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Microvascular Perfusion (microvascular + perfusion)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Apical Ballooning Syndrome in a Postoperative Patient with Normal Microvascular Perfusion by Myocardial Contrast Echocardiography

ECHOCARDIOGRAPHY, Issue 7 2005
Gautam Ramakrishna M.D.
Apical ballooning syndrome is classically described as transient left ventricular (LV) dysfunction, marked LV akinesia, and normal or near-normal coronary arteries. The etiology is unclear and there is limited information based on case reports and small case series. We describe a 35-year-old woman who underwent surgical hepatectomy and developed apical ballooning syndrome in the postoperative period. The novel use of myocardial contrast echocardiography (MCE) in this setting demonstrated intact microvascular perfusion and lack of coronary flow-limiting abnormalities despite apical akinesis. In select patients with similar clinical presentations, performing MCE is safe and may be pursued as an alternative to invasive coronary angiography. [source]

Microvascular Perfusion and Transport in the Diabetic Heart

MICROCIRCULATION, Issue 3 2000
PAUL F. McDONAGH
ABSTRACT Diabetes is a chronic disease of metabolic dysfunction that is increasing worldwide. The hyperglycemia associated with diabetes causes significant protein alterations and an oxidative stress. In the heart, all cell types are affected by diabetes; the myocyte, the vasculature and the blood cells. Four out of five diabetics die from ischemic heart disease and stroke, suggesting that the diabetic is quite vulnerable to ischemic injury. It is important to understand the pathophysiologic changes that occur in the diabetic heart in order to develop thoughtful treatments to limit this serious complication. This review focuses on the anatomical and functional alterations that occur in the diabetic circulation of the heart, with emphasis on the coronary microcirculation. Coronary microvascular dysfunction combined with blood cellular alterations are presented to explain the amplified oxidative stress that occurs in the diabetic heart under ischemic conditions. [source]

Remote Liver Injury is Attenuated by Adenovirus-Mediated Gene Transfer of Heme Oxygenase-1 During the Systemic Inflammatory Response Syndrome

MICROCIRCULATION, Issue 7 2004
SARAH D. MCCARTER
ABSTRACT Objectives: Adenovirus-mediated gene therapy is being investigated with increasing success for future treatment of autoimmune diseases. However, the use of adenoviruses is still limited by inflammatory and immune responses in the target organ. Previous work by the authors' laboratory established that the adenovirus encoding inducible heme oxygenase (Ad-HO-1) does not elicit the acute hepatic inflammation normally caused by adenoviruses, inviting further investigation in models of severe inflammation. Concurrently, there is increasing evidence for an endogenous protective role for heme oxygenase (HO) in the liver during the systemic inflammatory response syndrome (SIRS). Building on our previous results, this study investigated the effect of Ad-HO-1 pretreatment on remote liver injury during normotensive SIRS, induced by bilateral hind limb ischemia and reperfusion. Methods: Microvascular perfusion and hepatocyte death were quantified using established intravital videomicroscopy techniques. Hepatocellular injury and liver function were assessed using blood-borne indicators. Results: Microvascular perfusion deficits and increased hepatocyte death occurred following limb ischemia and 3 h of reperfusion in vehicle-pretreated animals; however, Ad-HO-1 pretreatment prevented these deficits. In contrast, the increase in serum alanine transaminase levels was unaffected by Ad-HO-1 pretreatment. Serum bilirubin levels were increased during systemic inflammation, predominantly in the conjugated form; and, this increase was prevented by administration of Ad-HO-1. Conclusions: These data indicate that gene transfer of inducible HO is an effective method to protect the liver during SIRS, providing incentive for further investigation into gene therapy strategies exploiting this anti-inflammatory enzyme. [source]

Increased asymmetric dimethylarginine and endothelin 1 levels in secondary Raynaud's phenomenon: Implications for vascular dysfunction and progression of disease

ARTHRITIS & RHEUMATISM, Issue 7 2003
Sanjay Rajagopalan
Objective To compare microvascular and macrovascular functions in a cohort of patients with primary and secondary Raynaud's phenomenon (RP) who were matched for demographic, risk factor, and severity profiles. Methods Forty patients with primary or secondary RP matched for vascular risk factors and severity scores underwent testing of endothelial function and cold pressor responsiveness of the brachial artery. Microvascular perfusion of the digital vasculature was assessed using laser Doppler fluxmetry in response to reactive hyperemia. Plasma was assayed for endothelin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesion molecule 1, vascular cell adhesion molecule 1 (VCAM-1), and monocyte chemoattractant protein 1 (MCP-1). Results Patients with RP had abnormal vasoconstrictor responses to cold pressor tests (CPT) that were similar in primary and secondary RP. There were no differences in median flow-mediated and nitroglycerin-mediated dilation or CPT of the brachial artery in the 2 populations. Patients with secondary RP were characterized by abnormalities in microvascular responses to reactive hyperemia, with a reduction in area under the curve adjusted for baseline perfusion, but not in time to peak response or peak perfusion ratio. Plasma ET-1, ADMA, VCAM-1, and MCP-1 levels were significantly elevated in secondary RP compared with primary RP. There was a significant negative correlation between ET-1 and ADMA values and measures of microvascular perfusion but not macrovascular endothelial function. Conclusion Secondary RP is characterized by elevations in plasma ET-1 and ADMA levels that may contribute to alterations in cutaneous microvascular function. [source]

Apical Ballooning Syndrome in a Postoperative Patient with Normal Microvascular Perfusion by Myocardial Contrast Echocardiography

Measurements of microvascular perfusion in healthy anesthetized dogs using orthogonal polarization spectral imaging

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2010
DACVECC, Deborah C. Silverstein DVM
No abstract is available for this article. [source]

Neurovascular Alignment in Adult Mouse Skeletal Muscles

MICROCIRCULATION, Issue 2 2005
SHAWN E. BEARDEN
ABSTRACT Objective: Muscle blood flow increases with motor unit recruitment. The physical relationships between somatic motor nerves, which control muscle fiber contraction, and arterioles, which control microvascular perfusion, are unexplored. The authors tested the hypothesis that motor axons align with arterioles in adult skeletal muscle. Methods: Transgenic mice (C57BL/6 background, n = 5; 10 months of age) expressing yellow fluorescent protein in all motor nerves underwent vascular casting (Microfil). Excised epitrochlearis, gracilis, gluteus maximus, and spinotrapezius muscles were imaged at 380× and 760× and a computer-integrated tracing system (Neurolucida) was used to acquire 3-dimensional digital renderings of entire arteriolar and neural networks within each muscle. Results: Arteriolar networks were typically ,3-fold longer than neural networks. Nerves coursed with arterioles until terminating at motor endplates. Across muscles, proximity analyses revealed that , 75% of total nerve length (9.8,48.8 mm) lay within 200 ,m of the nearest arteriole (diameters of 15,60 , m). Conclusions: Somatic motor nerves and arterioles align closely within adult mammalian skeletal muscle. Understanding the signals governing neurovascular alignment may hold important clues for the advancement of tissue engineering and regeneration. [source]

Small-volume resuscitation: from experimental evidence to clinical routine.

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2002
Advantages, disadvantages of hypertonic solutions
Background: The concept of small-volume resuscitatioin (SVR) using hypertonic solutions encompasses the rapid infusion of a small dose (4 ml per kg body weight, i.e. approximately 250 ml in an adult patient) of 7.2,7.5% NaCl/colloid solution. Originally, SVR was aimed for initial therapy of severe hypovolemia and shock associated with trauma. Methods: The present review focusses on the findings concerning the working mechanisms responsible for the rapid onset of the circulatory effect, the impact of the colloid component on microcirculatory resuscitation, and describes the indications for its application in the preclinical scenario as well as perioperatively and in intensive care medicine. Results: With respect to the actual data base of clinical trials SVR seems to be superior to conventional volume therapy with regard to faster normalization of microvascular perfusion during shock phases and early resumption of organ function. Particularly patients with head trauma in association with systemic hypotension appear to benefit. Besides, potential indications for this concept include cardiac and cardiovascular surgery (attenuation of reperfusion injury during declamping phase) and burn injury. The review also describes disadvantaages and potential adverse effects of SVR: Conclusion: Small-volume resuscitation by means of hypertonic NaCl/colloid solutions stands for one of the most innovative concepts for primary resuscitation from trauma and shock established in the past decade. Today the spectrum of potential indications envolves not only prehospital trauma care, but also perioperative and intensive care therapy. [source]

Increased asymmetric dimethylarginine and endothelin 1 levels in secondary Raynaud's phenomenon: Implications for vascular dysfunction and progression of disease

Lymphocyte function antigen-1 mediates leukocyte adhesion and subsequent liver damage in endotoxemic mice

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2004
Xiang Li
Sepsis is associated with leukocyte activation and recruitment in the liver. We investigated the role of lymphocyte function antigen-1 (LFA-1) in endotoxin-induced leukocyte,endothelium interactions, microvascular perfusion failure, hepatocellular injury and apoptosis in the liver by use of gene-targeted mice, blocking antibodies and a synthetic inhibitor of LFA-1 (LFA703). For this purpose, mice were challenged with lipopolysaccharide (LPS)+D -galactosamine (Gal), and intravital microscopy of the liver microcirculation was conducted 6 h later. The number of firmly adherent leukocytes in response to LPS/Gal was reduced by 48% in LFA-1-deficient mice. Moreover, endotoxin-induced increases of apoptosis and enzyme markers of hepatocellular injury were decreased by 64 and 69,90%, respectively, in LFA-1-deficient mice. Furthermore, sinusoidal perfusion was improved in endotoxemic mice lacking LFA-1. A similar protective pattern was observed in endotoxemic mice pretreated with an antibody against LFA-1. Thus, immunoneutralization of LFA-1 reduced endotoxin-induced leukocyte adhesion by 55%, liver enzymes by 64,66% and apoptosis by 42%, in addition to the preservation of microvascular perfusion. Administration of a novel statin-derived inhibitor of LFA-1, LFA703, significantly decreased leukocyte adhesion (more than 56%) and the subsequent liver injury in endotoxemic mice. Thus, this study demonstrates a pivotal role of LFA-1 in supporting leukocyte adhesion in the liver. Moreover, interference with LFA-1-mediated leukocyte adhesion protects against endotoxemic liver damage, and may constitute a potential therapeutic strategy in sepsis. British Journal of Pharmacology (2004) 141, 709,716. doi:10.1038/sj.bjp.0705634 [source]

Ischaemic preconditioning improves microvascular perfusion and oxygenation following reperfusion injury of the intestine,

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 9 2005
I. H. Mallick
Background: Ischaemia,reperfusion (IR) injury of the intestine occurs commonly during abdominal surgery. Ischaemic preconditioning (IPC) provides a way of protecting the organ from damage inflicted by IR. This study was designed to evaluate the beneficial effect of IPC, focusing on the intestinal microcirculation and oxygenation in intestinal IR injury. Methods: Rats were allocated to three groups. Animals in the IR and IPC groups underwent 30 min of intestinal ischaemia followed by 2 h of reperfusion. In the IPC group this was preceded by 10 min of ischaemia and 10 min of reperfusion. Animals in the third group underwent laparotomy but no vascular occlusion. Intestinal microvascular perfusion, oxygenation and portal venous blood flow (PVF) were monitored continuously. At the end of the reperfusion period, blood samples were obtained for measurement of lactate dehydrogenase (LDH) and biopsies of ileum for histological evaluation. Results: IPC improved intestinal microvascular perfusion and tissue oxygenation significantly at the end of the reperfusion period (P < 0·001). PVF improved significantly in the IPC compared with the IR group (P = 0·005). The serum LDH concentration was significantly lower in the IPC than the IR group (mean(s.e.m.) 667·1(86·8) versus 1973·8(306·5) U/l; P < 0·001) Histological examination showed that ileal mucosa was significantly less injured in the IPC group. Conclusions: This study demonstrated that IPC improves intestinal microvascular perfusion and oxygenation. Copyright © 2005 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]

Local heat-shock priming-induced improvement in microvascular perfusion in osteomyocutaneous flaps is mediated by heat-shock protein 32

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 3 2001
Dr M. Rücker
Background: Stress conditioning is thought to improve microvascular free flap survival but the mechanisms of protection are not clear. The aim of this study was to determine whether local induction of heat-shock protein (HSP) 32 improves microvascular perfusion in transferred osteomyocutaneous flaps. Methods: The hindlimb harvest region of osteomyocutaneous flaps in Wistar rats was subjected to stress conditioning by local heating (30 min, 42·5°C) 24 h before microvascular flap transfer. In a second group of animals, after heat-shock priming, the action of HSP-32 was inhibited by tin protoporphyrin IX. Animals with unconditioned flaps served as controls. After transfer, the microcirculation of the muscle, cutaneous, subcutaneous and periosteal tissue of the flap was analysed quantitatively for 6 h using intravital fluorescence microscopy. Results: Immunohistochemistry revealed that HSP-32 was detectable only after priming and not in unconditioned flaps. Priming did not alter functional capillary density or capillary red blood cell velocity compared with that in unconditioned flaps. However, heat-shock priming induced significant capillary dilatation (P < 0·05) and thus a substantial increase in capillary blood flow volume (P < 0·05) in all tissues of the transferred flaps. Inhibition of HSP-32 by tin protoporphyrin IX completely abolished the priming-induced improvement in capillary perfusion, as indicated by the lack of increased capillary diameters and volumetric blood flow. Conclusion: The present study demonstrated that stress conditioning by local heat-shock priming improves nutritive perfusion in osteomyocutaneous flaps by capillary dilatation, probably mediated through the vasoactive action of HSP-32. © 2001 British Journal of Surgery Society Ltd [source]

Blockade of Kupffer cells by gadolinium chloride or dichloromethylene diphosphonate influences hepatic microcirculation after sepsis and haemorrhagic shock

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 7 2000
C. Herzog
Background The liver plays a key role in the host defence response after haemorrhagic shock,resuscitation (H/R) and sepsis. Kupffer cells (KCs) have been shown to be a trigger and motor of the subsequent inflammatory response syndrome. This may lead to hepatocellular dysfunction, microcirculatory alterations and liver injury involving, for example, tumour necrosis factor ,, interleukin (IL) 1 and IL-6. In a double-blind study the effect of KC blockade with either gadolinium chloride or liposome-entrapped dichloromethylene diphosphonate (DMD) on hepatic microvascular flow after H/R and sepsis was investigated. Methods After pretreatment with intravenous gadolinium chloride 10 mg kg,1, DMD 1 mg kg,1 or saline 24 h before induction of shock, male Sprague-Dawley rats (n = 6,10 per group and time) were subjected to either haemorrhagic shock (mean arterial pressure 40 mmHg) for 60 min followed by resuscitation or lipopolysaccharide (LPS) 1 mg kg,1 intravenously. Microvascular flow was assessed by intravital microscopy of fluorescence-marked leucocytes in liver sinusoids at baseline, and 1, 6 and 12 h after shock induction. Results In saline groups, the mean(s.d.) leucocyte flow was significantly (P < 0·05) higher at 1 h (20 759(2901) ,m3 s,1) and 6 h (16 278(2916) ,m3 s,1) after H/R as well as at 6 h after LPS (17 661(3949) ,m3 s,1) compared with the baseline value (13 509(1580) ,m3 s,1). Animals pretreated with gadolinium chloride showed a significant flow increase compared with baseline (11 797(1124) ,m3 s,1) at l h following H/R (26 269(5909) ,m3 s,1). In DMD-pretreated animals leucocyte flow showed no significant change over time, following either H/R or LPS treatment. However, flow was significantly higher at baseline (18 054(998) ,m3 s,1) versus gadolinium chloride and saline groups. In addition, DMD-treated animals showed higher flow values 1 h after LPS challenge (20 665(2337) ,m3 s,1) compared with gadolinium chloride (13 110(1224) ,m3 s,1) and saline (15 311(800) ,m3 s,1) groups. Similarly, at 12 h after H/R the DMD group (21 782(1887) ,m3 s,1) had higher flow values than the gadolinium chloride (14 026(1616) ,m3 s,1) and saline (15 999(3175) ,m3 s,1) groups. Conclusion These results imply a significant influence of KCs on regulation of microvascular perfusion in liver sinusoids under normal conditions as well as after H/R and sepsis. The data indicate differential pathways and effects of blocking KCs by gadolinium chloride and DMD. © 2000 British Journal of Surgery Society Ltd [source]