to investigate whether superoxide and its precursors participate in the regulation of blood supply to single villi in this animal model. We found that indomethacin induced an increase in villous perfusion that was significantly reduced by N-acetylcysteine, indicating that superoxide and its precursors may participate in the regulation of blood supply to the mucosa in this animal model of intestinal inflammation.

Acetylcysteine↗

PubMed1997

The microcirculation of choroidal and ciliary body melanomas.

The microcirculation of ciliary body and choroidal melanomas is remodelled into patterns. The presence of microvascular networks, composed of back-to-back loops that encircle microdomains of tumour, and parallel vessels with cross-linking, are associated with death from metastatic melanoma. The formation of these complex vascular patterns may result from reciprocal interactions between the tumour cell and the extracellular matrix, and pattern formation may reflect an invasive tumour cell phenotype. Ciliary body and choroidal melanomas are among the few forms of cancer treated before a pathologist assigns a grade to indicate whether tumour is likely to follow a benign or aggressive course. There is evidence to suggest that prognostically significant microcirculatory patterns may be detectable by non-invasive imaging techniques that may provide a substitute for biopsy to guide the clinical management of patients with these sight- and life-threatening tumours.

Choroid Neoplasms↗

PubMed1976

Effect of the ligation of hepatic artery on the microcirculation in the cirrhotic liver in the rat.

The significance of the hepatic arterial supply in the intrahepatic microcirculation in normal and carbon tetrachloride-induced cirrhotic livers was studied by dye injection method and by ligation of the hepatic artery. The in vivo distribution of dye injected into the hepatic artery evidenced the presence of arterio-venous shunts in the cirrhotic liver. When the hepatic artery of the cirrhotic liver was ligated, the elevated portal venous pressure dropped significantly, and the fast-flowing population of microvessels and sinusoids in the bimodal frequency distribution plot disappeared. The fast-flowing microvessel and sinusoids appeared to be the "arterial" microvessels and sinusoids, and they were converted into the slow-flowing venous channels after hepatic arterial ligation. The transmission of arterial pressure via the A-V shunts may be of greater significance in the pathophysiology of portal hypertension than previously believed.

Animals↗

PubMed1987

Cerebrocortical microcirculation in different stages of hypoxic hypoxia.

This study investigated the relation between local cerebrocortical oxygen tension (PO2) and cerebrocortical microflow (CMF) during normoxia (FiO2 = 0.3) and hypoxic hypoxemia (FiO2 = 0.16 and 0.1). Measurements were performed on mechanically ventilated rats and rabbits anesthetized with 0.8% Ethrane and maintained within normocapnic limits. Polarographic techniques based on the use of multiwire surface electrodes were applied for measurements of local PO2 and CMF. In both species the mean tissue PO2 values were similar under normoxia (26.0 and 31.5 mm Hg for rats and rabbits, respectively). CMF histograms showed pronounced heterogeneity. The highest CMF values exceeded the lowest ones by a factor of 36 in the rat and by a factor of 26 in the rabbit. Mean CMF values were 6.67 +/- 0.72 and 4.09 +/- 0.14 relative units (for definition see text) in rats and rabbits, respectively. During hypoxemia, if the mean tissue PO2 was greater than 5 mm Hg, mean CMF did not change but a change in the pattern of microflow distribution was observed with increases in some CMF values (up to 670% of control) and decreases in others (down to 12% of control). When mean tissue PO2 values of less than 5 mm Hg were observed during hypoxemia, mean CMF increased in both species by approximately 50% on average. The increase in CMF could be seen in each individual CMF recording. We conclude that in the brain cortex local regulatory mechanisms are responsible for the change in the pattern of distribution of microcirculation during moderate tissue hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Cortical microcirculation in a new model of focal laser-induced secondary brain damage.

To study the causes of spatial and temporal evolution of progressive neuro-injury in focal brain ischemia, models with consistent lesion topography are required. In such models, continuous monitoring of the microcirculation in a penumbral area undergoing progressive damage could be possible. We used a fixed-pulse (1.0 s, 40 W) Nd-YAG laser (NYL) to produced discrete brain lesions in rats and monitored the cerebral blood flow (CBF) with laser-Doppler flowmetry (LDF) in nonirradiated areas directly adjacent to the maturing lesion. We also examined the time evolution of the lesion topography over a 4 day period. The lesion volume determined by histopathological methods increased from 3.1 +/- 0.5 to 4.5 +/- 0.5 mm3 (p less than 0.05) during the first 2 h. Simultaneously, LDF indicated severe hypoperfusion (-60 +/- 21%, p less than 0.01) at a zone (1 mm distance from the laser lesion) where progressive neuronal degeneration and increased tissue water content (80.0 +/- 3.3% versus 76.8 +/- 2.1% in normal tissue, n = 7, p less than 0.05) were also observed. At a 4 mm distance from the lesion, hyperemic CBF responses were observed, but no histopathological signs or edema. Secondary brain damage progressed up to 4 days (lesion volume of 6.0 +/- 0.7 mm3). The NYL-induced brain lesion produced a highly reproducible focal injury and progressive neuronal death in a spatial relationship with microcirculatory failure and edema formation. The model allows prospective study of tissue state at a discrete zone, which is separate from the initial injury, but susceptible to secondary brain damage.

Animals↗

PubMed1985

Influence of systemically applied angiotensin II on the microcirculation of glomerular capillaries in the rat.

The effect of intravenous infusion of angiotensin II on microvascular parameters of the renal microcirculation of rats was studied. With the aid of fluorescence microscopy and a high sensitivity video system we observed the passage of fluorescence-labeled erythrocytes through single glomerular capillaries on the surface of the rat kidney. From videotaped recordings, we measured the velocity and the flux of erythrocytes using a modified dual-slit technique with support of a microprocessor system. Angiotensin II was administered intravenously at a rate of either 0.2 or 0.4 microgram/min/kg of body wt. Angiotensin II decreased renal blood flow in a dose-dependent fashion (a 32% decrease with 0.2 microgram/min/kg and a 42% decrease with 0.4 microgram/min/kg). The higher rate of angiotensin II infusion had a variable effect on red cell velocity in glomerular capillaries with an overall effect to decrease velocity by 18%. Red cell flux in capillaries was similarly decreased by 25% with angiotensin II infusion. Three successive infusions of angiotensin II did not significantly diminish the effect of the peptide on red cell velocity or flux. Volume flow through the glomerular capillaries (calculated from erythrocyte velocity and vessel diameter) decreased during angiotensin II infusion (0.4 microgram/min/kg) from 3.2 to 2.4 nl/min despite no change in capillary diameter or hematocrit (ratio of erythrocyte flux to volume flow). These data indicate that alterations of the ultrafiltration coefficient (Kf) are not induced by uniform capillary vasoconstriction mechanisms, as others have suggested.

Angiotensin II↗

PubMed1997

Renal microcirculation and tissue damage during acute ureteral obstruction in the rat: effect of saline infusion, indomethacin and radiocontrast.

Radiocontrast agents and nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for the diagnosis and treatment of renal colic. We studied their impact during unilateral acute urinary outflow obstruction upon renal microcirculation and parenchymal integrity. Laser-Doppler and ultrasonic regional flow measurements demonstrated selective decline of outer medullary blood flow by 23 +/- 2% during an acute increase of intra-pelvic pressure to 50 to 55 cm H2O (N = 28, X +/- SEM, P < 0.01). In rats preconditioned with indomethacin, this manipulation reduced medullary blood flow by 50 +/- 4% (N = 16, P < 0.01 vs. obstruction alone), with cortical and total renal blood flow declining by 18 +/- 4% and 16 +/- 2%, respectively (P < 0.01). Unilateral obstruction alone for 24 hours in intact rats resulted in injury (hemorrhage and necrosis) to the papilla and fornix (formed laterally by inner stripe and medially by the inner medulla). These changes were detected as early as 30 minutes after ureteral ligature by staining for fragmented nuclear DNA (TUNEL). Mild damage of thick ascending limbs (mTALs) was associated with substantial medial fornix injury. Indomethacin markedly increased mTAL injury in obstructed kidneys, but attenuated inner medullary damage, both in the medial border of the urinary space and at the papilla. This latter protective effect, probably mediated by the decrease in intrapelvic pressure, was blunted by concomitant intravenous fluid load. Contrast media (iothalamate) and L-NAME (N omega nitro-L-arginine methyl ester) both augmented inner stripe and inner medullary damage in hydronephrotic kidneys. In rats concomitantly subjected to radiocontrast, indomethacin and L-NAME (an acute renal failure protocol, J Clin Invest 94:1069, 1994), unilateral obstruction augmented inner stripe hypoxic damage (65 +/- 6% vs. 24 +/- 11% of mTALs in contralateral kidneys, N = 7, P < 0.01). Injury was maximal at the fornix (93 +/- 6% vs. 39 +/- 14% of mTALs in the mid-inner stripe, P < 0.01) and extended to the outer stripe and medullary rays. Thus, in the rat acute ureteral obstruction alters medullary blood flow and within 24 hours produces medullary damage in both forniceal and inner medullary locations, that is exacerbated by concomitant measures which limit medullary oxygenation. Contrast studies, forced hydration and NSAIDs for renal colic are potentially harmful and their use should be re-evaluated.

Acute Disease↗

PubMed1997

Elevation of oxygen release by nitroglycerin without an increase in blood flow in the hepatic microcirculation.

The effect of nitroglycerin on oxygen (O2) release in the microcirculation was investigated by examining single, unbranched hepatic sinusoids of rats using dual-spot microspectroscopy. Nitroglycerin significantly increased O2 release from erythrocytes flowing in the sinusoids. Differences in O2 saturation of hemoglobin per unit length of the sinusoid were significantly enhanced, while there were no significant changes in erythrocyte velocity, hemoglobin concentration or oxyhemoglobin flow into the sinusoids, or in regional hepatic blood flow measured with a laser tissue blood flow meter. No change was noted for hepatic O2 consumption measured in isolated liver perfused with hemoglobin-free oxygenated buffer. Isosorbide dinitrate showed a similar but slower effect. These findings suggest that nitroglycerin and isosorbide dinitrate enhance O2 release from erythrocytes without significantly increasing tissue blood flow.

Animals↗