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PubMed1981

Classification of beta-adrenoceptors in the microcirculation of skeletal muscle.

Nervous and humoral beta-adrenergic, postjunctional effects on microvascular resistance, on precapillary sphincter tone, and on transcapillary fluid exchange in cat skeletal muscle (Lundvall & Järhult 1974, 1976 a, Lundvall & Hillman 1978 a, b) were evaluated with regard to the beta 1- or beta 2-specificity of the adrenoceptors. Marked beta 2-dilator responses but no significant beta 1-effects were observed. The conclusion was therefore reached that neurogenic as well as humoral beta-adrenergic control of the microcirculation in skeletal muscle is exerted via activation of beta 2-adrenoceptors.

Animals↗

PubMed1986

Testicular microcirculation in the rat studied by videophotometric capillaroscopy, fluorescence microscopy and laser Doppler flowmetry.

Testicular capillary blood flow was studied in rats using laser Doppler flowmetry, in vivo fluorescence microscopy and videophotometric capillaroscopy. All the methods revealed rhythmical oscillations in testicular microcirculation with a periodicity of 4-10 c.p.m. In arterioles, capillaries and small post-capillary vessels, periods of continuous blood flow alternated with periods of no or very low flow. No visible leakage of dextran-150 was observed from the testicular blood vessels. Four, 8 and 16 h after an s.c. injection of 200 IU hCG the blood flow was continuous and there was leakage of dextran-150 from the microvessels to the interstitial tissue. Twenty-four and 32 h after hCG the blood flow pattern was again rhythmical, and at 32 h there was no leakage of dextran-150. This suggests that hCG induces changes in blood flow and transvascular fluid exchange in the testis, perhaps by altering smooth muscle activity at the arteriolar-level.

Animals↗

PubMed1986

Effects of prostaglandin E1, E2 and 16,16-dimethyl-E2 on gastric mucosal microcirculation and basal acid output in the rat.

The effects of prostaglandins E1 (PGE1), E2 (PGE2) and 16,16-dimethyl-E2 (16,16-dm-PGE2) on the gastric mucosal microcirculation and (spontaneous) acid output were studied in anaesthetized rats. The superficial mucosal vessels were monitored on a TV screen using a microscope, TV camera and videorecorder for off-line analysis of red cell velocities (VRBC) and vessel diameters, from which the blood flow (QRBC) was calculated. The prostaglandins were either applied topically to the solution bathing the exposed mucosa or administered intravenously as a continuous infusion. Topical application of PGE1 (0.5 or 5 micrograms ml-1), PGE2 (5 or 50 micrograms ml-1) or 16,16-dm-PGE2 (0.005, 0.05 or 0.5 microgram ml-1) increased VRBC dose-dependently without altering acid output, except for the highest dose of PGE2 (50 micrograms ml-1) which inhibited acid output. The latter occurred in spite of a seven- to eight-fold increase in VRBC. Mucus secretion (evidenced by an impaired resolution of the TV image) also increased during topical application of the prostaglandins especially at higher doses. Intravenous PGE1, PGE2 (2.0 micrograms kg-1 min-1) or 16,16-dm-PGE2 (0.02 microgram kg-1 min-1) caused an initial and transient (5-10 min) fall in systemic arterial blood pressure and a decrease in VRBC and acid output. Intravenous 16,16-dm-PGE2 in a dose which did not affect secretion or systemic arterial blood pressure (0.002 microgram kg-1 min-1) still significantly reduced VRBC. Thus, topically applied PGE1, PGE2 or 16,16-dm-PGE2 dose-dependently increase VRBC while intravenous administration of the same prostaglandins reduce VRBC.

16,16-Dimethylprostaglandin E2↗

PubMed1999

Mechanisms of alterations in the microcirculation of the cochlea.

Labyrinthine function is tightly coupled to proper homeostasis. This includes appropriate blood flow that is under strict autoregulatory control. Perturbations in labyrinthine microcirculation can lead to significant cochlear and vestibular dysfunction. The etiology of many otologic disorders, including sudden sensorineural hearing loss, presbyacusis, noise-induced hearing loss, and certain vestibulopathies, are suspected of being related to alterations in blood flow. Some of the mechanisms responsible for hypoperfusion and possibly ischemia, within the cochlea, are addressed, with emphasis on the possibility that both noise and age contribute to localized low blood-flow states and stasis. This reduction in blood supply to the cochlea is likely, in part, responsible for reduced auditory sensitivity associated with chronic noise exposure and aging.

Age Factors↗

PubMed1986

Laser Doppler flowmetry: muscular microcirculation in anaesthetized horses.

Muscular microcirculation was studied in seven halothane anaesthetised horses in lateral recumbency using a laser Doppler flowmeter. A significant difference between the dependent and the uppermost triceps brachii was recorded. In the dependent muscles, microflow at first decreased and then increased up to the starting value. In the uppermost muscles, a significant rise of the microflow was measured.

Anesthesia, General↗

PubMed1975

The terminal hepatic microcirculation in the rat.

The hepatic microcirculation was observed microscopically in the transilluminated liver of the rat. The portal and hepatic venous microvessels were classified into four orders according to their branching hierarchy, and the hepatic sinusoids into branching, direct and interconnecting types according to their topographic arrangements. The diameters of the various orders of microvessels and types of sinusoids were measured by serial photomicrography, and the velocity of the erythrocytes in these various microvessels and sinusoids by the dual-slit photometric technique. The microvascular volume flows were calculated from these data. In both portal and hepatic venous systems, the erythrocyte velocity and the volume flow significantly decreased in successive orders of the microvessels in apparent relation to the cross-sectional areas. The diameters of the three types of sinusoids did not significantly differ, but the velocity of the erythrocytes in the direct sinusoid was significantly faster than that in the branching sinusoid while that in the inter-connecting sinusoid fluctuated widely.

Animals↗

PubMed1980

The arrangement of endocrine and exocrine pancreatic microcirculation observed in the living rabbit.

1. The microcirculation of the pancreas in the anaesthetized rabbit was examined by in vivo microscopy and micro-cinephotography. 2. The islets of Langerhans were identified by their appearance following the systemic injection of diphenylthiocarbazone. 3. Arterial injection of Evans blue demonstrated the arrangement of vessels within the pancreas. Blood leaving the islets passed via capillaries into the capillary meshwork; no islet was ever seen to be drained directly by a vein. 4. This significance of this portal arrangement is discussed.

Animals↗

PubMed1982

The influence of the sympathetic nervous system on individual vessels of the microcirculation of skeletal muscle of the rat.

1. Direct observations have been made on the responses of individual vessels of the microcirculation of rat spinotrapezius muscle to stimulation of the sympathetic paravascular nerve fibres and to topically applied catecholamines.2. All arteries and arterioles were constricted by sympathetic stimulation, the maximum response occurring at a stimulus frequency of 8-10 Hz. Primary and secondary arterioles (13-50 mum internal diameter) showed the greatest percentage change in diameter and remained constricted throughout the 1 min stimulation period whilst terminal arterioles (7-13 mum internal diameter) constricted initially but then returned towards their control diameter before the stimulus ceased.3. By contrast the venules and veins showed no response to sympathetic stimulation.4. In accord with these observations, fluorescence histochemical studies revealed a network of noradrenergic nerve fibres on all arterial vessels but showed no innervation of any venous vessels.5. Topically applied noradrenaline or adrenaline (10(-10)-10(-8) g/ml.) dilated the majority of arteries and arterioles while higher concentrations of either agent produced dose-dependent constrictor responses. In addition, many venules dilated in response to adrenaline (10(-9) g/ml.) while others constricted, but concentrations of either noradrenaline or adrenaline greater than 10(-8) g/ml. produced dose-dependent constriction of all venules and veins.6. The behaviour of the more proximal and more distal arterioles during sympathetic stimulation is in accord respectively with the changes in muscle vascular resistance and in capillary surface area recorded in previous studies during sympathetic stimulation.7. The observation that venous vessels are not influenced by sympathetic nerve fibres contrasts with the established view that venous vessels of skeletal muscle are strongly constricted during sympathetic stimulation. However, reappraisal of the evidence used to support this view indicates that such results may have been misinterpreted, while other available evidence supports the proposal that the present findings may be representative of skeletal muscle vasculature in general.

Adrenergic Fibers↗

PubMed1985

Direct observations of responses of mesenteric microcirculation of the rat to circulating noradrenaline.

The responses of mesenteric microcirculation of the rat to circulating noradrenaline were studied by in vivo microscopy, using a photo-electric device placed on a television monitor to measure changes in diameter of individual vessels. Blood flow was measured in the anterior mesenteric artery with an electromagnetic flow transducer, mesenteric vascular conductance was computed on-line from mesenteric artery flow and arterial pressure. I.V. injection of noradrenaline induced a decrease in diameter of arterioles (less than 30 microns) which began simultaneously with the rise in arterial pressure and averaged 15% at 15-20 s. By contrast small and principal arteries (30-40 microns and 80-350 microns respectively) generally showed a diameter increase which averaged 10% and began at the peak of the pressor response. Venules and veins (12-560 microns) showed a diameter decrease which averaged 12-15% at 25-30 s. Meanwhile mesenteric vascular conductance fell by 65-75% in 10 s and rose to 30-50% above control in 25-30 s. The diameter increases of small and principal arteries were not reflex dilator responses initiated by the rise in systemic arterial pressure, nor due to beta-adrenoreceptor stimulation. However, local application of phentolamine abolished responses of all sections of the vascular tree indicating that they all depended on activation of alpha-adrenoreceptors. During I.V. infusion of noradrenaline small arteries showed a maintained increase in diameter which began at the peak of the pressor response, while arterioles initially decreased in diameter but then relaxed, often attaining resting diameter before infusion ceased. Meanwhile mesenteric flow and conductance decreased transiently, but then returned to near control levels, i.e. 'autoregulatory escape' occurred. It is argued that noradrenaline induced alpha-mediated contraction of all sections of the vascular tree; the tendency of arteries to constrict was counteracted by the rise in intravascular pressure caused by arteriolar constriction, active constriction of venous vessels may have been augmented by passive collapse secondary to arteriolar constriction. The secondary relaxation of arterial vessels reflects an inherent property of their smooth muscle to relax from the constrictor influence of noradrenaline and is more marked in proximal than distal vessels. It is proposed that the initial decrease in mesenteric vascular conductance in response to circulating noradrenaline may be attributed to active constriction of distal arterioles and the secondary increase in conductance ('escape') to secondary relaxation of more proximal arterial vessels.

Animals↗

PubMed2002

ACh-induced endothelial NO synthase translocation, NO release and vasodilatation in the hamster microcirculation in vivo.

Studies in cultured cells show that activation of endothelial nitric oxide (NO) synthase (eNOS) requires the dissociation of this enzyme from its inhibitory association with caveolin-1 (Cav-1), and perhaps its translocation from plasma membrane caveolae to other cellular compartments. We investigated the hypothesis that in vivo NO-dependent vasodilatation is associated with the translocation of eNOS from the cell membrane. To this end, we applied ACh topically (10-100 microM for 10 min) to the hamster cheek pouch microcirculation and measured NO production, blood flow and vessel diameter, and assessed subcellular eNOS distribution by Western blotting. Baseline NO production was 54.4 +/- 5.2 pmol min(-1) (n = 16). ACh increased NO release, caused arteriolar and venular dilatation and elevated microvascular flow. These responses were inhibited by N(G)-nitro-L-arginine (30 microM). The maximal increase in NO production induced by 10 microM and 100 microM ACh was 45 +/- 20 % and 111 +/- 33 %, respectively; the corresponding blood flow increases were 50 +/- 10 % and 130 +/- 24 %, respectively (n = 4-6). Both responses followed a similar time course, although increases in NO preceded flow changes. In non-stimulated tissues, eNOS was distributed mainly in the microsomal fraction. ACh-induced vasodilatation was associated with eNOS translocation to the cytosolic and Golgi-enriched fractions. After 1.5, 3.0 or 6.0 min of application, 10 microM ACh decreased the level of membrane-bound eNOS by -13 +/- 4 %, -60 +/- 4 % and -19 +/- 17 %, respectively; at the same time points, 100 microM ACh reduced microsomal eNOS content by -38 +/- 9 %, -61 +/- 16 % and -40 +/- 18 %, respectively (n = 4-5). In all cases, microsomal Cav-1 content did not change. The close ACh concentration dependence and the concomitance between eNOS subcellular redistribution and NO release support the concept that eNOS translocation from the plasma membrane is part of an activation mechanism that induces NO-dependent vasodilatation in vivo.

Acetylcholine↗

PubMed2004

The microcirculation: a motor for the systemic inflammatory response and large vessel disease induced by hypercholesterolaemia?

There is abundant evidence that links hypercholesterolaemia to both vascular inflammation and atherogenesis. While atherosclerosis is a large vessel disease that is characterized by leucocyte infiltration and lipid deposition in the wall of lesion-prone arteries, the inflammatory response does not appear to be confined to these locations. There is evidence supporting a systemic inflammatory response that is characterized by endothelial cell activation in multiple vascular beds and the appearance of activated immune cells and a wide range of inflammatory mediators in blood. The mechanism(s) responsible for initiating this systemic response remain poorly defined, although several inciting factors have been proposed, including infectious agents and oxidative stress resulting from one or more of the cardiovascular risk factors (e.g. hypercholesterolaemia, hypertension). While cells within lesion-prone arteries are often inferred as the source of circulating inflammatory mediators during atherogenesis, the fact that endothelial cells throughout the vasculature are activated raises the possibility that the microvasculature (which encompasses a vast endothelial surface area) may contribute to creating the systemic inflammatory milieu that is linked to atherogenesis. This review addresses evidence that links the microvasculature to the inflammatory responses induced by hypercholesterolaemia and offers the hypothesis that inflammatory events initiated within the microcirculation may contribute to initiation and/or progression of large vessel disease.

Animals↗

PubMedDate not supplied

The Microcirculation Physiome Project.

Presented is a discussion of steps towards the creation of a database of the microcirculation encompassing anatomical and functional experimental data, and conceptual and computational models. The discussion includes issues of database utility, organization, data deposition, and linkage to other databases. The database will span levels from gene to tissue and will serve both research and educational purposes.

Animals↗

PubMedDate not supplied

Blood flow and leukocyte adhesiveness are reduced in the microcirculation of a peritoneal disseminated colon carcinoma.

Dynamic behavior of leukocytes in the microcirculation of solid tumor tissue was visualized using a fluorescent labeling technique combined with the use of a real-time confocal laser-scanning microscope (CLSM) system. Colon tumor cells (RCN-9) were inoculated into the peritoneal cavity of male Fischer 344 rats. Tumor-free rats were similarly injected with physiological saline (intraperitoneally). Ten days after tumor inoculation, the mesentery was exteriorized and subjected to vital microscopic observation under the CLSM system. Leukocytes were labeled with rhodamine 6G (100 microg kg(-1), intravenously), and their behavior within the microvessels (10-30 microm in diameter) was analyzed both in the solid tumor tissues and the normal mesentery. Wall shear rate was calculated from the measured values of vessel diameter and erythrocyte flow velocity. In tumor microvasculature of tumor-bearing rats, the centerline erythrocyte velocity (0.73 +/- 0.58 mm s(-1), mean +/- standard deviation) and wall shear rate (210 +/- 151 s(-1)) were significantly lower than those of the tumor-free rats (1.27 +/- 0.83 mm s(-1), 344 +/- 236 s(-1), respectively). Despite such reduced flow conditions, flux of the rolling leukocytes as well as density of the adhered leukocytes both decreased significantly in tumor microvasculature as compared with normal controls. The methods developed in this work show promise in improving our understanding of tumor biology and pathophysiology.

Adhesiveness↗

PubMed1998

Theoretical and experimental study of intermittent blood flows in microcirculation: application to the in-vivo determination of compliance.

A new theoretical approach was used to study the nonlinear response of a microvascular segment subjected to a pressure step at one end. The method is suitable for both large and small deformations of the vessel wall in the case of an elastic response of the segment. It is shown that the use of this simulation permits an indirect determination of the compliance of the vessel. The procedure is applied in two cases of major interest: first the in-vivo study of the intermittent blood flow in the microcirculation, and second, the analysis of experiments using micropipettes. The resulting values of the compliance agree with other values found in the previous studies. The theoretical method is particularly adapted to nonlinear equations.

Animals↗

PubMed1996

Interactions between electrical activity and cortical microcirculation revealed by imaging spectroscopy: implications for functional brain mapping.

Modern neuroimaging techniques use signals originating from microcirculation to map brain function. In this study, activity-dependent changes in oxyhemoglobin, deoxyhemoglobin, and light scattering were characterized by an imaging spectroscopy approach that offers high spatial, temporal, and spectral resolution. Sensory stimulation of cortical columns initiates tissue hypoxia and vascular responses that occur within the first 3 seconds and are highly localized to individual cortical columns. However, the later phase of the vascular response is less localized, spreading over distances of 3 to 5 millimeters.

Animals↗

PubMed1991

Retinal microcirculation in patients with diabetes mellitus: dynamic and morphological analysis of perifoveal capillary network.

The new scanning laser technique allows one to quantify the retinal microcirculation. A digital image analysing system was used to study capillary blood flow velocities and morphological parameters of perifoveal intercapillary areas and foveal avascular zones in normal and diabetic subjects. Diabetic patients showed a significant reduction in capillary blood cell velocities in comparison with normal subjects. Perifoveal intercapillary areas and foveal avascular zones were significantly increased in all stages of diabetic retinopathy, and both parameters increased with progressing diabetic retinopathy. Significant changes in the perifoveal intercapillary areas were observed between normal subjects and patients with no retinopathy.

Adult↗

PubMed2002

Inhibitory effect of losartan, an AT1 angiotensin II receptor antagonist, on increased leucocyte entrapment in retinal microcirculation of diabetic rats.

BACKGROUND: The effectiveness of losartan for the treatment of leucocyte entrapment in the retinal microcirculation of diabetic rats was evaluated quantitatively. METHODS: After diabetes was induced by injection of streptozotocin (STZ), the rats were divided into two subgroups. The first subgroup (n = 6), received no medications; the second subgroup (n = 6) was given fresh drinking water supplemented with losartan (5 mg/kg/day) for 4 weeks. Six rats that were not injected with STZ or given medications served as controls. 4 weeks after intervention, leucocyte dynamics in the retina were observed using acridine orange digital fluorography. Leucocyte entrapment in the retina was compared among the three groups. RESULTS: In the untreated diabetic rats, the number of trapped leucocytes (6.1 (SD 1.4) cells/mm(2)) increased significantly compared with control rats (2.8 (1.2) cells/mm(2); p = 0.005) and diabetic rats treated with losartan (3.1 (0.9) cells/mm(2); p = 0.0002). CONCLUSIONS: Losartan, an AT1 angiotensin II receptor antagonist, inhibited increased leucocyte entrapment in the diabetic retina. The authors demonstrated that losartan may have therapeutic efficacy in preventing development of diabetic retinopathy. Further clinical studies of the effect of the angiotensin receptor antagonist on preventing development of diabetic retinopathy are needed.

Acridine Orange↗

PubMed1972

The recovery of function and microcirculation in small intestinal loops following ischaemia.

Short loops of dog small intestine, filled with a buffered glucose solution, were subjected to one hour's total ischaemia by clamping the corresponding mesenteric artery and vein as well as the intestinal wall at each end of the loop. Immediately after the ischaemic period and 24 hours later, their functional capacity, together with that of neighbouring control loops, was determined by studying the absorption of phenylalanine and beta-methyl-glucoside in vitro and by measuring the levels of Na(+)-K(+)-ATPase in the mucosa. The release of lysosomal enzymes after the ischaemia was studied by gauging the levels of acid phosphatase in the venous blood draining the ischaemic loop. The state of the mucosal microcirculation was investigated by injection of indian ink into the mesenteric artery removal of the loop. Immediately after ischaemia, considerable structural damage was observed in the intestinal mucosa, with desquamation of the villous tips, oedema, vascular stasis, and haemorrhagic infiltration in the lamina propria. No dye was observed in the mucosal capillaries. All transport capacity was abolished, but ATPase levels were unchanged. A significant release of lysosomal enzymes into the venous blood was noted. One day later structural and functional recovery was complete, and vascularization of the villous core was restored.

Acid Phosphatase↗