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PubMedDate not supplied

Altered skin microcirculation in patients with systemic lupus erythematosus.

Although microvasculitis is one of the more common manifestations of systemic lupus erythematosus, there is no data on the hemodynamics of the skin microcirculation in such patients. The combination of dynamic capillaroscopy measuring capillary blood cell velocity (CBV) and laser Doppler fluxmetry (LDF) was used to simultaneously evaluate the nutritional and the total skin microcirculation in the fingers of 24 consecutive patients with SLE, using normal matched subjects as controls. The nutritional skin flow, as assessed by the CBV, was significantly impaired in patients, as compared with controls, both at rest (p = 0.001) and during postocclusive reactive hyperemia (p = 0.006). By contrast, no differences were observed in total skin microcirculation, as assessed by LDF (n.s.). There was no significant correlation between hemodynamic parameters and the presence of Raynaud's phenomenon, morphological capillary changes or anticardiolipine antibodies. There was no correlation between the magnitude of the alteration of the capillary blood flow and capillary morphological abnormalities, suggesting that the microvascular damage might be caused by different pathophysiological mechanisms.

Adolescent↗

PubMed1991

Functional distribution of alpha 1- and alpha 2-adrenergic receptors in the coronary microcirculation.

BACKGROUND: The goal of this study was to determine the functional distribution of alpha 1- and alpha 2-adrenergic receptors in the epicardial coronary microcirculation. This goal was accomplished by intracoronary administration of the selective alpha 1-adrenergic agonist phenylephrine and the selective alpha 2-adrenergic agonist BHT-933 during measurements of coronary microvascular diameters in the beating heart. METHODS AND RESULTS: Experimental measurements were made under conditions with intact vasomotor tone and during coronary hypoperfusion (i.e., under conditions with autoregulatory mechanisms intact and blunted, respectively). Administration of selective alpha 1- and alpha 2-adrenergic antagonists, prazosin and SKF 104078, respectively, confirmed that the agonists were preferentially activating the desired adrenergic receptor subtype because the vasoconstrictor effects of the agonists were completely blocked by the appropriate antagonist. With baseline coronary vasomotor tone intact, phenylephrine caused constriction (8 +/- 3% decrease in diameter, p less than 0.05) of small coronary arteries (vessels greater than 100 microns in diameter) but did not produce constriction of coronary arterioles (vessels less than 100 microns in diameter). During coronary hypoperfusion, phenylephrine caused constriction (p less than 0.05) of both small coronary arteries and arterioles, 6 +/- 2% and 11 +/- 3% decreases in diameter, respectively. BHT-933 did not cause significant changes in microvascular diameters under control conditions but substantially and selectively decreased arteriolar diameters during hypoperfusion (24 +/- 6% decrease in diameter, p less than 0.05). CONCLUSIONS: In the intact, autoregulating coronary circulation, coronary arterioles escape from the effects of adrenergic activation but coronary arteries do not; rather, they can exhibit alpha 1-adrenergic coronary vasoconstriction. During coronary hypoperfusion, when autoregulatory adjustments are blunted, coronary arterioles are sensitive to both alpha 1- and alpha 2-adrenergic agonists, demonstrating significant constrictor responses. Also, the magnitude of coronary alpha 2-adrenergic arteriolar constriction (24% decrease in diameter) is significantly greater than that of alpha 2-adrenergic constriction (11% decrease in diameter) (p less than 0.05). Thus, alpha 1- and alpha 2-adrenergic activation produce different constrictor effects in the coronary microcirculation under baseline conditions when autoregulatory adjustments are intact and during coronary hypoperfusion when autoregulation is blunted. The data suggest that alpha 2-adrenergic receptors are preferentially distributed in arterioles, whereas alpha 1-adrenergic receptors are located throughout the coronary microcirculation. Importantly, the data also suggest that intrinsic autoregulatory adjustments in tone (i.e., autoregulatory escape) can override either alpha 1- or alpha 2-adrenergic constriction in coronary arterioles.

Adrenergic alpha-Agonists↗

PubMed1998

Decreased coronary flow reserve in hypertrophic cardiomyopathy is related to remodeling of the coronary microcirculation.

BACKGROUND: Ischemia occurs frequently in hypertrophic cardiomyopathy (HCM) without evidence of epicardial stenosis. This study evaluates the hypothesis that the occurrence of ischemia in HCM is related to remodeling of the coronary microcirculation. METHODS AND RESULTS: End-diastolic septal wall thickness was significantly increased in patients with HCM (25.8+/-2.9 mm) in comparison with cardiac transplant recipients (control subjects: 11.4+/-3.0 mm; P<0.05). Although the diameter of the left anterior descending coronary artery was similar in both groups (3.0+/-0.8 versus 3.0+/-0.5 mm, P=NS), the coronary resistance reserve (CRR=CRRbasal/CRRhyperemic), corrected for extravascular compression (end-diastolic left ventricular pressure), was reduced to 1.5+/-0.6 in HCM (P<.05; control, 2.6+/-0.8). Arteriolar lumen (AL) divided by wall area was lower in HCM (21+/-5% versus 30+/-4%; P<.05), and capillary density tended to decrease (from 1824+/-424 to 1445+/-513 per mm2, P=.11) in HCM. CRR was linearly related to normalized AL according to the formula CRR=O.1 AL-0.45 (r=.57; P<.05). Further analysis revealed that CRR, AL, and capillary density were all linearly related to the degree of hypertrophy. CONCLUSIONS: Decrements in CRR were related to changes of the coronary microcirculation. Both the decrease in CRR and these changes in the coronary microcirculation were related to the degree of hypertrophy. All these factors might contribute to the well-known occurrence of ischemia in this patient group.

Adult↗

PubMed1989

The behavior of sonicated albumin microbubbles within the microcirculation: a basis for their use during myocardial contrast echocardiography.

The purpose of this study was to determine whether the behavior of sonicated albumin microbubbles accurately mimics red blood cell flow in the microcirculation and is thus consistent with their use as in vivo tracers of red blood cell flow during myocardial contrast echocardiography. Accordingly, microbubbles prepared from fluorescein-conjugated albumin and fluorescently labeled red blood cells were injected intravascularly in eight golden hamsters. Their intravascular distribution, velocities, arteriolar-to-venular transit and flux ratios at branch points were determined in the microcirculation of the cheek pouch. Albumin microbubbles (mean diameter, 4.9 +/- 3.6 microns) and red blood cells displayed a similar frequency of distribution across the arteriolar lumen (33% in the central 20% of the arterioles), and their arteriolar velocities were also similar (2.5 +/- 0.7 mm/sec and 2.3 +/- 0.7 mm/sec,p = NS). The mean velocities of microbubbles correlated well with those of red blood cells at baseline and after adenosine application (r = 0.97 and r = 0.89, respectively), as did the calculated maximum velocity (r = 0.98 and r = 0.80, baseline and adenosine, respectively). The velocity profiles across the lumen of the vessels for albumin microbubbles and red blood cells were similar at baseline and after adenosine-induced velocity changes. The flux ratios at branch points also correlated well (r = 0.92, p less than 0.001). Arteriolar-to-venular transit times of albumin microbubbles were similar to those of red blood cells in vessels ranging in size from 22 microns to 45 microns. We conclude that the behavior of albumin microbubbles in the microcirculation mimics that of red blood cells and supports their use as intravascular tracers of red blood cell flow during myocardial contrast echocardiography.

Animals↗

PubMed1994

Contrasting effects of vecuronium and succinylcholine on the renal microcirculation in rodents.

We assessed the effects of succinylcholine and vecuronium on renal function and on the renal microcirculation in a rodent model. Vecuronium (0.02 mg/kg followed by 0.2 mg.kg-1 x h-1) caused a significant decrease of 16.1% +/- 3.87% in inulin clearance from 0.92 +/- 0.07 to 0.71 +/- 0.05 mL.min-1 x gKW-1 (gram of kidney weight), and a decrease in para-aminohippuric acid clearance by 21.6% +/- 4.69% from 1.58 +/- 0.26 to 1.31 +/- 0.20 mL.min-1 x gKW-1 (P < 0.05), whereas succinylcholine (0.45 mg/kg followed by 2 mg.kg-1 x h-1) altered neither. The effect of these muscle relaxants was also determined on the renal microcirculation in separate experiments using videomicroscopy. Succinylcholine (n = 10; 10(-10) to 10(-6) M) and its parent compound, acetylcholine (n = 10, 10(-10) to 10(-6) M) used as a control, caused a significant vasodilation from baseline diameter in the interlobular, afferent, and efferent arterioles. The vasodilation caused by succinylcholine was significantly less than that observed with acetylcholine. Atropine blocked the response to succinylcholine, indicating the latter has a muscarinic effect. In contrast, vecuronium caused a significant, selective vasoconstriction from baseline diameter in the preglomerular vessels, but not in the postglomerular vessels. The vasoconstriction caused by vecuronium was significantly different than the vasodilation caused by succinylcholine. The preglomerular vasoconstriction observed with vecuronium may contribute to the decrease in renal plasma flow and glomerular filtration rate observed experimentally. The choice of a neuromuscular blocking drug can therefore have the potential to influence renal function by altering the renal microcirculation.

Animals↗

PubMed1994

[Observation of the rat gastric mucosal microcirculation by vital-microscopy].

The greater curvature of the stomach of fasted rats was cut under urethane anesthesia (1.25 g/kg, i.p.). The dorsal side of the glandular stomach was fixed in a plastic chamber by facing the mucosal side to the chamber and perfused with warm Tyrode solution at 37 degrees C. A window made by partial removal of the serosa, the muscularis externa and the submucosa allowed us to observe the basal part of the mucosal microcirculation through the muscularis mucosae. Images of the microcirculation were transmitted through a TV camera to a TV monitor screen and recorded on videotapes by a videotape-recorder. The diameters of the arterioles, collecting venules and venules were measured by an image analyzer. Arterioles, running along the muscularis mucosae, responded to acetylcholine and epinephrine applied on the window, by dilatation and constriction, respectively, but the collecting venules and venules showed no changes in diameter. Application of 50% ethanol on the mucosal side caused dilatation of the arterioles and constriction of the collecting venules and venules. This method may be useful for analyzing the mechanisms of gastric mucosal injury and those of the effects of vasoactive agents on the gastric mucosal microcirculation.

Animals↗

PubMed1994

Visualization of renal microcirculation in isolated Munich-Wistar rat kidneys: effects of endothelin-1 on renal hemodynamic activity.

The aim of the present study was to visualize the superficial glomeruli of the Munich-Wistar (MW) rat and to characterize the responses of the renal microvasculature to endothelin-1 (ET-1). We first examined the distribution of superficial glomeruli of the MW rat compared to that in a control strain (Wistar rat). Secondly, we examined the effects of ET-1 on the renal microcirculation of the MW rat. The right kidney was perfused with a Krebs-Ringer solution containing fluorescein isothiocyanate dextran (FITC-dextran) and was visualized under an epi-illuminated fluorescence microscope system. Changes in perfusion pressure and diameter of the microvessels accompanying the administration of ET-1 (10 fmole-300 pmole) were measured. The number of superficial glomeruli was greater in the MW rat than in the Wistar rat. ET-1 had long-lasting and dose-dependent pressor effects. Perfusion pressure showed a 3.5-fold increase compared with the control, and the afferent arterioles showed greater dose-dependent vasoconstriction than the efferent arterioles. These findings suggest that the MW rat is a useful animal model for the study of renal microcirculation and that the renal microcirculation is extremely sensitive to ET-1.

Analysis of Variance↗

PubMed1979

Central nervous system mediated stimulation by thyrotropin-releasing hormone of microcirculation in thyroid gland of rats.

The blood flow of thyroid, adrenal cortex and renal cortex in the pentobarbital anesthetized rat was assessed from hydrogen gas desaturation curve. The microcirculation of thyroid was markedly augmented within 2 min after an intraventricular injection of Thyrotropin-Releasing Hormone (TRH) while Met-Enkephalin (ENK) failed to influence. Both TRH and ENK stimulated the microcirculation of adrenal cortex moderately. ENK diminished the microcirculation of renal cortex whereas TRH did not exert any effect. The response of thyroid to TRH was abolished by vagotomy, thus the existence of a specific TRH-vagus -thyroid connection was indicated.

Adrenal Cortex↗

PubMed1991

Direct studies on the control of the renal microcirculation.

Recent advances in videomicroscopy combined with the development of several innovative in vivo and in vitro preparations now allow for direct study of the renal microcirculation. Blood flow in vasa recta capillaries of the rat can be studied by using video-microscopy, and changes in the flow of red blood cells in the renal cortex and papilla can be continuously monitored by using laser-Doppler flowmetry. All elements of the renal microcirculation can be visualized with the in vitro perfused juxtamedullary nephron or hydronephrotic kidney preparations. Pressures, blood flows, and vascular diameters in individual vessels can be directly measured in these preparations. Renal arterioles can be microdissected from the kidneys of several species and cannulated and pressurized in vitro for the study of pressure-diameter relationships and vascular responses to different agonists. In addition, membrane potentials and intracellular ion concentrations can now be measured in isolated renal arterioles by using microelectrodes and fluorescence microscopy. Thus, it is possible to study the control of renal vascular tone at all levels of integration from signal transduction in isolated cells to direct analysis of the regulation of hemodynamics in different regions of the microcirculation of the kidney in intact animals.

Animals↗

PubMed1975

Deterioration of the microcirculation in diabetes.

Studies of the microcirculation in diabetes in the last fifteen years have concentrated heavily on anatomic and biochemical abnormalities of the capillary basement membrane. Greater insights into basement membrane changes have eclipsed the previous picture of widespread progressive deterioration of the entire microcirculation. The history, variety of organ involvement, pattern of circulatory decline, and associated anatomic, physiologic, and biochemical findings are re-examined so that recently described potential mechanisms for the development of diabetic microangiopathy may be understood in a broader perspective. The possible contributions of seven categories of diabetic changes to damage of the microcirculation are outlined. The categories are: (1) altered basement membrane, (2) altered cellular function, (3) cell metabolic changes, (4) altered blood flow properties, (5) distrubed hemostasis, (6) altered oxygen transport, and (7) altered hormone production. The variety of clinical manifestations in long-standing diabetes related to microangiopathy appears to be due to a combination of a widely variable over-all rate of progression and a differing ability of body tissues and organs to accommodate to the sequential circulatory changes. The slow rate of deterioration in most diabetics suggests that several abnormalities must interact to produce the observed progression. A clear understanding of the interactions responsible for diabetic microangiopathy is becoming more important as new options in the management of diabetes become available.

Basement Membrane↗

PubMed1990

Hemodynamic changes in skin microcirculation induced by vibration stress in the conscious rabbit.

Cutaneous microcirculatory responses to vibration stress were observed by microphotoelectric plethysmography in a transparent round window installed in the ears of conscious rabbits. Vertical vibrations at frequencies ranging from 8 to 250 Hz were applied to the abdomen of the rabbits for 5 min. The vibrations produced an increase in heart rate and the index of discomfort, and a decrease in blood flow in the skin microcirculation. The maximum response was observed at 63 Hz. Rhythmic fluctuations in microcirculation were associated with two components: component A had a small amplitude and high frequency, and component B had a large amplitude and low frequency. Vibration exposure led to a large increase in component B and a smaller increase in component A. During vibration exposure, component A was suppressed by treatment with diltiazem, a calcium channel blocker, and was not affected by bunazosin, an alpha-1 adrenoceptor antagonist. The opposite changes were observed for component B. This indicates that components A and B of the rhythmic fluctuations are regulated by myogenic and neurogenic activities, respectively. Thus, the hemodynamic changes of skin microcirculation induced by vibration may actually be due to a neurogenic factor, especially sympathetic nerve activity. The responses appear to depend on the frequency of the vibrations.

Animals↗

PubMed1997

A review of the microcirculation of adipose tissue: anatomic, metabolic, and angiogenic perspectives.

Adipose tissue microcirculation is unique within the vascular system because of a capacity for this tissue to grow throughout most of adult life. A review of the microcirculation of adipose tissue has included a historical review of the early studies, which served as a foundation for later investigations on this topic, including basic hemodynamic measurements in mammalian adipose tissue. The various methods for measuring blood flow in white and brown adipose tissue are discussed with respect to studies of transport of substrates involved in adipose tissue metabolism. The role of innervation and vascular adrenergic receptors and the effects of diet and exercise on adipose tissue blood flow are also included. An in-depth analysis of the development of adipose tissue microvasculature indicates that angiogenesis often precedes adipogenesis. The clinical effects of hemodynamic adaptations to adipose tissue expansion are discussed in view of an epidemic increase in the prevalence of obesity and its co-morbidities. The recent discovery of sites of nuclear regulation of adipocyte differentiation, together with the identification of growth factors in adipose tissue, is an indication of the progress that is being made in the further understanding of molecular and cellular events that affect adipose tissue growth and, ultimately, adipose tissue microcirculation.

Adipose Tissue↗

PubMed1979

[Extracardiac effect of nitroglycerin in chronic ischemic heart disease according to the study of microcirculation].

Study of the dynamics of circulation in the microvessels of the eye conjunctiva under the effect of nitroglycerin in 50 patients with chronic ischemic heart disease showed short-lived dilatation of the postcapillaries and venules in most of them. Simultaneous fall in venous pressure may be evidence of a diminution of the venous tonus with a tendency to the storage of blood in the microcirculation system. The encountered shifts in the systemic hemodynamics may possibly be due to the reaction of the microcirculation channel, the labile character of which in the various "micro-areas" of the conjunctiva testifies to the complex reorganization of microcirculation under the effect of nitroglycerin.

Adult↗

PubMed1975

[Features of microcirculation in the liver during anaphylactic shock].

Microcirculation in the liver was studied in rats and dogs with anaphylactic shock. Injection of a reacting dose of the horse serum led to elevation of systemic arterial pressure by an average of 20 mm Hg; there also occurred spasm of the sinusoids, hepatic venules and an acceleration of blood flow in them With the following blood pressure reduction to 60-40 mm Hg there was blood congestion in the vessels, retarded circulation, intravascular aggregation of the blood formed elements, hemorrhages and ischemic changes. Restoration of systemic arterial pressure and of microcirculation occurred in parallel; no complete normalization of microcirculation in the liver ensued, yet.

Anaphylaxis↗

PubMed1975

[Microcirculation index--screening parameter for the assessment of dynamics of the terminal vascular system].

In this paper a new diagnostic method for the judgment of the dynamics of the terminal vascular system is presented. The microcirculation index which is to be obtained by means of the special technique of the phlebembraxis plethysmography was developed in investigations lasting several years and it was tested on persons with normal blood pressure and on hypertonics in comparison to recognized reference methods. Age-specific normal values were established and the differences found between normo- and hypertonics as well as between different decenniums were statistically ascertained. One group of hypertonics which underwent an antihypertensive long-term therapy showed a significant improvement of the microcirculation index after 8 weeks. According to the hitherto got results this index is fully suited for the utilization as screening method for serial examinations within the X-ray mass examinations and the research of cardio-criculatory diseases. It especially allows the selection of hypertonics who need treatment and through the increasing use of the multi-channel-occlusion-plethysmograph developed by the author the application in routine work for the judgment of the microcirculation and its influence by an antihypertensive therapy. For further foundation of the findings comparative methods with additional reference methods, especially electron microscopy are provided.

Adult↗

PubMed1975

[Study of the microcirculation of the wall of the stomach of white rats by the vital microscopy method].

Microcirculation of the gastric wall in the albino rat was studied by the method of vital microscopy in passing light. The conditions of the experiment permitted watching the microcirculation state during 5-6 hours. Intravital morphometry of the microcirculation bed vessels was made. The obtained data concerning the intravital angioarchitectonics of the gastric wall vascular bed were in good agreement with a conventional scheme of its blood supply. The role of arteriolevenular anastomoses in redistribution of blood within the bloodflow pathways was noted.

Animals↗

PubMed1975

Changes in microcirculation and oxygen pressure in the liver and kidneys in experimental traumatic shock.

Changes in microcirculation and oxygen pressure in the liver and kidneys were studied in experiments on 42 rats in the course of experimental traumatic shock elicited by Cannon's methoicroscope with a microphoto adapter MFN-12. Oxygen pressure was recorded with the aid of active open hemispheric platinum electrodes with diameters of 150-200 mum. With advencing shock, considerable disturbances of microcirculation and PO2 occurred in hepatic and renal tissues. By the end of the torpid phase of the shock, the PO2 in the liver sank to 1/2.4, and in the kidneys, to less than 1/4 of the respective initial values. The changes in microcirculation were of an ischaemic, vasospastic type in the kidneys, and of a mosaic pattern in the liver: ischaemic segments alternated with areas fully supplied with blood. A severe and rapid course of shock was accompanied by more marked disturbances of PO2 and circulation in hepatic and renal terminal vessels.

Animals↗

PubMed1992

[Physiopathology of venous stasis at the microcirculation level].

The division of the venous circulation in to two sectors, one constituted by the superficial and deep venous trunks (macrocirculation) and the other by the capillaries and precapillary venules (microcirculation), is surely schematical but aids the comprehension of many hemodynamic effects connected to hampered venous return and to the incompetence of the valvular devices. In fact many of the effects of stasis and venous hypertension (oedema, red cell diapedesis, skin dystrophies) cannot be explained merely by hydraulic mechanisms but require a primary alteration of the microvascular wall associated with structural changes of the perivascular connective tissue. The alterations that occur in microcirculation are of the utmost importance in the formation of the venules ulcerations. The passage of fibrinogen through large pores in the venules of the patients affected by venous hypertension derived from venous insufficiency creates a pericapillary fibrin deposition that cannot be removed because of inadequate blood and tissue fibrinolysis. This accumulation acts as a barrier to the diffusion of oxygen and other nutrients, determining a stasis dermatitis that may lead to tissue necrosis and ulceration. The more precise knowledge of the phenomena connected with the venous stasis at the level of microcirculation (pericapillary fibrin deposition, endothelial ischemia, blocked lymphatic drainage) will not only allow a deeper comprehension of the clinical signs but hopefully will lead to a more effective treatment of the postphlebitic syndrome.

Humans↗