About microcirculation

Analysis of the skin microcirculation

Effects of Propofol on Human Microcirculation

The Hepatic Microcirculation: Mechanistic Contributions

Microcirculatory Effects of Abciximab and Eptifibatide: A Critical Appraisal

Early changes in the skin microcirculation and muscle metabolism of the diabetic foot

Influence of Experimental Diabetes on the Microcirculation of Injured Peripheral Nerve

Effect of Hyperbaric Oxygenation on Microcirculation: Use in Therapy of Retinal Vascular Disorders

About microcirculation

The microcirculation is a term used to describe the small vessels in the vasculature which are embedded within organs and are responsible for the distribution of blood within tissues; as opposed to larger vessels in the macrocirculation which transport blood to and from the organs. The vessels on the arterial side of the microcirculation are called the arterioles, which are well innervated, are surrounded by smooth muscle cells, and are 10-100 µm in diameter. Arterioles carry the blood to the capillaries, which are not innervated, have no smooth muscle, and are about 5-8 µm in diameter. Blood flows out of the capillaries into the venules, which have little smooth muscle and are 10-200 µm. The blood flows from venules into the veins. In addition to these blood vessels, the microcirculation also includes lymphatic capillaries and collecting ducts. The main functions of the microcirculation include the regulation of 1. blood flow and tissue perfusion 2. blood pressure, 3. tissue fluid (swelling or edema), 4. delivery of oxygen and other nutrients and removal of CO2 and other metabolic waste products, and 5. body temperature. The microcirculation also has an important role in inflammation.

Most vessels of the microcirculation are lined by flattened cells, the endothelium and many are surrounded by contractile cells the smooth muscle or pericytes. The endothelium provides a smooth surface for the flow of blood and regulates the movement of water and dissolved materials in the plasma between the blood and the tissues. The endothelium also produce molecules that discourage the blood from clotting unless there is a leak. The smooth muscle cells can contract and decrease the size of the arterioles and thereby regulate blood flow and blood pressure.

Flow
Flow is determined by the diameter and the length of the vessels of the microcirculation. The Hagen–Poiseuille equation predicts the flow of blood through the vessels.

Capillary Exchange of Water
The Starling equation is an equation that describes the roles of hydrostatic and oncotic forces (the so-called Starling forces) in the movement of fluid across capillary endothelium.

Capillary Exchange of Solutes, e.g. glucose
Small solutes move across the endothelium by passing through the spaces formed by the tight junctions formed where the edges of adjacent endothelial cells abut.

This article comes from:

http://en.wikipedia.org/wiki/Microcirculation

Effects of Propofol on Human Microcirculation
　

It is increasingly believed that acute microvascular alterations may be involved in the development of organ dysfunction in critically ill patients. Propofol significantly decreases vascular tone and venous return, which can induce arterial hypotension. However, little is known about the microcirculatory effects of propofol in healthy humans.
Methods: We conducted a prospective, open-labelled trial in 15 patients anaesthetized by propofol for transvaginal oocyte retrieval. The sublingual microcirculatory network was studied before, during, and after propofol infusion using orthogonal polarization spectral imaging.
Results: Mean (SD) calculated propofol effect-site concentration was 6.5 (1.8) μg ml-1. During propofol administration, systemic haemodynamic and oxygenation variables were unchanged, but total microvascular density decreased by 9.1% (P<0.05). The venular density remained unchanged, but the density of perfused capillaries was significantly reduced by 16.7% (P<0.05). Microcirculatory alterations resolved 3 h after discontinuation of the propofol infusion.
Conclusions: Propofol infusion for anaesthesia in man reduces capillary blood flow.

Introduction
Propofol administration, at clinical doses, has significant haemodynamic effects. It has limited effects on the contractility of the heart, but induces arterial hypotension primarily by decreasing vascular tone and venous return. These effects are usually easily compensated by fluid administration, vasopressor agents, or both. In contrast to its systemic haemodynamic effects, little is known about the effects of propofol on the microcirculation. Acute microvascular alterations have been observed in patients with severe sepsis and in patients with severe cardiac failure,and these alterations are more severe in patients with a poor outcome. Experimental data suggest that an impaired microcirculation may lead to organ dysfunction;[14] although this is difficult to prove in man, it may be justified to avoid the agents that could further worsen microvascular perfusion. Some anaesthetic agents have been shown to alter the microcirculation in experimental conditions,leading to impaired oxygen extraction capabilities. However, these effects may be specific to the anaesthetic agent, its dosage, and its route of administration. We hypothesized that anaesthesia with propofol may be associated with microvascular alterations.

We used the orthogonal polarization spectral (OPS) imaging technique (Figure 1), a non-invasive method for assessing the microcirculatory blood flow in vivo in humans,[10-13] to study the effects of propofol on the human microcirculation in patients undergoing transvaginal oocyte retrieval for assisted reproductive techniques.
This article comes from:http://www.medscape.com/viewarticle/581346

The Hepatic Microcirculation: Mechanistic Contributions and (Therapeutic Targets in Liver Injury and Repair)
　

Institute for Experimental Surgery, University of Rostock, Rostock; and Institute for Clinical and Experimental Surgery, University of Saarland, Homburg-Saar, Germany
The complex functions of the liver in biosynthesis, metabolism, clearance, and host defense are tightly dependent on an adequate microcirculation. To guarantee hepatic homeostasis, this requires not only a sufficient nutritive perfusion and oxygen supply, but also a balanced vasomotor control and an appropriate cell-cell communication. Deteriorations of the hepatic homeostasis, as observed in ischemia/reperfusion, cold preservation and transplantation, septic organ failure, and hepatic resection-induced hyperperfusion, are associated with a high morbidity and mortality. During the last two decades, experimental studies have demonstrated that microcirculatory disorders are determinants for organ failure in these disease states. Disorders include 1) a dysregulation of the vasomotor control with a deterioration of the endothelin-nitric oxide balance, an arterial and sinusoidal constriction, and a shutdown of the microcirculation as well as 2) an overwhelming inflammatory response with microvascular leukocyte accumulation, platelet adherence, and Kupffer cell activation. Within the sequelae of events, proinflammatory mediators, such as reactive oxygen species and tumor necrosis factor-, are the key players, causing the microvascular dysfunction and perfusion failure. This review covers the morphological and functional characterization of the hepatic microcirculation, the mechanistic contributions in surgical disease states, and the therapeutic targets to attenuate tissue injury and organ dysfunction. It also indicates future directions to translate the knowledge achieved from experimental studies into clinical practice. By this, the use of the recently introduced techniques to monitor the hepatic microcirculation in humans, such as near-infrared spectroscopy or orthogonal polarized spectral imaging, may allow an early initiation of treatment, which should benefit the final outcome of these critically ill patients.
This article comes from: http://physrev.physiology.org/cgi/content/abstract/89/4/1269

Early changes in the skin microcirculation and muscle metabolism of the diabetic foot

BACKGROUND: Changes in the large vessels and microcirculation of the diabetic foot are important in the development of foot ulceration and subsequent failure to heal existing ulcers. We investigated whether oxygen delivery and muscle metabolism of the lower extremity were factors in diabetic foot disease. METHODS: We studied 108 patients (21 control individuals who did not have diabetes, 36 patients with diabetes who did not have neuropathy, and 51 patients with both diabetes and neuropathy). We used medical hyperspectral imaging (MHSI) to investigate the haemoglobin saturation (S(HSI)O2; % of oxyhaemoglobin in total haemoglobin [the sum of oxyhaemoglobin and deoxyhaemoglobin]) in the forearm and foot; we also used 31P-MRI scans to study the cellular metabolism of the foot muscles by measuring the concentrations of inorganic phosphate and phosphocreatine and calculating the ratio of inorganic phosphate to phosphocreatine (Pi/PCr). FINDINGS: The forearm S(HSI)O2 during resting was different in all three groups, with the highest value in controls (mean 42 [SD 17]), followed by the non-neuropathic (32 [8]) and neuropathic (28 [8]) groups (p<0.0001). In the foot at resting, S(HSI)O2 was higher in the control (38 [22]) and non-neuropathic groups (37 [12]) than in the neuropathic group (30 [12]; p=0.027). The Pi/PCr ratio was higher in the non-neuropathic (0.41 [0.10]) and neuropathic groups (0.58 [0.26]) than in controls (0.20 [0.06]; p<0.0001). INTERPRETATION: Our results indicate that tissue S(HSI)O2 is reduced in the skin of patients with diabetes, and that this impairment is accentuated in the presence of neuropathy in the diabetic foot. Additionally, energy reserves of the foot muscles are reduced in the presence of diabetes, suggesting that microcirculation could be a major reason for this difference.
　

This article comes from:

http://www.ncbi.nlm.nih.gov/pubmed/16291064

Effect of Hyperbaric Oxygenation on Microcirculation: Use in Therapy of Retinal Vascular Disorders

The physiopathologic effects of oxygen, especially under hyperbaric conditions, on the retina and microcirculation were reviewed. The therapeutic effects of oxygen on ischemic (vascular) retinal disorders toere evaluated in 7 cases--2 with central retinal artery occlusion, one with exudative disciform retinopaihy, one with central serous retinopathy, and 3 with diabetic retinopathy. Whereas no definite improvement in the visual function teas noted under oxygen therapy, the changes in the scotoma related to vascular occlusion and angioscotoma and the vasodilatation noted in diabetic retinopathy are phenomena previously not described and whose significance is yet to be defined.
　

This article comes from:

http://www.iovs.org/cgi/content/abstract/4/6/1141

Influence of Experimental Diabetes on the Microcirculation of Injured Peripheral Nerve(Functional and Morphological Aspects)

Regeneration of diabetic axons has delays in onset, rate, and maturation. It is possible that microangiopathy of vasa nervorum, the vascular supply of the peripheral nerve, may render an unfavorable local environment for nerve regeneration. We examined local nerve blood flow proximal and distal to sciatic nerve transection in rats with long-term (8 month) experimental streptozotocin diabetes using laser Doppler flowmetry and microelectrode hydrogen clearance polarography. We then correlated these findings, using in vivo perfusion of an India ink preparation, by outlining the lumens of microvessels from unfixed nerve sections. There were no differences in baseline nerve blood flow between diabetic and nondiabetic uninjured nerves, and vessel number, density, and area were unaltered. After transection, there were greater rises in blood flow in proximal stumps of nondiabetic nerves than in diabetic animals associated with a higher number, density, and caliber of epineurial vessels. Hyperemia also developed in distal stumps of nondiabetic nerves but did not develop in diabetic nerves. In these stumps, diabetic rats had reduced vessel numbers and smaller mean endoneurial vessel areas. Failed or delayed upregulation of nerve blood flow after peripheral nerve injury in diabetes may create a relatively ischemic regenerative microenvironment.

Patients with diabetes are susceptible to peripheral nerve injury from entrapment and other causes. Regeneration in peripheral nerves can be complicated by relative ischemia, as may occur in cases of nerve infarction. The intact peripheral nerve endoneurial vascular nutritive compartment is well supplied by extrinsic “feeding” vessels arising from its epineurial plexus. Ischemia after nerve injury may be “normally” averted by increasing endoneurial nerve blood flow to address the increased nutrient and oxygen consumption of regenerating axons and cellular elements during repair. For example, rises in blood flow, or hyperemia, may be mediated by vasodilation of the extrinsic vasa nervorum by neuropeptides (notably calcitonin gene-related peptide [CGRP], substance P, and vasoactive intestinal peptide [VIP]) and mast cell-derived histamine. Macrophage- and endothelial-derived nitric oxide (NO) also likely augments nerve blood flow at the injury site through vasodilation. At later stages of regeneration and repair, extensive neoangiogenesis may maintain a persistent hyperemic state. Revascularization from angiogenesis into a peripheral nerve graft often precedes regenerating axons, with fibers near blood vessels having the fastest regeneration rates .

Regenerative success in diabetes is impaired as a result of defects in the onset of regeneration , in elongation rate of axonal sprouts , and subsequently in nerve fiber maturation of experimental and human diabetes. The regenerative program could be compromised by a failed upregulation of neurotrophins , defective transport of cytoskeletal elements, or inadequate microvascular support. Diabetic nerve microvessels exhibit basement membrane thickening (as a result of accumulation of type IV collagen), endothelial cell hyperplasia, as well as intimal and smooth muscle cell proliferation that all increase with the severity of diabetic polyneuropathy and may impair vasoreactivity. Diabetes has been noted to impair vascular hyperemic responses to agents such as heat and injury, to surgical exposure of nerve, and to epineurial application of capsaicin. A diminished supply of vasoactive peptides such as CGRP, substance P, and VIP in intact diabetic nerve and dorsal root ganglion, along with excessive scavenging of NO, results in blunted vasodilation and hyperemia. Increased intervascular distance in diabetic rats after nerve injury may further predispose the regenerating nerve to ischemia.

In this work, we explored the response of vasa nervorum to sciatic nerve injury in rats with chronic experimental diabetes. We examined physiological measures of nerve blood flow by two approaches—laser Doppler flowmetry (LDF) and microelectrode hydrogen clearance (HC) polarography—to address selectively flow dominated by the epineurial plexus and flow within the endoneurial vascular compartment, respectively. These measures were correlated with quantitative morphometric studies of nerve microvessels using in vivo perfusion of an India ink preparation and study of luminal profiles from unfixed nerve sections. Assessment of two time points (48 h and 2 weeks) after injury allowed us to examine two distinct but sequential and related stages of injury-induced hyperemia. The findings suggest that there are substantial alterations in how diabetic vasa nervorum respond to injury and how they may support regeneration
　

This article comes from:

http://diabetes.diabetesjournals.org/content/51/7/2233.full

Microcirculatory Effects of Abciximab and Eptifibatide: A Critical Appraisal

The coronary microcirculation is critically important in the maintenance of myocardial nutritive blood flow. Even in situations where measures of epicardial blood flow appear normal, abnormalities in microcirculatory integrity secondary to microvascular occlusion may precipitate myocardial infarction and regional myocardial dysfunction. Atherothrombotic embolization of the distal microcirculation may occur spontaneously following plaque rupture during acute coronary syndromes or may occur secondary to percutaneous coronary intervention (PCI) induced plaque disruption. The debris produced by coronary stent deployment is composed of atherosclerotic plaque components (fibrin, necrotic core, foam cells, cholesterol clefts) as well as organized thrombus of variable degree. In addition, platelet as well as white cell-platelet aggregates which form at the site of endoluminal vessel injury or on the surface of the metallic stent prosthesis contribute to the process of embolization and distal microvascular occlusion. As the pathogenesis of microvascular obstruction is multi-factorial, both pharmacologic and mechanical strategies for embolic protection have been devised. All three currently available platelet glycoprotein (GP) IIb/IIIa receptor blockers have been demonstrated to reduce the incidence of periprocedural myocardial infarction associated with PCI as reflected by CK-MB elevation. The mechanism for this benefit is attributed in large part to a reduction in platelet aggregates and platelet embolization and to a lesser extent, preservation of side branch integrity following coronary stent deployment. The degree of “protection” provided by GP IIb/IIIa receptor blockade is influenced by the pathophysiologic substrate and is not demonstrable following PCI of saphenous vein graft stenoses, possibly reflecting the burden of atherothrombotic debris produced.1,2
Indeed, atherosclerotic plaque disgorgement and plaque volume reduction following coronary stent deployment as demonstrated by intravascular ultrasound evaluation, has been directly correlated with periprocedural CK-MB elevation, particularly in patients who present with unstable angina pectoris.3 Thus, it is no surprise that platelet GP IIb/IIIa blockade provides variable and incomplete protection against microvascular occlusion considering the multiple diverse factors which contribute to this phenomenon.
Various techniques to evaluate microcirculatory integrity have been proposed and validated in specific patient subsets. Most notably, these have included Doppler flow wire assessment of coronary flow reserve, contrast echocardiography, TIMI myocardial perfusion or “blush” grade (TMBG) and the magnitude of electrocardiographic ST segment resolution (> 70%) following mechanical or pharmacologic reperfusion for ST segment elevation acute myocardial infarction (MI).
In the current issue of the Journal, Stoupakis et al.4 purport to demonstrate similarity in microvascular preservation following elective coronary stent deployment in a consecutive series of patients undergoing PCI for stable angina.

This article comes from:

http://www.invasivecardiology.com/article/2019

Analysis of the skin microcirculation

Exploring the heterogeneity of skin microcirculation
The study of capillary functionality in man is limited to the vascular bed. However, the skin capillary network can be elegantly studied by using nailfold videocapillaroscopy. This technique enables the clinical operator to assess their morphology, density and the blood flow within them.

The skin blood supply originates from perforating vessels rising from the underlying muscles and subcutaneous fat forming the lower horizontal plexus, at the point of the dermal–subcutaneous interface. From the lower plexus, paired arterioles and venules rise and establish direct connections with the subpapillary plexus, which is situated in the papillary dermis; from this point arise the capillary loops of the dermal papillae. The majority of the skin microcirculation resides in the papillary dermis 1–2 mm below the skin surface.

The microvessels in the papillary dermis range in size from 10 to 35 nm whereas those located in the mid and deep dermis are 40–50 nm with arterioles large as 100 nm being occasionally observed. The capillary architecture, in particular the loop region, may vary according to the skin area and the age of the subject under examination.

The toe and at the finger nail fold level are the sole skin body areas in wich the terminal row of dermal capillary loops lies parallel to the skin surface.

                           Perpendicular vs. parallel

(A) A capillaroscopic image of the nailfold microvascular network taken in a healty subject. The capillaries lie parallel to the skin surface.
(B) A capillaroscopic image of the microvascular network from another skin body area. The main capillary loop axis is perpendicular to the skin surface and capillaries show a characteristic dot shape.
(images are used under permission of Professor Walter Grassi)When moving from the distal part to the proximal one along the finger, the orientation of capillaries changes and become perpendicular or oblique to the skin surface. The overall capillary density varies according to the boby skin area and slight differences have been reported over small areas such as the dorsum of the foot.

Ageing is generally accompanied by a significant loss in dermal volume, a reduction in capillary density, a shortening of capillary loops and a rarefaction of larger microvessels.
　

This article comes from:

http://www.capillaroscopia.it/html/cnt/en/skin_microcirculation.asp

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