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PubMed1998

Blood volume redistribution on fluid treatments after burn-blast combined injury, especially with respect to the regulation role of microcirculation due to the Fåhraeus effect.

Considering the Fåhraeus effect and the blood volume regulation role of the microcirculation, we used a new method for calculating the blood volume change in microcirculation, macrocirculation as well as the whole circulation (delta Vmic, delta Vmac, delta Vb), to compare fluid therapy effects of hypertonic saline dextran solution (HSD) and lactic Ringer's solution at the early stage after burn-blast combined injury (BBI). The measurement of plasma viscosity was used in this calculation. The results showed that, with calculation of the blood volume change in microcirculation and macrocirculation, this method could more exactly and distinctly display the change and distribution of blood volume during the therapy. It confirms that HSD treatment can increase blood pressure and attenuate tissue edema, by significantly increasing total blood volume, recouping delta Vmac. The study suggests that a desirable and practical clinical method for blood volume change can be developed based on the present study.

Animals↗

PubMed1998

The effect of pentaerithrityl-tetranitrate on parameters of the microcirculation.

AIM OF THE STUDY: The effect of organic nitrates on microcirculation was first studied in 1964 and with regard to glyceroltrinitrate (GTN) an "internal hemodilution" (i.e. a fluid shift from the extravascular fluid to the intravascular compartment) was observed. Therefore, we found it of interest to study the effects of the long-acting PETN on parameters of hemorrheology. METHODS: The effects of single doses of 25, 50, and 80 mg PETN, 0.4 mg GTN, and of placebo were investigated on the capillary erythrocyte velocity (CEV; Capiflow), the tissue oxygen tension (tcpO2), the deformability of red blood cells, the plasma viscosity and of the fibrin content of the plasma in a single-blind, randomized study over 12 h in 12 healthy female and male volunteers. The CEV and the tcpO2 were measured in the nailfold of the fourth finger and on the skin of its end phalanx, respectively. Statistical analysis was performed by analysis of variance, the calculation of epsilon (Greenhouse-Geisser), and the multiple t test. RESULTS: After administration of 50 or 80 mg PETN the CEV decreased by 30% over a period of 2 or 4 h (p = 0.02 or 0.002). A decrease by 11% was measured 1 and 2 h after administration of GTN (p = 0.034). Under the same PETN doses tcpO2 increased from 1.41 to 1.78 mm mercury (p = 0.002). The deformability of red blood cells was slightly increased after 50 and 80 mg PETN under share rates of 60 Pa from 55.5 to 58.0% 8 and 12 h after intake. The plasma viscosity was decreased after intake of 50 mg PETN 4 to 8 h (1.36 vs. 1.34 Pa x s, p = 0.023) and after intake of 80 mg 2 to 12 h post dose (1.36 vs. 1.33 Pa x s, p = 0.015). The systolic or diastolic blood pressure decreased, but was not significant. CONCLUSIONS: The PETN-induced decrease in CEV can be explained with the pre- and afterload decreasing properties of the nitrates. The increase in tcpO2 and erythrocyte deformability and the decrease in viscosity are additional advantageous effects on the microcirculation. If the results are transferred from the nailfold of the finger to the myocardium, the benefit of nitrates could not only be seen in the decrease in preload due to their vasodilating properties, but also in improving the parameters of microcirculation. The internal hemodilution and the slightly enhanced deformability might provide an additional supply of myocardial capillaries in case of myocardial ischemia.

Administration, Oral↗

PubMed1996

[Effects of aspirin and nifedipine alone or in combination on mesenteric microcirculation of rats].

AIM: To study the effects of the combination of aspirin (Asp) and nifedipine (Nif) on mesenteric microcirculation of rats. METHODS: Acute microcirculation disturbance (AMD) was produced by high molecular weight dextran (M(r) 480,000, 360 mg.kg-1 i.v.). Arteriole and venule blood flow velocity and diameter (ABFV, VBFV, AD, VD) and blood flow state (BFS) were observed by intravital microcirculation method. RESULTS: Asp 2.5, 5 mg.kg-1, Nif 0.05, 0.1 mg.kg-1, Asp + Nif (1 + 0.025), (2.5 + 0.05) mg.kg-1, i.v. had the significant increase of 11.1%, 31.3%, 18.5%, 19.3%, 30.5%, 39.8% of ABFV and 12.5%, 25.7%, 12.6%, 15.2%, 29.6%, 36.1% of VBFV respectively, the marked improvement of BFS, and the distinctive increase of 4.3%, 17.9%, 35.9%, 39.7%, 15.2%, 42.8% of AD and 2.2%, 4.2%, 26.2%, 27.4%, 3.4%, 28.9% of VD separately, and got a raise in the number of capillaries. Asp + Nif (1 + 0.025), 2.5 + 0.05) mg.kg-1 i.v. could reverse AMD. CONCLUSION: Asp was superior to Nif in the increase of BFV, but Nif was superior to Asp in expansion of blood vessel. Asp in combination with Nif produced marked synergistic action and protection againist AMD.

Animals↗

PubMed1998

[Understanding microcirculation deficits as the key to surgical planning in visceral surgery].

It was the aim of our investigation to analyse microcirculatory disorders in order to optimize surgical decision-making intra- and perioperatively. Acute pancreatitis: The surgical principle to operate less and later is based on an improved ICU therapy. Using intravital microscopic quantification of pancreatic microcirculation it could be shown experimentally that in the early phase pancreatic necroses can be limited by improvement of pancreatic microcirculation. Hemodilution with dextran is superior to other regimens. Liver resection: The expansion of liver resections requires a reduction of ischaemia/reperfusion injury. Preconditioning of the liver, i.e. induction of short-term ischaemia prior to the main ischaemic period, results in an induction of protective mechanisms with increased tolerance to ischaemia. Liver transplantation: Liver microcirculation is a reliable parameter to predict graft quality intraoperatively and to monitor therapeutic approaches to ischaemia/reperfusion injury. With the analysis of microcirculatory disorders, a basic understanding for organ dysfunctions which lead to operation or are a result of surgical therapy can be gained.

Animals↗

PubMed1996

First clinical realization of continuous monitoring of liver microcirculation after transplantation by thermodiffusion.

To date, no method is available for the continuous long-term monitoring of liver microcirculation in patients. Experimentally, thermodiffusion has been validated in the quantification of hepatic perfusion. In an attempt to investigate the practicability of thermodiffusion technology in patients after liver transplantation thermodiffusion probes were inserted into the graft in seven patients during liver transplantation. Continuous monitoring started intraoperatively and was performed until day 7, when the probes were extracted transcutaneously. No probe-related complications (i.e., hemorrhage, infection) were observed. In four patients with normal graft function, liver perfusion recovered within 12 h from the intraoperative reduction to a range between 85 and 93 ml/100 g per min. In contrast, primary graft failure (n = 1) was characterized by a constant decrease of hepatic perfusion (< 50 ml/100 g per min). In prolonged reperfusion injury (n = 1), a second peak of transaminases was paralleled by an impairment of liver microcirculation. In one patient, R2 rejection on day 7 was preceded by a drop in hepatic perfusion 48 h earlier. Thus, thermodiffusion is a safe and reliable method for the continuous quantification of liver microcirculation after transplantation in patients. Measurements are reproducible for at least 7 days. Changes in hepatic perfusion during postoperative complications can be detected. The characteristics of microcirculatory disorders will have to be defined in a larger number of patients.

Adolescent↗

PubMed1996

Microcirculation in the footsole as a function of mechanical pressure.

OBJECTIVE: In this study an experimental set-up for measuring skin microvascular responses of the footsole to changes in externally applied pressure was analysed. DESIGN: A clinical study. Skin microvascular blood flow was measured in healthy volunteers, during and after external mechanical pressure of different magnitudes. BACKGROUND: During standing and walking the footsole is commonly exposed to high static and dynamic mechanical pressure, resulting in changes in the microcirculation of the footsole. In diabetic patients a disturbed interaction between externally applied pressure and skin microvascular response seems to be involved in the development of a foot ulcer. METHODS: Eleven volunteers participated in the study. Static loads were applied to the heel part of the footsole with the person in a supine position. Contact pressure and skin blood flux, based on the laser Doppler technique, were simultaneously monitored. The pressure used was varied in five discrete steps between 10 and 160 kPa and applied during a period of 5 min each. The microcirculation was measured during as well as after pressure loading. RESULTS: Pressures of 40 kPa and higher do stop the blood flow in the skin microcirculation. Releasing the applied pressure resulted in a hyperaemic response. This response appears to increase in amplitude at increasing pressures up to 800% of the baseline laser Doppler fluxmetry level. Beyond a pressure level of 80 kPa the hyperaemic response seems not to be influenced by the pressure level. The time needed to achieve the maximal laser Doppler fluxmetry level decreased when the pressure was raised from 10 to 80 kPa, but increased again when higher pressures were applied (P = 0.051). An intraindividual variation of 11-50% was observed for the parameters describing the blood flux before, during, and after pressure application. CONCLUSION: Simultaneously measuring changes in contact pressure and laser Doppler flux of the footsole is a useful method to study the interaction of external mechanical pressure and skin microvascular reactions. Pressures above 40 kPa stop skin microvascular blood flow. Releasing the applied pressure results in a hyperaemic response, which increases when the applied pressure increases from 40 to 80 kPa. Higher pressures do not influence the amplitude in skin microvascular response, but result in a longer delay to maximal hyperaemia.

Journal Article↗

PubMed2005

Hepatic microcirculation after continuous 7-day elevated intra-abdominal pressure in cirrhotic rats.

It is well known that IAP elevation, even at the level of 10mmHg used for laparoscopic surgery leads to an increase in portal pressure and decrease in portal blood flow. Since hepatic hemodynamics are already disturbed in cirrhotics, we decided to investigate the possible role of chronically elevated intra-abdominal pressure thus simulating ascites under tension-in liver perfusion and function in cirrhotic portal hypertensive rats. Four groups of 10 rats each were studied, including two control and two CCl(4)(-) induced cirrhotic groups. These were subdivided into normal and increased IAP. Elevation and maintenance of increased IAP to 20mmHg for 7 consecutive days was achieved by means of an intraperitonially placed balloon filled with water. Liver microcirculation was assessed by means of laser-Doppler technique, while venous blood samples were obtained for determination of the biochemical parameters of liver function. Cirrhotic rats showed a significant decrease in liver microcirculation in relation to controls (15.7+/-2.5 versus 23.2+/-2.2, p=0.001). Elevation of IAP led to a significant decrease (p=0.001) of liver microcirculation in both groups, i.e. from 15.7+/-2.5 to 12.7+/-1.7 units of flow in cirrhotics and from 23.2+/-2.2 to 15.9+/-2.6 units of flow in control rats. Alkaline phosphatase, alanine aminotransferase and bilirubin concentrations were found increased in cirrhotics in comparison to controls (p=0.05). IAP elevation resulted in a further impairment of liver function, but the differences, were not statistically significant. In conclusion, chronically elevated IAP in cirrhotic rats is associated with a significant impairment of the already decreased hepatic blood flow due to liver cirrhosis. Thus, the possible consequences of decreased liver perfusion must be taken under consideration in any case of severe cirrhosis presented with ascites under tension.

Journal Article↗

PubMed1995

Isovolemic hemodilution with dextran prevents contrast medium induced impairment of pancreatic microcirculation in necrotizing pancreatitis of the rat.

BACKGROUND: Previous studies demonstrated that intravenous contrast medium (CM), as used in contrast enhanced computed tomography, aggravates the impairment of pancreatic microcirculation (PM) characteristic of severe pancreatitis and increases necrosis and mortality in necrotizing pancreatitis (NP) in rats. This study evaluates the use of isovolemic hemodilution, which can enhance the microcirculation in severe pancreatitis, for preventing CM-induced injury. METHODS: NP was induced in 30 dextran-tolerant Wistar rats by intraductal glycodeoxycholic acid and intravenous cerulein for 6 hours. PM was quantified by intravital microscopy using fluorescein isothiocyanate labeled erythrocytes. Based on previous results, areas with low blood flow (< 1.6 nL/min/cap) were identified and baseline recordings of capillary blood flow taken. A reduction of hematocrit to 75% of baseline was achieved by replacement of 5 mL/kg of blood with 25 mL/kg Ringer's lactate (RL) or by exchange of 8 mL/kg of blood for the same amount of dextran 70.6%. Thereafter, the nonionic CM iopamidol (Solutrast, Byk Gulden, Konstanz, Germany) was injected during 1 minute and PM measurements repeated after 30 and 60 minutes. RESULTS: Despite hemodilution with RL, pancreatic capillary perfusion was significantly decreased to 87% of baseline (0.83 +/- 0.04 mL/min/cap; n = 216) 60 minutes after CM infusion (P < 0.05). In contrast, capillary blood flow was significantly increased to 161% (1.56 +/- 0.05 nL/min/cap; n = 278) in the group treated with dextran. Moreover, the percentage of capillaries developing complete stasis was significantly lower in the dextran group (2.3 +/- 1.2%) compared to animals diluted with RL (22.3 +/- 4.8%) (P < 0.002). CONCLUSION: Isovolemic hemodilution with dextran prevents the additional impairment of pancreatic microcirculation induced by CM in NP.

Acute Disease↗

PubMed1994

Therapy of hypertensive cardiac hypertrophy and impaired coronary microcirculation.

In arterial hypertension, cardiac remodeling comprises myocyte hypertrophy, interstitial fibrosis, and functional and structural alterations of the coronary microcirculation. This leads to diastolic and systolic dysfunction of the left ventricle and impairment of coronary flow reserve. Consequently, antihypertensive treatment should aim at repairing hypertensive cardiac remodeling through reversing myocyte hypertrophy, restoring myocardial structure, and improving coronary flow reserve along with blood pressure normalization. Although it has been shown that regression of left ventricular hypertrophy (LVH) can be achieved by suitable antihypertensive therapy, more insight regarding the ability to repair coronary microcirculation is needed. In spontaneously hypertensive rats (SHRs), it has been shown that coronary reserve was enhanced after hydralazine administration without concomitant regression of LVH. Likewise, administration of the calcium-channel blocker felodipine led to a reversal of medial hypertrophy in coronary resistance vessels. The angiotensin-converting enzyme inhibitor lisinopril was shown to improve coronary reserve and to reserve both medial hypertrophy and myocardial fibrosis in SHRs. Increase in length density of capillaries with either nifedipine or moxonidine treatment was also found in experimental hypertension. First clinical data indicate that, after prolonged antihypertensive treatment, coronary flow reserve can be improved in hypertensive patients with microvascular disease. Further studies are warranted to elucidate whether improved coronary flow reserve after medical treatment for arterial hypertension is due to an influence of myocardial factors, such as LVH or myocardial fibrosis or to repair of the structurally remodeled microcirculation.

Animals↗

PubMed1999

Effects of N(omega)-nitro-L-arginine (L-NOARG) on blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension.

The role of N(omega)-nitro-L-arginine (L-NOARG), a nitric oxide (NO) synthase inhibitor, in the control of blood flow and vasomotion in rat diaphragm microcirculation during hemorrhagic hypotension was investigated by means of laser Doppler flowmetry (LDF). Fifty-six Sprague-Dawley rats were divided into seven groups. Ten minutes after one-stage hemorrhage to 40-60% of initial blood pressure, the rats received 15 min topical superfusion of saline (group 1, time control), 0.1 mM L-NOARG (group 2), 10 mM L-arginine (group 3), or vehicle (0.1% DMSO and 0.9 mN NaOH, group 4). For groups 5 and 6, L-NOARG or its vehicle was superfused for 15 min without hemorrhage. In group 7, the vasodilator responses to the endothelium-dependent vasorelaxant acetylcholine (ACH) and the endothelium-independent vasorelaxant sodium nitroprusside (SNP) were assessed at rest and after 25 min of hemorrhagic hypotension. The results showed no significant differences in blood flow, fundamental frequency, or relative amplitude of the rat diaphragm microcirculation before or after administration of the test agents among the first four groups during hemorrhagic hypotension or in groups 5 and 6 during sham operation without hypoperfusion. Hemorrhagic hypotension significantly decreased the vasodilator response to ACH (p = 0.003), but not to SNP. We conclude that NO did not play an important role in the regulation of blood flow or vasomotion in rat diaphragm microcirculation during acute hemorrhagic hypotension.

Animals↗

PubMed2005

Capillaroscopy and videocapillaroscopy assessment of skin microcirculation: dermatologic and cosmetic approaches.

BACKGROUND: Different noninvasive bioengineering techniques exist to study the microvasculature of the skin and the dynamics of the microcirculation. The goal of these techniques is to visualize the skin capillary circulation easily and directly. Indeed, this information is irreplaceable to study the physiology and physiopathology of the skin capillary circulation efficiently. AIMS: Capillaroscopy and video-capillaroscopy techniques are presented with different methods to study the capillary structure of the skin. METHODS: The methods presented in this work include image processing analysis combining morphology, statistics, geometry, and neural network detection designed to quantify the microcirculation and to follow its evolution. To illustrate the combination of these techniques and methods, different examples of their application are described, in dermatology (hypertension, venous insufficiency, age-related changes) as well as in cosmetology (rosacea and erythrosis assessment). CONCLUSION: The determination of structural or dynamic changes in the cutaneous microcirculation belongs to the noninvasive techniques of the biometrological domain. Thus, every capillary modification resulting from topical cosmetic products, or chemical agents can be observed. In pathology, numerous conditions can be better examined with this system. Associated with the potential of numerical image analysis, capillaroscopy techniques will probably extend their application fields to the assessment of the influence of arterial and venous diseases on the skin nutritional circulation.

Journal Article↗

PubMed2002

Toxigenic Helicobacter pylori induces changes in the gastric mucosal microcirculation in rats.

BACKGROUND AND AIMS: One of the key components of inflammation is changes in vascular structure and function. This suggests that the microcirculation may be a key target of Helicobacter pylori released factors. It has previously been shown in vivo that pooled H pylori extracts from duodenal ulcer/gastritis patients induce platelet aggregation but no leucocyte activation within rat gastric mucosal microcirculation (GMMC). However, infection with strains associated with ulcer disease as compared with gastritis may exert greater effects on the microcirculation. This study used fluorescent in vivo microscopy to determine the acute effects of extracts of genotypically different H pylori strains on the GMMC. METHODS: Three H pylori extracts, with different cagA and VacA toxigenic status, were individually administered to the gastric mucosa of anaesthetised Wistar rats. The mucosal surface was visualised via an incision made in the exteriorised stomach. Fluoroscein isothiocyanate conjugated to bovine serum albumin (FITC-BSA) or acridine orange was used to quantify macromolecular leak (MML) and leucocyte/platelet activity respectively for 120 minutes. Changes in capillary and post-capillary venule (PCV) diameters were also monitored. RESULTS: The cagA(+) VacA toxigenic strain 60190 induced significant and sustained MML by five minutes (p<0.01). Transient and less leakage was observed with its isogenic VacA(-) mutant and other non-toxigenic strains regardless of cagA status. Significant increases in leucocyte adhesion (p<0.05), platelet aggregation (p<0.05), and PCV vasoconstriction (p<0.05) were only observed with the cag A(+) and toxigenic strain. CONCLUSION: Extracts of H pylori are capable of inducing marked disturbances within the rat GMMC. These disturbances seem to be dependent on the production of an active vacuolating cytotoxin. Varying effects on the GMMC may explain the clinically diverse outcomes associated with genotypically different strains.

Animals↗

PubMed2000

Chronic 17beta-estradiol replacement increases nitric oxide-mediated vasodilation of guinea pig coronary microcirculation.

BACKGROUND: Estrogen is cardioprotective of the coronary circulation by mechanisms incompletely understood. This study determined the effect of chronic 17beta-estradiol replacement on dilator responses to acetylcholine and sodium nitroprusside of the isolated coronary microcirculation. METHODS AND RESULTS: Adult female guinea pigs were ovariectomized, and a 21-day-release pellet containing 0.0, 0.1, 0.25, 0.5, or 1.0 mg 17beta-estradiol was implanted subcutaneously. Serum estradiol concentrations ranged from 3.9 to 74.9 pg/mL, increasing with the dose of estradiol. After 19 to 20 days, the animals were euthanized, and their hearts were removed and perfused with buffer at constant flow on an isolated heart apparatus. Both perfusion pressure and contractile force were measured in prostaglandin F(2alpha)-constricted hearts. Vasodilation to the cumulative addition of the endothelium-dependent agonist acetylcholine (10(-9) to 10(-5) mol/L) and the nitric oxide (NO) donor sodium nitroprusside (10(-9) to 10(-5) mol/L) was measured before and after NO synthesis inhibition by nitro-L-arginine (LNA, 10(-4) mol/L). Baseline coronary resistance was unaltered by estradiol, although LNA increased resistance in estradiol-treated hearts more than in ovariectomized controls. Chronic 17beta-estradiol increased sensitivity (measured by -log EC(50) values) but not maximal response to acetylcholine compared with ovariectomized controls. Differences were abolished by LNA at all doses of estradiol. Sodium nitroprusside-induced dilation was unaffected by estradiol replacement. CONCLUSIONS: Chronic 17beta-estradiol replacement, at doses producing hormone levels within the physiological range, enhances dilator sensitivity of the coronary microcirculation through enhanced NO production by the endothelium, independent of changes in NO sensitivity of the vascular smooth muscle. Thus, estradiol enhances NO production as a protective mechanism of the coronary microcirculation.

Animals↗

PubMed1987

Laser-induced endothelial damage inhibits endothelium-dependent relaxation in the cerebral microcirculation of the mouse.

This study demonstrates endothelium-dependent relaxation in the surface arterioles of the brain. A helium-neon laser was used to injure endothelium in situ following i.v. injection of Evans blue dye, which sensitizes the bed to the laser. Areas 18 or 36 micron in diameter were injured and no longer relaxed to either 1 ml of acetylcholine chloride or bradykinin triacetate, 80 micrograms/ml delivered for 60 seconds. Dilations to sodium nitroprusside (30 micrograms/ml) were unaffected. Normal responses to nitroprusside, plus electron microscopy, established that vascular smooth muscle was uninjured. Endothelium-dependent relaxation was impaired when only minor ultrastructural damage was present. Dilation was inhibited downstream and upstream as far as 80 micron from the center of the laser beam. This suggests a spread of endothelium injury around the site of laser impact. However, inhibition was somewhat more marked downstream than upstream, implying that a portion of the downstream response was dependent on a substance released from an upstream site. To date, very few studies have reported endothelium-dependent relaxation in vivo, especially in the microcirculation. The present study accomplishes this. Moreover, in contrast to in vitro observations of endothelium-dependent relaxation in large vessels, the in vivo elimination of endothelium-dependent relaxation in the microcirculation required neither removal of endothelium nor injury to large numbers of endothelium cells. Since endothelium-dependent relaxation in the microcirculation has now been demonstrated using three different techniques to injure endothelium, it is reasonable to conclude that the phenomenon is real.

Acetylcholine↗

PubMed1996

Pentoxifylline maintains cochlear microcirculation and attenuates temporary threshold shifts following acoustic overstimulation.

The etiology of noise-induced hearing loss is poorly understood despite years of clinical experience and experimental investigations. One potential mechanism which may contribute to noise-induced temporary threshold shifts (TTS) are vascular pathologies in the microcirculation of the cochlea. Several studies have demonstrated histologic evidence of reduced cochlear blood flow following noise exposure. Recent studies utilizing intravital microscopy (IVM) complement these histologic studies and furthermore demonstrate localized ischemia during noise exposure. The purpose of the current study was to attempt to maintain cochlear blood flow during noise exposure by treating with pentoxifylline, a xanthine derivative which promotes blood flow in capillary beds. The possibility that preserved cochlear microcirculation with pentoxifylline treatment attenuates noise-induced TTS was also examined in this study. The results show treatment with pentoxifylline maintains cochlear microcirculation as assessed by continuous red blood cell movement through capillaries. Pentoxifylline treatment did not prevent vasoconstriction or increased permeability often observed in the cochlear microvasculature during noise. Treatment with this drug reduced noise-induced TTS.

Animals↗

PubMed1999

Studies on the flow and distribution of leukocytes in mesentery microcirculation of rats.

AIM:To study the effect of leukocyte-endothelium interaction (LEI) on the flow and distribution of leukocytes in microcirculation under physiological condition.METHODS:A microcirculation image multiple parameter computer analysis system (MIMPCAS) was used to study the flow and distribution of leukocytes in mesentery microcirculation of rats in vivo.RESULTS:The difference of visible leukocyte flux (VLF) was as high as 131 times in the arterioles and venules with similar diameter and blood velocity. The visible leukocytes rolled along the blood vessel wall as a jerky movement. The frequency distribution of the visible leukocyte velocity (VLV) showed a two peak curve. The low peak value was on 10&mgr;m/s-15&mgr;m/s while the high peak fell between 25&mgr;m/s-30&mgr;m/s. With the increase of diameter of venules, VLF increased while the VLV remained at the same level. With the increase of RBC velocity, VLV trends to elevate and VLF to fall down.CONCLUSION:The results herein might provide a basic theory for the study on the mechanism of LEI under physiological condition and novel methods for the prevention and treatment of high LEI in many pathological processes.

Journal Article↗

PubMed1985

Abnormalities of the coronary microcirculation in acute murine Chagas' disease.

Chronic Chagasic heart disease has many features characteristic of other congestive cardiomyopathies, including ventricular and atrial chamber enlargement, hypertrophy, focal scarring, and mural thrombi. Histologically, there is often lymphocytic inflammation, spotty necrosis, and few parasites. Although immunologic mechanisms have been invoked to explain the development of myocardial degeneration, there have been suggestions that the focal alterations in the heart are secondary to abnormalities of the coronary microcirculation. Based on work from our laboratories which has demonstrated microvascular hyperreactivity in several other models of congestive cardiomyopathy, we investigated whether the cardiac microcirculation of mice acutely infected with Trypanosoma cruzi was also abnormal. We perfused animals at 15-17 days post-infection with silicone rubber which fills the arterioles, capillaries, and venules of the beating heart. After clearing the tissue, we observed numerous areas of focal vascular constriction, microaneurysm formation, dilatation, and proliferation of microvessels which were not present in control animals. These lesions were similar to those we have observed in other congestive cardiomyopathies. Since at this stage of infection there is minimal cardiac degeneration or fibrosis, the presence of these vascular lesions even early in Chagas' disease, may be significant for the pathogenesis of focal myocardial damage. These observations during acute infection provide additional support for the suggestions of others that the myocardial microcirculation is abnormal in Chagas' disease.

Aneurysm↗

PubMed2004

[Changes of cat cerebral microcirculation and blood-brain barrier in early stage of craniocerebral gunshot wound in the hot and humid environment].

OBJECTIVE: To study the changes of cat cerebral microcirculation in early stage after craniocerebral gunshot wound in the hot and humid environment to provide laboratory evidence for clinical treatment of such wound. METHODS: Craniocerebral gunshot wound was induced in 24 cats according to the method described by Carey with modifications, and the cats were placed in a cabin with environmental temperature and humidity of 25 degrees Celsius and 50% (group A), and 35 degrees Celsius and 85% (group B), respectively, to observe the changes in all the indices of cerebral microcirculation. RESULTS: All the cats survived and notable changes occurred in the morphology and permeability of cerebral microvascular along with obvious pathological changes in the brain tissue, and the vital signs, hemorheology and blood-brain barrier were significantly different between groups A and B. CONCLUSION: Hot and humid environment induces obvious changes in cat cerebral microcirculation and blood-brain barrier function in the early stages after craniocerebral gunshot wound.

Animals↗