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PubMed1995

Characterization of alpha 1-adrenoceptors mediating vasoconstriction to noradrenaline and nerve stimulation in the isolated perfused mesentery of rat.

1. The objective of this study was to investigate the alpha 1-adrenoceptor subtype(s) mediating vasoconstrictor responses to perfused and neuronally-released noradrenaline (NA) in the isolated perfused mesentery preparation of rat. 2. Isolated mesenteric preparations (with gut attached) from male Sprague Dawley rats (250-300g) were perfused via the superior mesenteric artery with oxygenated Krebs solution at approximately 6 ml min-1. The effects of antagonists on vasoconstrictor responses to either perfused (+/-)-NA or periarterial nerve stimulation (70 V, 2 ms pulse width, 10 s train) were determined. 3. Vasoconstrictor responses to perfused NA were antagonized by prazosin (pA2 = 9.3 +/- 0.1), WB4101 (pA2 = 9.6 +/- 0.1), 5-methyl urapidil (5-MU: pA2 = 9.0 +/- 0.1), (+)-niguldipine (insurmountable) and spiperone (pA2 = 7.7 +/- 0.1). The insurmountable nature of the antagonism by (+)-niguldipine (0.1 nM) was greatly reduced by co-perfusion with prazosin (10 nM). Chloroethylclonidine (CEC: 100 microM for 20 min, followed by 40 min washout) caused an approximate twofold increase in the EC50 for (+/-)-NA and reduced the maximum response by approximately 25%. Pre-treatment of tissues with CEC (100 microM as above) did not significantly alter affinity estimates for prazosin (pA2 = 9.2 +/- 0.1), WB4101 (pA2 = 9.3 +/- 0.1) or 5-MU (pA2 = 8.7 +/- 0.2). Vasoconstrictor responses to periarterial nerve stimulation were antagonized by WB4101 > 5-MU > prazosin >> spiperone. CEC (100 microM as above) reduced nerve-stimulated responses by approximately 50%. 4. The affinity estimates for the various antagonists studied suggest that vasoconstrictor responses to both exogenous and neuronally-released NA are mediated via the same a,-adrenoceptor subtype. The pharmacological profile most resembles the 'classical' alpha l A-adrenoceptor, which, in turn, appears to be a rat homologue of the cloned bovine alpha lc-adrenoceptor.

Adrenergic alpha-1 Receptor Agonists↗

PubMed2003

An experimental study on the vasoconstriction effect of calcium hydroxide using rat mesentery.

Calcium hyroxide has been used for eliminating persistent intracanal exudation. In order to address the mechanism behind this action, we investigated whether calcium hydroxide solutions cause the constriction of microvessels in the mesenteric microcirculation bed of rats. The exteriorised mesentery from anaesthetised rats was spread in a chamber, and arterioles, venules and capillaries were viewed under a digital microscope. Various concentrations of calcium hydroxide solutions were applied for 10 sec, and the diameter of the microvessels was recorded. In arterioles, calcium hydroxide solutions caused rapid and transient constriction. A statistically significant difference versus original diameter was detected 1 min after the application of 4.0 x 10(-3) mol/l and 1.0 x 10(-2) mol/l solutions (p < 0.05, one-way analysis of variance and Tukey-Kramer test). No statistically significant constriction occurred in capillaries and venules. It was concluded that the arteriolar constriction might be an explanation for the exudation-controlling effect of intracanal calcium hyroxide dressings.

Analysis of Variance↗

PubMed1989

Hydroxylamine dilates resistance blood vessels of the perfused rat kidney and mesentery.

Hydroxylamine (ED50 values, 47 +/- 8.9 nmol and 320 +/- 39 nmol) dilates resistance arterioles of the perfused noradrenaline-preconstricted rat kidney and mesentery. In this respect hydroxylamine was approximately 63x and 320x less potent than acetylcholine (ACh) and 15x and 128x less potent than nitroprusside in the two perfused organs studied. The vasodilator effect of hydroxylamine (unlike that of ACh) was unaffected by CHAPS de-endothelialization suggesting that its effect is independent of endothelium-derived relaxing factor (EDRF).

Acetylcholine↗

PubMed2001

Leukocyte rolling in rat mesentery venules: distribution of adhesion bonds and the effects of cytoactive agents.

A new method of analyzing in vivo measurements of leukocyte WBC rolling along venular endothelium (EC) has been developed to extract insightful information on the dynamics of WBC-EC bond formation and disruption. The rolling velocity of WBCs was obtained by intravital microscopy of rat mesenteric venules. For the "spontaneous" rolling observed following exteriorization of the mesentery, we estimated that the average distance between clusters of adhesion bonds which tether a rolling cell to the venular wall was about 2 microm, and that the average lifetime of a bond cluster at the trailing edge of the rolling cell, from its exposure to the tensile force to its release, was on the order of 0.05 s. Both the inter-cluster distance and the lifetime were significantly reduced by treatments with the chemoattractant N-formyl-methionyl-leucyl-phenylalanine and the cytokine interleukin-1, while the average lifetime of the stretched bond clusters was not significantly changed by treatment with the cytoskeleton-modifying agents cytochalasin B and colchicine. Each of the four treatments significantly reduced the heterogeneity in the cell rolling velocity, presumably by the selective recruitment of WBC subsets from the circulating WBC population or by a reduction in the heterogeneity of endothelial adhesiveness. These results were analyzed in the context of in vitro data in the literature on molecular bonds of cell adhesion. The findings suggest that, in the case of "spontaneous" rolling, there are on average approximately 2-3 clusters of adhesion bonds between a rolling cell and the vessel wall, and approximately five bonds in each cluster.

Animals↗

PubMed2005

Clostridium perfringens epsilon-toxin increases permeability of single perfused microvessels of rat mesentery.

Epsilon-toxin, the primary virulence factor of Clostridium perfringens type D, causes mortality in livestock, particularly sheep and goats, in which it induces an often-fatal enterotoxemia. It is believed to compromise the intestinal barrier and then enter the gut vasculature, from which it is carried systemically, causing widespread vascular endothelial damage and edema. Here we used single perfused venular microvessels in rat mesentery, which enabled direct observation of permeability properties of the in situ vascular wall during exposure to toxin. We determined the hydraulic conductivity (L(p)) of microvessels as a measure of the response to epsilon-toxin. We found that microvessels were highly sensitive to toxin. At 10 microg ml(-1) the L(p) increased irreversibly to more than 15 times the control value by 10 min. At 0.3 microg ml(-1) no increase in L(p) was observed for up to 90 min. The toxin-induced increase in L(p) was consistent with changes in ultrastructure of microvessels exposed to the toxin. Those microvessels exhibited gaps either between or through endothelial cells where perfusate had direct access to the basement membrane. Many endothelial cells appeared necrotic, highly attenuated, and with dense cytoplasm. We showed that epsilon-toxin, in a time- and dose-dependent manner, rapidly and irreversibly compromised the barrier function of venular microvessel endothelium. The results conformed to the hypothesis that epsilon-toxin interacts with vascular endothelial cells and increases the vessel wall permeability by direct damage of the endothelium.

Animals↗

PubMed2005

Effect of oxygen consumption by measuring method on PO2 transients associated with the passage of erythrocytes in capillaries of rat mesentery.

Mathematical models have predicted the existence of Po(2) gradients between erythrocytes in capillaries in the usual case where plasma contributes substantial resistance to oxygen diffusion. According to theoretical predictions, these gradients could be detected as rapid Po(2) fluctuations (erythrocyte-associated transients, EATs) along the capillary. However, verification of a model and correct choice of its parameters can be made only on the basis of direct experimental measurements. We used phosphorescence quenching microscopy to measure Po(2) in 52 capillaries of rat mesentery to obtain plasma Po(2) values 100 times/s at a given point along a capillary. A 532-nm laser generated 10-mus pulses of light, concentrated by a x100 objective, onto a spot 0.9 mum in diameter. The presence of erythrocytes in the excitation region was detected on the basis of phosphorescence amplitude (PA), proportional to the amount of plasma encountered by the laser beam, and on the basis of the intensity of transmitted laser light (LT), detected by a photodiode placed under the capillary. The data revealed correlated waveforms in PA, LT, and Po(2) in capillaries. The magnitude of the Po(2) gradients between erythrocytes and plasma was correlated with average capillary Po(2). EATs in Po(2) were more readily detected in capillaries with relatively low oxygenation. The correlation coefficients between PA and Po(2) for the half of the capillaries (n = 26) below the median Po(2) (mean Po(2) = 17 mmHg; R = -0.72) was higher than that for the other half (mean Po(2) = 39 mmHg; R = -0.38). These results support the theoretical predictions of EATs and plasma Po(2) gradients in capillaries.

Animals↗

PubMed2004

Disodium cromoglycate stabilizes mast cell degranulation while reducing the number of hemoglobin-induced microvascular leaks in rat mesentery.

Blood substitutes, such as diaspirin cross-linked Hb (DBBF-Hb), have been considered for use during blood transfusions. Unfortunately, bolus injection of modified Hb has been shown to rapidly increase the leakage of microvessels to plasma albumin. This effect may result from production of excess reactive oxygen species (ROS) and could be linked to the observed increase in degranulated mast cells (DMC). Disodium cromoglycate (cromolyn) stabilizes mast cells and therefore might minimize the venular permeability in the rat mesentery. In 10 anesthetized Sprague-Dawley rats, the mesenteric preparation was continuously suffused with cromolyn while the microvasculature was filled with DBBF-Hb solution (10 mg/ml) for 10 min. Six animals received cromolyn pretreatment [two intravascular injections over 30 min (experiment A)] and four animals received pretreatment with 2% HEPES-buffered saline (HBS)-BSA (experiment B). Two more animals were pretreated with HBS-BSA without DBBF-Hb infusion but with cromolyn suffusion (experiment C). Another set of experiments was performed on five animals without cromolyn suffusion or any pretreatment but with DBBF-Hb infusion (experiment D). All groups then received a 1-min perfusion of FITC-albumin, fixation for 60 min, and microscopic examination. Experiments A and B demonstrated a significant reduction in the number of venular leaks and DMC compared with experiment D, but not in the area of venular leaks. These results suggest mast cell degranulation is not a major contributor to microvascular leakage induced by DBBF-Hb.

Animals↗

PubMed2005

Erythrocyte-associated transients in PO2 revealed in capillaries of rat mesentery.

Mathematical models have predicted the existence of Po(2) gradients between erythrocytes in capillaries in the usual case where plasma contributes substantial resistance to oxygen diffusion. According to theoretical predictions, these gradients could be detected as rapid Po(2) fluctuations (erythrocyte-associated transients, EATs) along the capillary. However, verification of a model and correct choice of its parameters can be made only on the basis of direct experimental measurements. We used phosphorescence quenching microscopy to measure Po(2) in 52 capillaries of rat mesentery to obtain plasma Po(2) values 100 times/s at a given point along a capillary. A 532-nm laser generated 10-micros pulses of light, concentrated by a x100 objective, onto a spot 0.9 microm in diameter. The presence of erythrocytes in the excitation region was detected on the basis of phosphorescence amplitude (PA), proportional to the amount of plasma encountered by the laser beam, and on the basis of the intensity of transmitted laser light (LT), detected by a photodiode placed under the capillary. The data revealed correlated waveforms in PA, LT, and Po(2) in capillaries. The magnitude of the Po(2) gradients between erythrocytes and plasma was correlated with average capillary Po(2). EATs in Po(2) were more readily detected in capillaries with relatively low oxygenation. The correlation coefficients between PA and Po(2) for the half of the capillaries (n = 26) below the median Po(2) (mean Po(2) = 17 mmHg; R = -0.72) was higher than that for the other half (mean Po(2) = 39 mmHg; R = -0.38). These results support the theoretical predictions of EATs and plasma Po(2) gradients in capillaries.

Animals↗

PubMed1991

Sulfated polysaccharides inhibit leukocyte rolling in rabbit mesentery venules.

Before firm adhesion, leukocytes roll slowly along the walls of small venules at velocities ranging from 0.7 to 36% of mean blood flow velocity. To investigate the nature of the adhesive process underlying leukocyte rolling, synthetic (dextran sulfate) and naturally occurring sulfated polysaccharides (heparin, chondroitin sulfates, keratan sulfate, and heparan sulfate) were infused via glass micropipettes into the lumen of small venules (20-60 microns diam) of the rabbit mesentery. Leukocyte rolling was observed and quantified using both transmitted light and incident fluorescence intravital microscopy. Rolling leukocytes accounted for 27-80% of total leukocyte flux, exhibiting a wide range of individual velocities (0.01-0.84 mm/s) with a mean value of 4% of centerline velocity. Dextran sulfate (Mr 500,000) inhibited leukocyte rolling very effectively [half-effective concentration (ED50) approximately 10 micrograms/ml] and was able to almost completely abolish rolling at 500 micrograms/ml. Heparin (ED50 approximately 50 micrograms/ml), chondroitin 6-sulfate C (ED50 approximately 500 micrograms/ml), and heparan sulfate (ED50 approximately 5 mg/ml) also reduced leukocyte rolling. At 5 mg/ml, chondroitin 4-sulfate B (dermatan sulfate) was marginally effective, but chondroitin 4-sulfate A and keratan sulfate were ineffective. The present data suggest that an adhesion receptor-ligand system distinct from the leukocyte integrins may be underlying transient leukocyte adhesion (rolling). Endothelial glycoproteins or proteoglycans containing sulfated side chains may be involved in mediating this adhesive process.

Animals↗

PubMed1994

Endothelial actin cytoskeleton in rat mesentery microvasculature.

The actin cytoskeleton plays a key role in maintaining and modulating cellular morphology and thus is important in various aspects of endothelial cell function, yet few studies to date have studied the endothelial actin cytoskeleton in the microvasculature, where many of the specialized endothelial functions take place. We developed a method to fix and stain the microvasculature of the rat mesentery under physiological conditions and used a confocal microscope to observe the pattern of actin filaments in individual endothelial cells throughout the intact vascular network. We observed several distinct patterns of actin filaments in the endothelial cells depending on the caliber and type of vessel. The endothelial cells of large arterioles and venules (> 50 microns in diameter) displayed a prominent circumferential rim of actin, with few central actin fibers. Endothelium of midsized (20-50 microns) arterioles (and some midsized venules) displayed prominent abluminal actin fibers across the central portion of the cell, aligned parallel to the longitudinal axis of the vessel, in addition to a peripheral rim of actin. The endothelium of capillaries contained few actin fibers but instead typically displayed diffuse staining throughout the cell. The endothelial cells in the postcapillary venules generally displayed a thin peripheral rim of actin and occasional short central fibers. These results indicate that the local environment dictates the actin pattern in endothelial cells and suggests that specialized endothelial function is correlated with specialized endothelial actin architecture.

Actins↗

PubMed1999

Modified hemoglobins produce venular interendothelial gaps and albumin leakage in the rat mesentery.

Cross-linked hemoglobin (alphaalpha-Hb) and polyethylene glycol (PEG)-conjugated Hb have both been considered as possible "blood substitutes." Previously, we showed that PEG-Hb extravasates rapidly in the intestinal mucosa and causes transient epithelial sloughing, resulting in temporary opening of the intestinal epithelial barrier. In the present study, the rat mesenteric preparation was used to quantify the effects of the two Hbs on microvascular leakage to albumin and to investigate possible changes in the integrity of the interendothelial cell junctions and the endothelial actin cytoskeleton. In anesthetized Sprague-Dawley rats, the microvasculature of a mesenteric window was perfused with HEPES-buffered saline (HBS) containing 0.5 mg/ml BSA and 2 mg/ml alphaalpha-Hb (n = 16) or PEG-Hb (n = 5) for 2 or 10 min. Controls (n = 4) just received HBS-BSA. In some experiments (n = 9 for alphaalpha-Hb; n = 5 for PEG-Hb), the perfusate was then replaced by FITC-albumin in HBS-BSA for the next 3 min. The vasculature was then perfusion fixed, stained for filamentous actin and for mast cells, and viewed microscopically. In the remaining experiments, the mesenteric microvasculature was stained with silver nitrate to determine the number of endothelial junctional gaps per length of venules. Both Hbs increased the number and area of leaks per micrometer of venular length compared with control, but alphaalpha-Hb increased to a greater extent than PEG-Hb. Formation of leaks was accompanied by changes in the endothelial actin cytoskeleton and by an increased number of endothelial gaps. Mast cell degranulation was significantly greater (P < 0.05) in Hb-treated preparations compared with controls, but there was no direct correlation between sites of degranulation and albumin leakage. These Hbs appear to induce venular leakage in the mesentery by mechanisms similar to those previously observed after treatment with histamine or nitric oxide synthase inhibitors.

Actins↗

PubMed2000

Influence of erythrocyte aggregation on leukocyte margination in postcapillary venules of rat mesentery.

The role of erythrocyte (red blood cell; RBC) aggregation in affecting leukocyte (white blood cell; WBC) margination in postcapillary venules of the mesentery (rat) was explored by direct intravital microscopy. Optical techniques were refined and applied to relate the light-scattering properties of RBCs to obtain a quantitative index of aggregate size (G), which, under idealized conditions, represents the number of RBCs per aggregate. WBC margination, defined as the radial migration of WBCs to the venular wall and their subsequent rolling along the endothelium, was measured as the percentage of the potentially maximal WBC volumetric flux within the microvessel lumen (F(WBC)(*)). In normal blood, F(WBC)(*) increased exponentially fourfold, and G increased from 1 to 1.15 as wall shear rates () were reduced from a steady-state value of approximately 600 to <100 s(-1) by proximal occlusion with a blunt microprobe. Enhancement of aggregation by infusion (iv) of dextran 500 (428 kDa), to attain a systemic concentration of 3 g/100 ml, resulted in a four- and sevenfold increase in G and F(WBC)(*), respectively, as was reduced below 100 s(-1). Inhibition of RBC aggregation by infusion of dextran 40 (37.5 kDa) caused F(WBC)(*) to fall to one-half of its steady-state level for < 100 s(-1). Thus it appears that the well-known increase of WBC margination with reductions in is strongly dependent on the occurrence of RBC aggregation. Increasing the extent of RBC aggregation during reductions in also increased the firm adhesion of WBCs to the endothelium because of an enhanced probability of contact between leukocytes and the postcapillary venular wall.

Animals↗

PubMed1975

Haemostatic plug formation and stability in the rabbit mesentery after femoral fracture.

The effect of standardised trauma (femoral fracture) on the formation time and stability of haemostatic plugs in transected microvessels of the rabbit mesentery was studied in relation to alterations in fibrinogen concentration, platelet count, platelet adhesiveness, and haematocrit. In contrast to most other studies, platelet adhesiveness as a percentage was found to decrease post-traumatically. One week after trauma, the haemostatic plugs were maximally stable and at the same time venular haemostatic plug formation time was significantly reduced. These findings coincide with high levels of fibrinogen and increased numbers of circulating adhesive platelets.

Animals↗

PubMedDate not supplied

Characterization of postsynaptic alpha-adrenergic receptors by [3H]-dihydroergocryptine binding in muscular arteries from the rat mesentery.

Alpha-adrenergic receptors are likely to be important determinants of the effects of catecholamines on vascular resistance. To study the alpha-adrenergic receptor in muscular arteries of the type that determine vascular resistance, we characterized and quantitated alpha-adrenergic receptors in a particulate fraction of the highly reactive, richly innervated arteries of the rat mesentery. With the ligand [3H]-dihydroergocryptine ([3H]-DHEC), specific binding (displaceable by 5 microM phentolamine) is saturable. There is a single class of binding sites with a dissociation constant (Kd) of 2.9 nM and a maximal binding capacity of 68 fmoles of [3H]-DHEC per mg of particulate fraction protein. Catecholamines compete for [3H]-DHEC binding stereospecifically and with the alpha-adrenergic potency series of (-)epinephrine greater than (-)norepinephrine greater than (-)isoproterenol. Binding is rapid (t 1/2 less than or equal to 2 mins) and rapidly reversible (t 1/2 less than or equal to 2 mins). Inhibition of [3H]-DHEC binding by the alpha-adrenergic antagonist phentolamine (Kd = 3.0 nM) is much greater than by the beta-adrenergic antagonist propranolol (Kd = 8200 nM). The alpha 1-selective antagonist prazosin (Kd = 63 nM) is 20 times more potent in competing for [3H]-DHEC binding than is the alpha 2-selective antagonist yohimbine (Kd = 1250 nM), thus suggesting that the alpha-adrenergic receptor identified is predominantly of the alpha 1 subtype that is responsible for vascular smooth muscle contraction. This extension of radioligand binding techniques to highly innervated muscular arteries of the type contributing to vascular resistance will allow the study of the role of the vascular alpha-adrenergic receptor in various physiologic states and models of hypertension.

Adrenergic alpha-Antagonists↗

PubMed1990

Effect of wall shear rate on thrombogenesis in microvessels of the rat mesentery.

The role of hemodynamics on platelet thrombus formation was studied in venules and arterioles of the rat mesentery. Thrombus formation was induced by the fluorescent dye/light method for examination of the following factors: 1) the effect of wall shear rate on thrombus initiation, 2) the effect of wall shear rate on the growth of thrombi, and 3) the relation between platelet thrombus initiation and intraluminal velocity profile. The range of wall shear rate was up to approximately 1,000 1/sec in venules and from 640 to 2,900 1/sec in arterioles. Platelet thrombus initiation occurred more rapidly at higher wall shear rate in venules and at lower wall shear rate in arterioles. Thrombus initiation time was shortest around a wall shear rate of 900 1/sec in venules and around 700 1/sec in arterioles. Thrombus growth rate in venules was greatest at a wall shear rate of 1,500-2,000 1/sec. Thrombus initiation and its relation to blood flow was also examined in branched and curved microvessels. In these vessels platelet thrombi were also first initiated at the sites of higher wall shear rate in venules and of lower wall shear rate in arterioles.

Animals↗

PubMed2004

Isoflurane pretreatment supports hemodynamics and leukocyte rolling velocities in rat mesentery during lipopolysaccharide-induced inflammation.

UNLABELLED: We hypothesized that the protective effects of isoflurane (ISO) pretreatment on the vasculature may be attributed, in part, to altered leukocyte-endothelial interactions. Rats were anesthetized with pentobarbital and then randomized into four groups: control, ISO-control (pretreatment with 30 min of 1.4% ISO), lipopolysaccharide (LPS; 10 mg/kg IV), and ISO-LPS (ISO pretreatment and then LPS). The mesentery was prepared for intravital videomicroscopy. Mean arterial blood pressure (MAP), along with microcirculatory variables that included postcapillary venular and arteriolar blood flow velocity and leukocyte dynamics (number of rolling and adherent leukocytes and individual rolling leukocyte velocities), were measured hourly (baseline and at 0-4 h). In LPS rats, ISO pretreatment significantly (P < 0.05) attenuated the decrease in MAP at 2 and 4 h after LPS and increased leukocyte rolling velocities after 2-4 h. Four hours after LPS, leukocyte rolling velocities were >200% more rapid (63.7 +/- 27.6 microm/s versus 19.8 +/- 6.4 micro m/s) in ISO-LPS versus LPS rats. In control rats, ISO pretreatment had no effect on MAP or leukocyte rolling velocities but increased the number of rolling leukocytes. ISO pretreatment had no effect on arteriolar and postcapillary venular blood flow velocity in LPS rats or leukocyte adherence in LPS or control rats. In conclusion, ISO pretreatment supported hemodynamics and increased leukocyte rolling velocities but did not alter the number of rolling or adherent leukocytes in the mesenteric microcirculation during LPS-induced inflammation. IMPLICATIONS: Isoflurane pretreatment supported hemodynamics and increased leukocyte rolling velocities in the mesenteric microcirculation during lipopolysaccharide-induced inflammation. Faster rolling velocities may reduce the incidence of inflammation by decreasing leukocyte-endothelial interactions and cellular injury.

Anesthetics, Inhalation↗

PubMed1991

Propagation properties of vasomotion at terminal arterioles and precapillaries in the rabbit mesentery.

A vasomotion activity in the mesentery of anesthetized rabbits were studied by simultaneous measurements of inside diameters at multiple sites in arterioles, precapillaries and their bifurcations. A frame-by-frame diameter determination technique was used with a microcomputer-assisted laser video disk recorder and video-image analysis system. Simultaneous intensity profiles across microvessels were continuously obtained. Applying an automatic wall surface tracer and a graphic editor to construct temporal sequences of intensity profiles, we obtained digitized data of inside diameters of microvessels, and implemented cross-correlation analysis between data sets to calculate phase differences of vasomotion at separated sites. The present analysis of the propagation of vasomotion showed that the vasomotion originated from the orifice of precapillaries at the bifurcations, spreading downstream in the precapillary. The vasomotion wave spreads both upstream and downstream along single arterioles from various origins of the vasomotion activity. The propagation velocity of vasomotion was 0.17 +/- 0.03 mm/sec (n = 19), and it became significantly slower through the branching points than along the arterioles. It is suggested that the vasomotion in terminal arterioles and precapillaries may spread through some mechanical transmission factors.

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↗