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PubMedDate not supplied

Retinal microcirculation as revealed by SEM corrosion casts in the rat.

The morphology of the retinal microcirculation has been extensively studied by different techniques. Nevertheless, some problems concerning the capillary bed lamination and pre- and postcapillary patterns have not yet been clarified. In the present study the SEM corrosion cast technique was employed to study the three-dimensional relationships of rat retinal vessels and to follow the smallest vascular branches. Rat retina is considered a useful experimental model for a number of pathologies which affect the microvascular bed deeply. Two precapillary patterns have been observed. Precapillary arterioles gave rise to capillaries both as terminal branches or as collaterals. The former pattern of ramification allows only a regulation of flow in a whole group of capillaries downstream, the latter pattern could provide a finer regulation of blood flow. SEM corrosion casts have shown very well the lamination of the capillary bed: one can easily realize this by seeing the overlapped meshes of the two different planes, vessels in between the two capillary laminae can always be followed from one meshwork to the other. This three-dimensional organization is an interesting model for retinal circulation because it shows many features in common with the retina of humans and primates.

Animals↗

PubMed2001

Microcirculation in chronic venous insufficiency.

In this review, the anatomy and physiology of the venous system and its pathophysiology are described. Theories regarding the possible causes of disturbances in venous microangiopathy are summarized. The theories concern the deoxygenation of red blood cells, arteriovenous shunts, fibrin cuffs, and the trapping of growth factors and/or white blood cells. Furthermore, microlymphatic, neurologic and hemorheologic disturbances in venous disease are outlined. Findings in venous microangiopathy obtained from histology, capillary microscopy, microlymphography, laser Doppler fluxmetry and transcutaneous oxygen partial pressure are detailed. Finally, the recently discovered pattern of perfusion in microcirculation within and around venous ulcers is discussed.

Blood Vessels↗

PubMed2006

A review of the microcirculation in skin in patients with chronic venous insufficiency: the problem and the evidence available for therapeutic options.

Impairment of the cutaneous microcirculation is a major predisposing factor in inflammation and ulceration in patients with chronic venous insufficiency (CVI). Increase of capillary filtration rate predisposes to the formation of edema. Local lymphedema is a complication of CVI, often underdiagnosed. This review is focused on CVI but excludes the complication of ulceration. Treatment of microcirculatory dysfunction can be done by pharmacologic intervention or compression therapy or using a combination of both. This review is focused on drugs that have been evaluated by randomized prospective controlled trials. The following compounds are discussed: horse chestnut seed extracts, flavonoids, red vine leaves extracts, total triterpenic fraction of Centella asiatica (L), prociadins, calcium dobesilate, and pentoxifylline. The microcirculatory effects of compression therapy using bandages or stockings are also reviewed. The major microcirculatory effects that have been shown are the reduction of capillary filtration rate and improvements in levels of transcutaneous partial pressures of oxygen and carbon dioxide (TcPO(2) and TcPCO(2)). Available data suggest that a combination of pharmacologic and compression therapy may have some additive effects.

Chronic Disease↗

PubMed2006

Role of the microcirculation in diabetic foot ulceration.

The concept of microcirculation being implicated in the pathogenesis of diabetic foot disease is being challenged by evidence that fails to confirm it. However, there is evidence of structural changes with capillary and in the basement membrane that do not permit the concept to be denied either. The lack of evidence should not be a reason to argue against surgery in the diabetic foot.

Blood Flow Velocity↗

PubMed2006

Store-operated Ca2+ channel in renal microcirculation and glomeruli.

Store-operated Ca2+ channel (SOC) is defined as a channel that opens in response to depletion of the internal Ca2+ stores. During the last decade, many investigators have made a great effort to identify and characterize SOC, and to evaluate its physiologic function and pathophysiologic relevance in a variety of cell lines, primary cultures, and native tissues. To date, accumulating evidence has demonstrated that SOC is an essential Ca2+ entry mechanism in vascular smooth-muscle cells of renal microvasculature and glomerular mesangial cells, both of which tightly control glomerular hemodynamics and filtration. Store-operated Ca2+, combined with other types of Ca2+ entry channels, constitutes a profile of Ca2+ changes in response to physiologic vasoconstrictors and, thereby, regulates renal microcirculation and mesangial function. In addition, SOC is associated with altered Ca2+ signaling occurring in diseased kidneys, such as diabetic nephropathy. Although the gating mechanism and molecular identity of SOC are still enigmatic and may be cell-type and tissue specific, data from several independent groups suggest that protein kinase C plays an important role in SOC activation and that certain isoforms of canonical transient receptor potential (TRPC) proteins are candidates of SOC in renal microvessels and mesangial cells.

Calcium↗

PubMed1994

Three-dimensional relationships between tumor cells and microcirculation with double cyanine immunolabeling, laser scanning confocal microscopy, and computer-assisted reconstruction: an alternative to cast corrosion preparations.

The morphology of the microcirculation of uveal melanomas is a reliable market of tumor progression. Scanning electron microscopy of cast corrosion preparations can generate three-dimensional views of these vascular patterns, but this technique sacrifices the tumor parenchyma. Formalin-fixed wet tissue sections 100-150 microns thick from uveal melanomas were stained with the lectin Ulex europaeus agglutinin I (UEAI) and proliferating cell nuclear antigen (PCNA) to demonstrate simultaneously the tumor blood vessels and proliferating tumor cells. Indocarbocyanine (Cy3) was used as a fluorophore for UEAI and indodicarbocyanine (Cy5) was used for PCNA. Double labeled sections were examined with a laser scanning confocal microscope. Images of both stains were digitized at the same 5-microns intervals and each of the two images per interval was combined digitally to form one image. These combined images were visualized through voxel processing to study the relationship between melanoma cells expressing PCNA and various microcirculatory patterns. This technique produces images comparable to scanning electron microscopy of cast corrosion preparations while permitting simultaneous localization of melanoma cells expressing PCNA. The microcirculatory tree can be viewed from any perspective and the relationship between tumor cells and the tumor blood vessels can be studied concurrently in three dimensions. This technique is an alternative to cast corrosion preparations.

Antigens, Neoplasm↗

PubMedDate not supplied

Acute alterations of endothelin-1 and iNOS expression and control of the brain microcirculation after head trauma.

The biosynthetic equilibrium between endothelin-1 (ET-1, a vasoconstricting agent) and nitric oxide (NO, a gas with vasodilating effects) is thought to play a role in the autoregulation of microvessel contractility and maintenance of adequate perfusion after traumatic brain injury. ET-1 is a constitutively expressed peptide, while the gene that encodes for the inducible nitric oxide synthase (iNOS, an enzyme responsible for the synthesis of excessive and toxic amounts of NO) is solely activated after brain injury. We employed the Marmarou acceleration impact model of brain injury (400 g from 2 m) to study the effect of closed head trauma on the rat brain microcirculation. Following head trauma we analyzed changes of cerebral cortex perfusion using laser Doppler flowmetry and ultrastructural alterations of endothelial cells. We temporally correlated these changes with the expression of ET-1 (immunocytochemistry) and iNOS (in situ hybridization) to assess the role of these vasoactive agents in vascular contractility and cortical perfusion. Cortical perfusion was reduced by approximately 50% during the second hour as compared to values during preceding time points after TBI, reached a peak minutes before 3 h, and subsequently showed a trend towards normalization. A significant reduction in the lumen of microvessels and severe distortion of their shape were observed after the fourth hour post-trauma. At the same time period ET-1 expression in endothelial cells was stronger than in microvessels of control animals. ET-1 expression was further increased at 24 h after TBI. iNOS mRNA synthesis was strongly upregulated in the same cells at 4 h but was undetectable at 24 h post trauma. Our combined functional, cellular and molecular approach supports the notion that ET-1 and iNOS are expressed differentially in time within individual endothelial cells of cortical microvessels for the control of cortical blood flow following closed head trauma. This differential expression further indicates a reciprocal interaction in the synthesis of these two molecules which may underlie the control of microvascular autoregulation.

Animals↗

PubMed2003

Platelet-endothelial interaction in tumor angiogenesis and microcirculation.

Activated platelets release angiogenic growth factors and have therefore been proposed to contribute to tumor angiogenesis within a potentially prothrombotic tumor microcirculation. The aim of the study was to investigate interactions of platelets with the angiogenic microvascular endothelium of highly vascularized solid tumors during growth and in response to endothelial stimulation in comparison with normal subcutaneous tissue. Experiments were performed in the dorsal skinfold chamber preparation of C57BL/6J mice bearing the Lewis lung carcinoma (LLC-1) or methylcholanthrene-induced fibrosarcoma (BFS-1). Fluorescently labeled rolling and adherent platelets, red blood cell velocity, and vessel diameters were assessed by intravital fluorescence microscopy on days 1, 3, 8, and 14 after tumor cell implantation. Slightly elevated numbers of rolling platelets were observed in the early stages of tumor angiogenesis at day 1 (control, 1.7 +/- 0.6; LLC-1, 3.4 +/- 1.8; BFS-1, 3.0 +/- 0.7 [1/mm/s], P <.05) and day 3 (control, 1.6 +/- 0.6; LLC-1, 4.1 +/- 1.7, P <.05; BFS-1, 2.3 +/- 0.5 [1/mm/s]) after tumor cell implantation. Endothelial stimulation with calcium ionophore A23187 at day 14 after tumor cell implantation resulted in a minor increase to 2.1 +/- 0.4 (LLC-1) and 1.8 +/- 0.8 (BFS-1) rolling platelets (1/mm/s) in tumor microvessels compared with 4.9 +/- 0.9 in controls (P <.05). Platelet adherence was not observed. We therefore conclude that in the 2 experimental tumors under study, (1) slightly increased platelet rolling is a transient phenomenon after tumor cell implantation, and (2) platelet-endothelial interaction in response to endothelial stimulation is reduced in tumor microvessels.

Animals↗

PubMed2005

The non-invasive documentation of coronary microcirculation impairment: role of transthoracic echocardiography.

Transthoracic Doppler echocardiographic-derived coronary flow reserve is an useful hemodynamic index to assess dysfunction of coronary microcirculation. Isolated coronary microvascular abnormalities are overt by reduced coronary flow reserve despite normal epicardial coronary arteries. These abnormalities may occur in several diseases (arterial hypertension, diabetes mellitus, hypercholesterolemia, syndrome X, aortic valve disease, hypertrophic cardiomyopathy and idiopathic dilated cardiomyopathy). The prognostic role of impaired microvascular coronary flow reserve has been shown unfavourable especially in hypertrophic or idiopathic dilated cardiomyopathies. Coronary flow reserve reduction may be reversible, for instance after regression of left ventricular hypertrophy subsequent to valve replacement in patients with aortic stenosis, after anti-hypertensive treatment or using cholesterol lowering drugs. Coronary flow reserve may increase by 30% or more after pharmacological therapy and achieve normal level >3.0. In contrast to other non invasive tools as positron emission tomography, very expensive and associated with radiation exposure, transthoracic Doppler-derived coronary flow reserve is equally non invasive but cheaper, very accessible and prone to a reliable exploration of coronary microvascular territories, otherwise not detectable by invasive coronary angiography, able to visualize only large epicardial arteries.

Clinical Trials as Topic↗

PubMed2005

The microcirculation as a functional system.

This review examines experimental evidence that the microvascular dysfunction that occurs early in sepsis is the critical first stage in tissue hypoxia and organ failure. A functional microvasculature maintains tissue oxygenation despite limitations on oxygen delivery from blood to tissue imposed by diffusion; the density of perfused (functional) capillaries is high enough to ensure appropriate diffusion distances, and arterioles regulate the distribution of oxygen within the organ precisely to where it is needed. Key components of this regulatory system are the endothelium, which communicates and integrates signals along the microvascular network, and the erythrocytes, which directly monitor and regulate oxygen delivery. During hypovolemic shock, a functional microvasculature responds to diminish the impact of a decrease in oxygen supply on tissue perfusion. However, within hours of the onset of sepsis, a dysfunctional microcirculation is, due to a loss of functional capillary density and impaired regulation of oxygen delivery, unable to maintain capillary oxygen saturation levels and prevent the rapid onset of tissue hypoxia despite adequate oxygen supply to the organ. The mechanism(s) responsible for this dysfunctional microvasculature must be understood in order to develop appropriate management strategies for sepsis.

Animals↗

PubMed2006

Skin microcirculation and vasopressin infusion: a laser Doppler study.

Use of arginine vasopressin in the management of refractory vasodilatory shock has been associated with development of ischaemic skin lesions. Because of the increasing popularity of arginine vasopressin, it is important to evaluate its effects on microcirculatory blood flow. Such studies are crucial if we are to appreciate the microcirculatory consequences of our various resuscitation strategies. However, methodological issues must always be considered because they can significantly influence interpretation of the results. Some aspects of use of laser Doppler to evaluate the microcirculation are reviewed within the context of recent findings presented by Luckner and coworkers in this issue of Critical Care.

Arginine Vasopressin↗

PubMed2005

Acute hyperglycemia does not affect the reactivity of coronary microcirculation in humans.

OBJECTIVE: There is some evidence that acute hyperglycemia (H) may cause vascular dysfunction in normal subjects. This study investigates whether acute, short-term H affects coronary vasodilatory function in healthy subjects. DESIGN: Diastolic peak flow velocity in the left anterior descending coronary artery was measured at rest and after dipyridamole (0.56 mg/kg over 4 min) using transthoracic color Doppler echocardiography in 13 healthy men. Coronary flow reserve (CFR) was defined as the ratio of dipyridamole-induced coronary peak diastolic to resting peak diastolic flow velocity. CFR was measured both in euglycemia (E) and after 3 h H ( approximately 14 mmol/liter) by a variable infusion of glucose and octreotide (0.4 mg/h) to prevent increase in insulin concentration. RESULTS: Fasting plasma glucose increased to 14.3 +/- 0.33 mmol/liter during the study and maintained variability within less than 10%. Plasma insulin remained nearly stable during H. Resting diastolic flow velocity was 18.5 +/- 0.6 cm/sec in E and increased to 20.0 +/- 0.7 cm/sec during H (P < 0.005). Dipyridamole infusion produced a marked increase in coronary flow velocity, which reached values of 50.8 +/- 2.9 cm/sec in E and 51.8 +/- 2.1 cm/sec in H (P = not significant). CFR was 2.78 +/- 0.16 in E and 2.59 +/- 0.12 in H (P = not significant). CONCLUSION: Our study indicates that short-term hyperglycemia does not affect the vasodilatory response of coronary microcirculation in healthy subjects.

Acute Disease↗

PubMed2003

Changes in cerebral microcirculation during and after abdominal aortic cross-clamping in rabbits: the role of thromboxane A2 receptor.

UNLABELLED: Little is known about any changes in cerebral hemodynamics, during and after abdominal aortic cross-clamping and unclamping, especially in the cerebral microcirculation. We studied the effects of abdominal aortic cross-clamping and unclamping on cerebral pial vessel diameter in the presence or absence of the thromboxane (Tx)A(2) receptor antagonist using a closed cranial window in 27 rabbits. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 min (maximum, -17% for large [> or =75 micro m] and -28% for small arterioles [<75 micro m] compared with baseline). Topical administration of a TxA(2) receptor antagonist, seratrodast, at 10(-7) M and 10(-6) M, significantly attenuated the constriction of large and small arterioles (at 60 min, -9% and -13% constriction for 10(-7) M, and -6% and -7% for 10(-6) M). Release of a 20-min aortic cross-clamp induced a sustained pial arteriolar constriction. Because this unclamping-induced vasoconstriction was attenuated by topical administration of seratrodast, it was likely partially mediated via the washout of TxA(2) produced in the ischemic region during the clamp and after cross-clamp release. IMPLICATIONS: Abdominal aortic unclamping after a 20-min clamp caused an initial dilation followed by a sustained constriction of pial arterioles. Seratrodast, a thromboxane A(2) receptor antagonist, attenuated the vasoconstriction suggesting that it is at least partly mediated by thromboxane A(2) washed out from the region rendered ischemic by clamping.

Animals↗

PubMed2003

The comparative effects of prostaglandin E1 and nicardipine on cerebral microcirculation in rabbits.

UNLABELLED: We compared the effects of the systemic hypotensive drugs prostaglandin E1 (PGE1) and nicardipine on the cerebral microcirculation and on the cerebrovascular reactivities to hypercapnia and hypoxia. In isoflurane-anesthetized rabbits (n = 48), we measured cerebral pial vessel diameters using a cranial-window preparation: (a) during IV PGE1- or nicardipine-induced mild or moderate hypotension (to 80% or 60% of initial mean arterial blood pressure), (b) after topical administration of these drugs, and (c) during hypercapnia or hypoxia induced during such mild or moderate hypotension. Pial arteriolar diameters were (a) unchanged when hypotension (mild or moderate) was induced by PGE1 but increased when it was induced by nicardipine and (b) increased dose-dependently by topical administration of nicardipine but not PGE1. Only small changes in cerebral venular diameter were observed in these experiments. The pial arteriolar dilator response to hypercapnia was potentiated during hypotension (mild or moderate) when it was induced by PGE1 but decreased when it was induced by nicardipine, whereas the response to hypoxia was maintained during PGE1-induced hypotension but decreased during nicardipine-induced hypotension. In conclusion, as a systemic hypotensive drug, PGE1 does not dilate cerebral arterioles and maintains cerebrovascular reactivities to hypercapnia and hypoxia, whereas nicardipine dilates such vessels and reduces these cerebrovascular reactivities. IMPLICATIONS: When given systemically to produce mild or moderate hypotension, prostaglandin E1 does not induce cerebral vasodilation and maintains cerebrovascular reactivity to hypercapnia and hypoxia, whereas nicardipine dilates cerebral vessels and reduces both reactivities.

Alprostadil↗

PubMed1992

A possible involvement of central atrial natriuretic peptide in cerebral cortical microcirculation.

The possible involvement of atrial natriuretic peptide (ANP) in cerebral cortical microcirculation was investigated in rats by means of laser-Doppler flowmetry and immunohistochemistry. In the laser-Doppler study, local cerebral blood flow (LCBF) changes after the administration of 10(-6) to 10(-8) mol/LANP solution or vehicle (saline solution) as an intracortical injection for 5 minutes were continuously monitored throughout the 30 minutes of the study and were expressed as percentages of preinjection values represented as 0%. The administration of 10(-6) to 10(-8) mol/LANP caused a significant decrease in LCBF; the onset of LCBF responses occurred within a few minutes after the start of the injection and the decrease in LCBF reached the maximum level within 7 to 10 minutes after the completion of the administration, after which LCBF gradually recovered. In the immunohistochemical study, no specific ANP immunoreactivity was found associated with the intraparenchymal blood vessels; however, ANP-immunoreactive neurons were observed primarily in the hypothalamus and septum, in which high concentrations of ANP-containing neurons have been identified. The data from the laser-Doppler study suggest that central ANP may produce a vasoconstriction of the intraparenchymal blood vessels, regardless of whether through direct action on these vessels or through the mediation by some system in the central nervous system. Because there is no evidence for ANP-containing nerves around these vessels, the role of central ANP in the cerebral circulation must await identification of the source of perivascular ANP.

Animals↗

PubMed1994

A new model for in vivo observation of the feline spinal microcirculation: the closed spinal window.

A new experimental model is described that uniquely allows the in vivo observation and quantification of vascular caliber changes on the dorsal surface of the feline spinal cord. The model consists of a rectangular Plexiglas window that is sutured to the lumbar dura and is supported by a special holder. Inlet and outlet tubes attached to the window serve for topical applications of mock cerebrospinal fluid or vasoactive agents to the surface of the cord and for continuous monitoring of intrathecal pressure. Pial vessels below the window were observed at 200-fold magnification with the aid of a microvideo camera. Spinal arterioles reacted to hypercarbia and superfusion with acetylcholine solution in a manner similar to cerebral arterioles. Tests with increased intrathecal pressure showed that the window remained watertight between 25 and 130 mm Hg, with an average leakage pressure of 57.8 +/- 33.5 mm Hg. To promote the use of this model in other laboratories, the authors give a detailed description of the closed spinal window preparation and report their experiences gained from 50 experiments. It is concluded that the closed spinal window is a highly reproducible model, suitable for the study of the feline spinal microcirculation for several hours in vivo.

Animals↗

PubMed2004

Ampulla ('takotsubo') cardiomyopathy of both ventricles: evaluation of microcirculation disturbance using 99mTc-tetrofosmin myocardial single photon emission computed tomography and doppler guide wire.

An 84-year-old woman was admitted to hospital with chest pain at rest. An electrocardiogram showed ST-segment elevation in leads II, III, aV(F) and V(2-6), and the 2-dimension echocardiogram showed apical ballooning akinesis and basal hyperkinesis of both ventricles. (99m)Tc-tetrofosmin myocardial single photon emission computed tomography (SPECT) showed severely reduced uptake in the apex. Coronary angiography did not show any organic stenosis, and epicardial coronary spasm was not provoked by the ergonovine loading test. Left ventriculography showed apical ballooning akinesis and basal hyperkinesis, which were also apparent on right ventriculography. The coronary flow velocity pattern showed rapid diastolic acceleration and deceleration times, and the coronary flow reserve measured with a Doppler guide wire was severely decreased. (99m)Tc-tetrofosmin myocardial SPECT showed improvement in the findings after 14 days, and the coronary flow velocity pattern and coronary flow reserve improved after 30 days. Left and right ventriculography both revealed mild improvement in the wall motion. These findings suggested that a microcirculation disturbance caused ampulla ('Takotsubo') cardiomyopathy.

Aged↗

PubMed1999

[Microcirculation in the myocardium].

The coronary artery supplies the arterial blood that contains oxygen and nutrients for the myocardial tissue to produce high-energy phosphates aerobically. The left anterior descending and circumflex coronary arteries run on the epicardial surface of the left ventricle, turn toward the endocardium at a right angle, and nourish the tissues of the subendocardinal layers with the arterial blood. Cessation of coronary blood flow makes the myocardium ischemic. The endocardium is particularly susceptible to ischemia because the arteries that run to the endocardium are pressed due to extravascular compression during every systole. Coronary vasodilators are still used as anti-anginal drugs. However, a potent coronary vasodilator may cause coronary-steal and thereby worsen the ischemia-induced myocardial injury. We will demonstrate changes in the microcirculation of the ischemic myocardium caused by coronary vasodilators and demonstrate that a coronary vasodilator is not always effective on the ischemic myocardium.

Coronary Vessels↗