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PubMed1987

The structure and reactions of the microcirculation in a subcutaneous air pouch in the rat.

Studies by a combination of vascular perfusion, histological and electron microscopic techniques show that subcutaneous injection of air into rats excites no acute inflammatory response, but leads to the formation of a pouch lined by avascular fibrous tissue. Existing subcutaneous blood vessels are displaced by the pouch but no new blood vessels are formed. By contrast injection of carrageenan with the air or into a preformed air pouch leads to a severe inflammatory reaction and the rapid development of a thick layer of granulation tissue. Either type of pouch is a useful system in which to study inflammation. However because the distribution and ultrastructure of small blood vessels in the pouch wall is quite different from the known characteristics of the microcirculation of synovial membrane, the air pouch is an unsuitable model for the study of injury to joints or experimental arthritis.

Animals↗

PubMed1997

Study of microcirculation by coloured microspheres and NMR-microscopy in isolated rat heart: effect of ischaemia, endothelin-1 and endothelin-1 antagonist BQ 610.

Although the investigation of coronary microcirculation is of great importance, available methods have severe restrictions. They do not allow the study of vasodynamics of resistance vessels and microscopic conductance vessels simultaneously in the isolated beating rat heart. We now demonstrate that the combined measurement of perfusion which reflects the state of resistance vessels and cross-sections of microscopic conductance vessels is feasible in the model of the isolated constant flow perfused rat heart. Perfusion measurement was based on injection of coloured microspheres. Cross-sections of microscopic conductance vessels (diameter >140 micron) were determined by NMR-microscopy by flow weighted imaging. Both methods were established recently by our group. The combined measurement was applied to hearts which were subjected to ischaemia and reperfusion (group 1: n=5, 15 min ischaemia/group 2: n=7, 30 min ischaemia/measurements before ischaemia and 15/30 min after reperfusion), 200 pmol endothelin-1 bolus application (group 3: n=6/measurements before and 5 min after drug application), continuous infusion of the endothelin-1 antagonist BQ 610 (group 4: n=6/measurements before and 20 min after onset of infusion), and 200 pmol endothelin-1 application superimposed on 20 min of continuous BQ 610 infusion (group 5: n=7/combined measurement before BQ 610 infusion and 5 min after endothelin-1 application). In group 1, 15 min reperfusion restored the pre-ischaemic perfusion state, whereas conductance vessels were dilated (80.8+/-2.6%), after 30 min reperfusion pre-ischaemic conditions were also restored for conductance vessels. In group 2, a redistribution of perfusion from left ventricular endocardium to the right ventricular wall was observed. Post-ischaemic rhythm disturbances made NMR-imaging in this group impossible. In group 3, a shift of perfusion from the left ventricular myocardium to the right ventricular wall was observed. Similarly, the cross-section of left ventricular conductance vessels decreased (-32.6+/-2.1%), whereas size of right ventricular vessels increased. In group 4, BQ 610 had no effect on perfusion nor on vessel size and antagonized the effect of endothelin-1 on perfusion and vessel size in group 5.

Animals↗

PubMed1998

Inflammatory alterations in the myocardial microcirculation.

Inflammatory mechanisms are involved in the pathophysiology of cardiovascular disease and the present review focus us on the association between inflammation and microvascular endothelial dysfunction in the heart, i.e. reduced endothelium dependent vasodilation of coronary resistance vessels. This abnormality is caused by reduced bioactivity of nitric oxide (NO), and it is found in a variety of conditions, including ischemic heart disease, cardiac allograft vasculopathy, diabetes, hypercholesterolemia, and smoking. At the level of the myocardial microcirculation, reperfusion injury manifests itself as endothelial dysfunction, no-reflow, and increased permeability, which are all probably the result of reperfusion-induced augmentation of the inflammatory response. In other animal models of cardiovascular disease, inflammatory alterations have been described that can contribute to microvascular endothelial dysfunction and reactive oxygen species, neutrophils, tumour necrosis factor-alpha, and inducible NO synthase are among the mediators that have been incriminated. Circulating levels of inflammatory mediators may serve as molecular markers of cardiovascular disease, and antiinflammatory interventions hold some promise for future cardiovascular therapy.

Endothelium, Vascular↗

PubMed1995

Beta-adrenergic modulation of the collateral-dependent coronary microcirculation.

The effect of chronic, collateral-dependent perfusion on beta-adrenergic coronary microvascular responses was examined. Ameroid constrictors were placed on the proximal left circumflex (LCx) coronary artery in 16 pigs. In 8 pigs, heparinized saline containing vascular endothelial growth factor (VEGF) was administered into the perivascular space of the proximal LCx artery using an implanted osmotic pump. After 5-7 weeks, coronary arterial microvessels (70-150 microns) were studied in a pressurized (40 mm Hg) no-flow state with video-microscopy. beta-Adrenoceptor-mediated relaxations of isolated microvessels from the collateral-dependent LCx region to isoproterenol (P < 0.01) were markedly reduced, as were those to the adenylate cyclase activator forskolin (P < 0.01), compared to the respective response of vessels from the normally perfused left anterior descending artery region. Responses to the Gs-protein activator NaF showed a similar trend, but the differences were not significant. Chronic treatment with VEGF normalized responses to isoproterenol, NaF, and forskolin in the collateral-dependent LCx region. Blood flow in the LCx region increased in both control (P < 0.01) and VEGF-treated (P < 0.05) groups during rapid atrial pacing. The absolute increase in LCx blood flow was greater in the VEGF group than in the control group at rest (P < 0.05), but not during rapid pacing. Thus, beta-adrenergic microvascular relaxation is impaired in the collateral-dependent coronary microcirculation. The periadventitial delivery of VEGF improves myocardial perfusion to the collateral-dependent area and preserves beta-adrenergic-mediated relaxation of microvessels in the collateral-dependent myocardium.

Animals↗

PubMed1995

Superoxide dismutase attenuates effects of platelet-activating factor on gastric microcirculation.

This study examined the effect of Cu-Zn superoxide dismutase (SOD) on platelet-activating factor (PAF)-induced alterations of the gastric microcirculation. In separate experiments using an ex vivo canine gastric segment, changes in vascular resistance, filtration, and circulating neutrophil counts were measured during intra-arterial infusion of PAF (0.12 to 150 nM, n = 6) alone and with SOD (10 U/ml, n = 5). PAF produced dose-related increases in vascular resistance and filtration. SOD pretreatment attenuated changes in these measurements in response to 9 and 38 nM PAF. PAF also produced dose-related increases in the difference between arterial and venous neutrophil counts across the gastric segment. SOD significantly reduced this neutrophil flux at 0.5, 2, 9, and 38 nM PAF. Our results suggest that PAF causes both mucosal ischemia due to increased vascular resistance and microvascular injury as evidenced by increased filtration, as well as enhanced neutrophil adhesion to the microvasculature. The protective effects of SOD suggest that these responses to PAF involve the generation of oxygen-derived free radicals. In addition, these responses to PAF appear to be dependent upon circulating neutrophils.

Animals↗

PubMed1996

Effect of endotoxemia on intestinal villus microcirculation in rats.

Intestinal mucosal hypoperfusion with subsequent ischemia during endotoxemia might cause a breakdown of the gut barrier with translocation of bacteria and their toxins into the systemic circulation, thus maintaining a "gut-derived" septic state. The aim of this study was to investigate the influence of endotoxin on the microcirculation of intestinal villi, which represent the most vulnerable part of the mucosa. The changes in blood flow and in the diameters of the central villus arterioles located in the distal ileum were monitored in control rats without lipopolysaccharide (LPS) exposure (n=7), and in rats receiving 1.5 mg/kg b.w. LPS (n=7) or 15 mg/kg b.w. LPS (n=7) over 60 min. The blood flow and the arteriolar diameters were determined using in vivo videomicroscopy at baseline, and 60 min and 120 min later. In control animals, no change in blood flow and arteriolar diameters were observed during the entire experiment. Administration of 1.5 mg/kg b.w. LPS reduced the blood flow to 69.5 +/- 9.0% of the baseline value at the end of the study period. This decrease in blood flow was associated with a decrease in the villus arteriolar diameters by 17.4 +/- 2.5% from the baseline values. In animals exposed to 15 mg/kg b.w. LPS, the decrease in villus blood flow at 60 min was 64.8 +/- 10.9% of baseline, and at 120 min 66.9 +/- 12.6% of baseline. The diameters of the villus arterioles were reduced by 11.5 +/- 2.4% and 15.1 +/- 1.7%, respectively. In the control group and in the 1.5-mg/kg LPS group, the mean arterial blood pressure did not change during the entire study period. In the 15-mg/kg LPS group, the mean arterial pressure tended to decrease after 60 min. These data suggest a reduction of villus blood flow due to vasoconstriction in the central villus arterioles during normotensive endotoxmia, which might represent the mechanism for the mucosal ischemia observed in critically ill patients.

Animals↗

PubMed1996

The effect of gabexate mesilate on pancreatic and hepatic microcirculation in acute experimental pancreatitis in rats.

Microcirculatory derangements are important early features in many organs during the process of acute pancreatitis. However, dynamic evaluation of these factors has been difficult. Antiprotease has long been used for the treatment of acute pancreatitis, although its effects and mechanism have not been fully elucidated. The involvement of proteases and microcirculatory derangement early in the course of acute pancreatitis are the main concern of this study. A severe acute pancreatitis model in male Sprague-Dawley rats (225-275 g) was established by adding caerulein (15 microg/kg/ hr) in intravenous infusion fluid and intraductal injection of 0.1 ml glycodeoxycholic acid (5 mM). Gabexate mesilate [GM; ethyl-4-(6-guanidinohexanoyloxy)benzoate methanesulfonate], a synthetic antiprotease, was infused intravenously in doses of 0.01, 0.1, 1, and 10 mg as a therapeutic intervention in this model. Pathology hematocrit, serum amylase level, and glutamic-oxaloacetic transaminase (GOT) levels were used to confirm the severity of disease and effect of therapy. In vivo microscopic technique was used as a investigating tool in this study of microcirculatory derangement in pancreas and liver, 8 hr after induction of acute pancreatitis. GM can significantly improve pathologic criteria and changes of serum amylase levels in the range of 1-10 mg/kg/hr. The severity of changes of hematocrit and GOT was significantly lessened with GM in the range of 0.1-10 mg/kg/hr. This agent also could improve the microcirculatory environment in pancreas and liver after induction of acute pancreatitis according to the parameters, such as flow velocity and rolling leukocyte phenomenon, in the range of 1-10 mg/kg/hr. According to our observation, severity of hyperpermeability had not changed with the treatment of GM. These results indicated the beneficial effects of GM on pancreatic and hepatic microcirculation early in the course of acute pancreatitis. The beneficial effects were noted in serum parameters and hematocrit. The importance of protease activation and remote organ dysfunction is emphasized in the course of acute pancreatitis from this study.

Acute Disease↗

PubMed2000

Detrimental effects of octreotide on intestinal microcirculation.

BACKGROUND: Octreotide (OCT) is used for the protection of pancreato-intestinal anastomoses and for treatment of acute pancreatitis. Its effect on jejunal microcirculation after ischemia-reperfusion has not been investigated. MATERIAL AND METHODS: Intestinal ischemia was induced in Wistar rats (n = 8) by occlusion of the superior mesenteric artery for 40 min. Prior to reperfusion infusion of OCT (7.5 microgram/h) was started (n = 8). Microvascular perfusion of the jejunal mucosal and muscle layers was assessed and compared with that of groups without intervention (n = 16) by means of intravital microscopy. RESULTS: Ischemia-reperfusion decreased mucosal functional capillary density from 838.4 +/- 12.6 to 418.9 +/- 9.6 cm(-1). Mucosal capillary red blood cell velocity was reduced from 0.53 +/- 0.01 to 0.35 +/- 0.01 mm/s (P < 0.05). Permanent leukocyte adherence was increased. OCT without ischemia-reperfusion decreased functional capillary density (735.4 +/- 13.5 cm(-1)) and red blood cell velocity (0.46 +/- 0.01 mm/s). After reperfusion OCT led to perfusion heterogeneity demonstrated by villous stasis (26 +/- 4%) and a decrease in the index of mucosal perfusion (0.38 +/- 0.02). Functional capillary density was further decreased compared with ischemic controls (234.0 +/- 11.8 cm(-1)). Capillary red blood cell velocity was lower (0.30 +/- 0.01 mm/s) than in ischemic controls. CONCLUSIONS: OCT impairs microvascular perfusion of the jejunum both under physiological conditions and after ischemia-reperfusion.

Animals↗

PubMed2002

A compartmental model for oxygen transport in brain microcirculation in the presence of blood substitutes.

A compartmental model is developed for oxygen (O(2)) transport in brain microcirculation in the presence of blood substitutes (hemoglobin-based oxygen carriers). The cerebrovascular bed is represented as a series of vascular compartments, on the basis of diameters, surrounded by a tissue compartment. A mixture of red blood cells (RBC) and plasma/extracellular hemoglobin solution flows through the vascular bed from the arterioles through the capillaries to the venules. Oxygen is transported by convection in the vascular compartments and by diffusion in the surrounding tissue where it is utilized. Intravascular resistance and the diffusive loss of oxygen from the arterioles to the tissue are incorporated in the model. The model predicts that most of the O(2) transport occurs at the level of capillaries. Results computed from the present model in the presence of hemoglobin-based oxygen carriers are consistent with those obtained from the earlier validated model (Sharan et al., 1989, 1998a) on oxygen transport in brain circulation in the absence of extracellular hemoglobin. We have found that: (a) precapillary PO(2) gradients increase as PO(2) in the arterial blood increases, P(50 p) (oxygen tension at 50% saturation of hemoglobin with O(2) in plasma) decreases, i.e. O(2) affinity of the extracellular hemoglobin is increased, the flow rate of the mixture decreases, hematocrit decreases at constant flow, metabolic rate increases, and intravascular transport resistance in the arterioles is neglected; (b) precapillary PO(2) gradients are not sensitive to (i) intracapillary transport resistance, (ii) cooperativity (n(p)) of hemoglobin with oxygen in plasma, (iii) hemoglobin concentration in the plasma and (iv) hematocrit when accounting for viscosity variation in the flow; (c) tissue PO(2) is not sensitive to the variation of intravascular transport resistance in the arterioles. We also found that tissue PO(2) is a non-monotonic function of the Hill coefficient n(p) for the extracellular hemoglobin with a maximum occurring when n(p) equals the blood Hill coefficient. The results of the computations give estimates of the magnitudes of the increases in tissue PO(2) as arterial PO(2) increases,P(50 p) increases, flow rate increases, hematocrit increases, hemoglobin concentration in the plasma increases, metabolic rate decreases, the capillary mass transfer coefficient increases or the intracapillary transport resistance decreases.

Animals↗

PubMed1993

Pathophysiological characteristics of cutaneous microcirculation in patients with liver cirrhosis: relationships to cardiovascular hemodynamics and plasma neurohormonal factors.

To elucidate pathophysiological characteristics of the peripheral circulation in liver cirrhosis, cutaneous microcirculation was analyzed at the finger, palm, toe, and arch of the foot using laser Doppler spectroscopy in 19 patients with liver cirrhosis, and the results were correlated with cardiovascular hemodynamics (n = 10) and plasma neurohormonal factors (n = 8). Cutaneous blood flow at each area was all significantly reduced (P < 0.001, < 0.05, < 0.01, < 0.001, respectively) in patients with liver cirrhosis compared to those in normals (n = 20). Cutaneous blood mass was also significantly reduced (P < 0.05, < 0.01, < 0.001, respectively) except at the arch of foot in patients with liver cirrhosis. There were significant correlations between finger cutaneous blood flow and systemic vascular resistance (r = -0.73, P < 0.05), plasma norepinephrine level (r = -0.84, P < 0.01), plasma renin activity (r = -0.77, P < 0.01), plasma concentrations of aldosterone (r = -0.76, P < 0.05) and angiotensin II (r = -0.76, P < 0.05), between palm blood flow and plasma vasoactive intestinal polypeptide concentration (r = 0.83, P < 0.05). From these results and our previous data demonstrating increased forearm muscular blood flow in patients with liver cirrhosis, increases in arteriovenous anastomotic flow and the contribution of neurohormonal factors will represent pathophysiological mechanisms for these changes.

Adult↗

PubMed1993

Improvement of microcirculation abnormalities in sickle cell patients upon buflomedil treatment.

The efficacy of the vasoactive compound buflomedil on previously described microcirculation abnormalities observed in sickle cell disease (SCD) was investigated using bulbar conjunctival angioscopy (BCA) and laser doppler flux metering. Eleven sickle cell disease patients at steady state were studied in a double-blind randomized parallel-versus-placebo study (5 patients were given placebo and 6 patients received 600 mg buflomedil per day for 21 days after a washout period of 15 days). The blood flux score measured by BCA improved, indicating reduced entrapment of sickle red blood cells. There was a striking improvement of reactive alterations of vasomotion in the buflomedil group, particularly in postocclusive reactive hyperemia; the half return time was also significantly reduced. These results encourage further studies with buflomedil to investigate long-term effects of this compound in SCD, potential prevention of acute vaso-occlusive events, and degenerative complications.

Adult↗

PubMed1994

Responses of cutaneous microcirculation to cold exposure and neuropathy in vibration-induced white finger.

In order to clarify the mechanisms of cold temperature on vibration-induced white finger (VWF), three groups of forestry chain saw operators served as the subjects of this study. Groups I and II worked in a cold high-altitude area, and group III worked in a warm low mountain climate. Group I workers had VWF sign [VWF(+)] but groups II and III did not [VWF(-)]. In the present study, finger nailfold microcirculation before and after cold exposure, finger skin sympathetic alpha receptor response, and sympathetic skin response were measured. The results showed that there was no significantly different neuropathy in any of the groups. However, vibration-induced microcirculatory disturbances including blood stasis and red blood cell aggregation were more prominent in VWF(+) group, whereas both of the VWF(-) groups (groups II and III) had no significant difference in microcirculatory disturbances. This suggests that the severity of the microcirculatory disturbances is dose-effect correlated and is aggravated by cold in vibration syndrome. Thus it can be realized that a cold working environment is an important contributing factor in causing microcirculatory disturbances of VWF.

Altitude↗

PubMed1994

Intestinal microcirculation and leukocyte behavior in ischemia-reperfusion injury.

Polymorphonuclear leukocytes are thought to play a pivotal role in the generation of ischemia-reperfusion-induced mucosal injury; however, their behavior in the intestinal microvasculature following this injury has not been directly examined. In this study intravital microscopy was used to investigate the dynamics of blood flow and leukocyte behavior in the villus, serosal, and mesenteric microcirculation during ischemia-reperfusion in anesthetized hamsters. Thirty minutes of ischemia and 90 min of reperfusion resulted in almost complete microvascular stasis in the villi of control animals, whereas only a few serosal and mesenteric microvessels exhibited stasis. Following reperfusion, there was a significant increase in leukocyte accumulation in all three tissues; however, significantly fewer leukocytes adhered in the villus microvasculature than in the rest of either the mucosa, serosa, or mesentery. Treatment with gamma-hydroxybutyrate (GHB), a compound that we have previously demonstrated to be highly effective in preventing ischemia-reperfusion injury, significantly reduced both the microvascular stasis and leukocyte accumulation in all three vascular beds. This study demonstrates that there are significant differences in the response to ischemia-reperfusion in various intestinal layers and that areas most susceptible to damage are not necessarily those exhibiting the greatest leukocyte accumulation.

Animals↗

PubMed1995

A new fluorescence microscopy for tomographic observation of microcirculation by using dual-beam slit laser illumination.

By designing a new epi-illumination system with dual slit laser beams, we have developed a fluorescence microscope for tomographic observations of in vivo microcirculation. Two beams of an Argon ion laser were converted into thin slit beams of thickness 28 to 60 microns by optical lenses and were illuminated onto tissue to intersect at the focal plane of the objective. The fluorescent light emitted from a FITC tracer by this cross-illumination was picked up by the microscope through a filter, with no "out of focus" noise from the tracer above and below the crossing zone. The results of in vitro experiments by using glass micropipettes (20-80 microns i.d.) filled with FITC-dextran and skeletal muscle tissue certified uniform tracer excitation in the crossing zone and the augmentation of the beam thickness due to light scattering in the tissue to be 1.7 and 2.5 times at depths of 100 and 200 microns from the surface, respectively. In vivo tests in the rabbit tenuissimus muscle revealed that this system can realize microvasculature tomography, with adequate vertical zone selectivity and spatial resolution to reconstruct its three-dimensional mapping, and long-term monitoring of tracer leakage from a single capillary to the surrounding tissue, with sufficient quantitative reliability to determine the capillary permeability and its heterogeneity along the channel.

Animals↗

PubMed1996

Dynamic coherence analysis of vasomotion and flow motion in skeletal muscle microcirculation.

The aim of our study was to determine the cause of fluctuations in microvascular blood flow measured by laser Doppler perfusion monitoring (LDPM) in microvessels of the hamster skin fold preparation. LDPM flow fluctuations (flow motion) were compared to simultaneous records of diameter changes obtained from arterioles and venules. Time-varying coherence analysis was used to quantify the frequency of flow and diameter changes in awake hamsters in control conditions and during sodium nitroprusside-induced vasodilation. Power spectrum analysis of LDPM signals of order 4 and 3 arterioles indicated frequencies of 0.06 +/- 0.01 and 0.08 +/- 0.02 Hz, respectively. Order 3 arterioles exhibited significant temporal coherence between flow motion and vasomotion signals at a frequency of the order of 0.1 Hz. There was lack of coherence when vasomotion was absent in arterioles. Order 4 arterioles had several coherent frequencies in addition to that around 0.1 Hz. In conclusion, time-variant coherence analysis indicated that spontaneous fluctuations in flow are caused by vasomotion of order 3 arterioles with frequency around 0.1 Hz that appears to coordinate local control processes in the microcirculation. Additional frequency components present in LDPM signals are unrelated to vasomotion.

Animals↗

PubMed1997

Venular oscillatory flow during hemorrhagic shock and NO inhibition in hamster cheek pouch microcirculation.

Blood flow oscillations (flowmotion) during hemorrhagic shock (HS) were recorded with laser Doppler perfusion monitoring (LDPM) and red blood cell (RBC) velocimetry in arterioles and venules in hamster cheek pouch microcirculation. Experiments were carried out after baroceptor denervation or inhibition of nitric oxide (NO) synthesis with NG-monomethyl-L-arginine prior to and during HS. Flowmotion was characterized by spectral analysis with fast Fourier transform and autoregressive modeling. Low frequency flowmotion was detected in LDPM and RBC velocity tracings derived from arterioles while high frequency oscillations dominated in venules under baseline conditions. Venular blood flow was significantly higher compared with arteriolar flow during HS, while large amplitude low frequency flowmotion was found in venules but not in arterioles where dominated small amplitude high frequency oscillations coincident with respiratory or heart rates. Baroceptor denervation did not affect venular blood flow and low frequency flowmotion during HS. NO inhibition reduced significantly venular blood flow compared with control and abolished low frequency flowmotion in venules. High frequency oscillations remained in arterioles during HS. In conclusion, LDPM low frequency flowmotion was not originated by variations in the diameter of vessels, but corresponded to RBC velocity changes. A compensatory higher blood flow and concomitant low frequency flowmotion in venules appeared to be related to NO production during HS, independently of neural mechanism.

Animals↗

PubMed1998

Alpha adrenoceptors in the rabbit ear thermoregulatory microcirculation.

The rabbit ear microcirculation was analyzed in a chronic unanesthetized model to evaluate alpha adrenergic microvascular control in a thermoregulatory end organ. This model allowed direct measurement of microcirculatory responses without the effects of anesthetics or inflammatory responses induced by acute surgical intervention. The ipsilateral facial artery was catheterized for drug injections into the experimental ear. Microvascular diameter changes following stimulation or blockade of adrenoceptor (AR) subtypes were observed directly through a chronic microvascular chamber implanted in the rabbit ear. Vascular alpha1- and alpha2-ARs appear to be distributed differently across the arterioles and AVAs of the rabbit ear. Both alpha1- and alpha2-ARs appear to contribute to vasoconstriction of AVAs in the conscious rabbit ear. In contrast, alpha1-AR's (vs alpha2-ARs) appear to predominate in adrenergically mediated sympathetic vasoconstriction of arterioles.

Adrenergic alpha-Agonists↗

PubMed1998

In vivo measurement of morphometric and hemodynamic changes in the microcirculation during angiogenesis under chronic alpha1-adrenergic blocker treatment.

The effect of chronic administration of the alpha 1 blocker prazosin on microvascular angiogenesis was studied in rabbit ear chamber to investigate the role of concomitant increase in flow-oriented wall shear stress in vascular remodeling during angiogenesis. Rabbits were treated with prazosin hydrochloride (50 mg/liter in water) orally after ear chambers were installed. The microcirculation in the chamber was observed and recorded from 4 to 23 postoperative day (POD) by an intravital videomicroscope. The total vascular area (TA) were quantified as a morphometric parameter. Changes in wall shear stress in venules (20-40 micron ID) were calculated from flow velocity, vessel diameter, and in vivo blood viscosity. TA was significantly increased in the prazosin-treated animals. The levels of shear stress, which was increased 1.43 times by prazosin on 9 POD, gradually decreased toward the control level on 13 POD and they almost coincided on 21 POD. These findings experimentally provided supporting evidence that shear stress is probably involved in the adaptive response as one of mechanical factors regulating vascular remodeling during angiogenesis.

Adrenergic alpha-Antagonists↗