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At least 1,099 records · Page 61Linked to original sources

PubMed1980

[Microcirculation disturbances at the onset of diabetic retinopathy. New therapeutic procedures? (author's transl)].

The generalized capillary dilatation demonstrable at the early stage of diabetic retinopathy can now, on the basis of recent results in biochemistry, be assessed as an attempt at autoregulation in relative hypoxia of tissue. In patients with diabetic retinopathy, an elevated HbA1c concentration in the blood can be observed. The DPG level, however, is reduced. Both facts cause reduced oxygen transmission from blood to tissue. Rheologic changes such as augmented aggregation of erythrocytes, decreased deformability of erythrocytes and increased viscosity of blood and plasma finally lead to disturbances of microcirculation in the terminal vascular system. From these latest findings concerning the development of microcirculation disorders in diabetic retinopathy possible consequences for new therapeutic procedures can be derived.

Blood Glucose↗

PubMedDate not supplied

Platelet-vessel wall interactions in the microcirculation.

Platelet adhesion in the microcirculation is being reported and studied in a growing number of animal models of human disease. The adhesion molecules utilized by platelets to attach to the walls of microscopic blood vessels have been defined in most model systems, with P-selectin-PSGL-1, GPIIb/IIIa-fibrinogen-ICAM-1, and vWF-GPIba interactions serving as major adhesion pathways. The binding of platelets to adherent leukocytes appears to contribute significantly to the platelet-vessel wall interactions elicited in many models of disease. Shear forces generated by the movement of blood through the microcirculation exert an important influence on platelet adhesion. Physiologic regulation of platelet adhesion is mediated by both nitric oxide and superoxide, with the former inhibiting and the latter promoting platelet adhesion. The interactions between platelets and the walls of microscopic blood vessels appear to have important implications in the initiation and/or progression of tissue injury associated with different experimental models of human disease.

Blood Platelets↗

PubMed1995

Intravenous contrast medium aggravates the impairment of pancreatic microcirculation in necrotizing pancreatitis in the rat.

BACKGROUND: Previous reports demonstrated that radiographic contrast medium, as used in contrast-enhanced computed tomography, increases acinar necrosis and mortality in experimental pancreatitis. The authors studied the possibility that these changes may be related to an additional impairment of pancreatic microcirculation. METHODS: Fifty Wistar rats had acute pancreatitis induced by intraductal glycodeoxycholic acid (10 mmol/L for 10 min) and intravenous cerulein (5 micrograms/kg/hr for 6 hrs). After rehydration (16 mL/kg), pancreatic capillary perfusion was quantified by means of intravital microscopy at baseline before intravenous infusion of contrast medium (n = 25) or saline (n = 25), and 30 and 60 minutes thereafter. In addition to total capillary flow, capillaries were categorized as high- or low-flow (> or < 1.6 nL/min). RESULTS: Pancreatic capillary flow did not change in either high- or low-flow capillaries after saline infusion. However, contrast medium infusion induced a significant decrease of total capillary flow (p < 0.001). Analysis according to the relative flow rate revealed that this was primarily because of a significant additional reduction of perfusion in low-flow capillaries (p < 0.0001). Furthermore, complete capillary stasis was observed in 15.9 +/- 3.4% after contrast medium as compared with 3.2 +/- 1.2% after saline infusion (p < 0.006). CONCLUSION: Radiographic contrast medium aggravates the impairment of pancreatic microcirculation in experimental necrotizing pancreatitis.

Acute Disease↗

PubMed2002

Effects of hypothermia and rewarming on the mucosal villus microcirculation and survival after rat intestinal ischemia-reperfusion injury.

OBJECTIVE: To determine the effects of hypothermia and rewarming on changes in the villus microcirculation induced by intestinal ischemia-reperfusion (I/R). SUMMARY BACKGROUND DATA: The small intestine is extremely sensitive to I/R injury, and although hypothermia can reduce cellular injury, its capacity to influence the villous microcirculation after intestinal I/R is unclear, especially after the return to normothermic conditions. METHODS: Core body temperature of PVG rats was maintained at either 36 degrees to 38 degrees C (n = 12) or 30 degrees to 32 degrees C (n = 24) and then subjected to 30 minutes of intestinal ischemia. A subgroup of hypothermic animals (n = 12) were returned to normothermic conditions 120 minutes after clamp removal. The mucosal surface was visualized in an exteriorized ileal segment and macromolecular leak (MML) and leukocyte adhesion were monitored using in vivo microscopy (n = 6 in each group). MML from individual villi and numbers of adherent leukocytes within villi were determined for 2 to 4 hours after clamp removal. Heart rate and mean blood pressure were monitored in all animals. Control animals underwent sham surgery (n = 12). RESULTS: Ten of 12 normothermic animals failed to survive the reperfusion period, whereas all hypothermic animals and 11 of 12 of the hypothermic animals that were returned to normothermic conditions survived. MML was significantly increased in all animals subjected to I/R, although leakage was more marked in animals subjected to continuous normothermia. Enhanced leukocyte adhesion and decreased blood flow were observed only in normothermic animals. CONCLUSIONS: Hypothermia might prove to be an effective strategy for preventing adverse side effects in clinical settings in which intestinal I/R can be predicted.

Animals↗

PubMed1998

Effect of hemorrhage on cerebral microcirculation during normal and high cerebrospinal fluid pressure in pigs.

Studies on cerebral blood flow during hypotension and high intracranial pressure are scarce. Accordingly, this study examines the effects of increased cerebrospinal fluid (CSF) pressure on the cerebral circulatory response to hemorrhage. Measurements of cerebral microcirculation with laser Doppler flowmetry was performed in 12 pentobarbital-anesthetized pigs during hemorrhage, with and without high CSF pressure. Arterial and CSF pressures were monitored. Laser Doppler microprobes were positioned on the brain surface and in the gray and white matter. High CSF pressure (80% of mean arterial pressure) was induced by infusion of artificial CSF into the cisterna magna in eight pigs, whereas four animals served as controls. The response to rapid arterial bleeding at normal and high CSF pressure was recorded. When CSF pressure was normal, bleeding of 15% and 25% of the total blood volume caused a drop of cerebral perfusion pressure to 73 and 71 mmHg, respectively, causing a decrease in the laser Doppler signal to 90+/-8% of the baseline value. During high CSF pressure, the cerebral perfusion pressure was 23 mmHg and the laser Doppler signal was 52+/-29% of baseline. Bleeding of 15% of blood volume reduced the laser Doppler signal to 0 (equal to postmortem values) in three pigs, and bleeding of 25% of the blood volume reduced the laser Doppler signal to 0 in seven of eight pigs. Consequently, a blood loss that is of minor importance for the cerebral microcirculation in the normal state may be deleterious to the circulation when combined with high CSF pressure.

Animals↗

PubMed2001

Cerebral hypoxemia-ischemia and reoxygenation with 21% or 100% oxygen in newborn piglets: effects on extracellular levels of excitatory amino acids and microcirculation.

OBJECTIVE: To determine whether reoxygenation with 21% oxygen is preferable to 100% oxygen in normalizing extracellular levels of excitatory amino acids in the brains of hypoxic-ischemic newborn piglets and to compare this model of combined hypoxemia-ischemia to a previously used model of global hypoxemia. DESIGN: Prospective, randomized animal study. SETTING: Surgical research laboratory. SUBJECTS: Twenty-four anesthetized piglets, 1-3 days old. INTERVENTIONS: Hypoxemia-ischemia was achieved by normoventilation with 8% oxygen and temporary occlusion of the common carotid arteries. After 20 mins, reoxygenation-reperfusion was started with 21% oxygen (HI 21% group, n = 12) or 100% oxygen (HI 100% group, n = 12) for 30 mins followed by 21% oxygen. All piglets were observed for 2 hrs. MEASUREMENTS AND MAIN RESULTS: We measured extracellular concentrations of amino acids in striatum and hypoxanthine in cerebral cortex (microdialysis), microcirculation in cerebral cortex (laser Doppler), plasma hypoxanthine, and mean arterial pressure. During the 2-hr reoxygenation-reperfusion period, levels of amino acids were significantly higher in the HI 21% group compared with the HI 100% group (glutamate, p = 0.02; aspartate, p = 0.03). Mean arterial pressure was significantly lower in the HI 21% group (p = 0.04). Microcirculation decreased to <10% of baseline during hypoxemia-ischemia and normalized during reoxygenation-reperfusion in the HI 100% group, but it remained at a significantly lower level in the HI 21% group (p = 0.03). CONCLUSIONS: Significantly higher levels of excitatory amino acids in striatum, significantly lower mean arterial pressure, and a significantly greater degree of hypoperfusion in cerebral cortex were found after reoxygenation with 21% oxygen compared with 100% oxygen in normocapnic, hypoxemic-ischemic newborn piglets. This suggests a less favorable outcome in the group receiving room air.

Journal Article↗

PubMed1994

Display of the characteristics of endothelium-derived hyperpolarizing factor by a cytochrome P450-derived arachidonic acid metabolite in the coronary microcirculation.

1. In addition to nitric oxide (NO) and prostacyclin (PGI2) an endothelium-derived factor, which hyperpolarizes vascular smooth muscle cells via activation of K+ channels, contributes to the dilator effect of bradykinin in different vascular beds. Since this so-called endothelium-derived hyperpolarizing factor (EDHF) also seems to play an important role in the coronary circulation, we investigated its nature and mechanism of action in the rat isolated perfused heart (Langendorff preparation). 2. Bolus injections of bradykinin (1, 10, and 100 pmol) elicited a transient dose-dependent dilator response (e.g., 12 +/- 2% decrease in coronary perfusion pressure (CPP) at 10 pmol bradykinin, n = 41). Administration of the cyclo-oxygenase inhibitor, diclofenac (1 microM), augmented the bradykinin-induced dilation approximately twofold (n = 9 P < 0.01). Combined treatment with the NO synthase inhibitor, NG-nitro-L-arginine (30 microM) and diclofenac (1 microM) significantly reduced the duration, but increased the amplitude of the dilator response to bradykinin (27 +/- 2% decrease in CPP, n = 24, P < 0.01). 3. The abolition of this NG-nitro-L-arginine/diclofenac-insensitive dilator response to bradykinin by tetrabutylammonium (0.3 mM), an inhibitor of Ca(2+)-dependent K+ channels (4 +/- 1% decrease in CPP, n = 6, P < 0.01), supports the view that the dilator compound released in the coronary microcirculation is EDHF. 4. This EDHF-type dilation was reversibly inhibited by the phospholipase A2 inhibitor, quinacrine (3 microM, 9 +/- 3% decrease in CPP, n = 6, P < 0.01) and by the cytochrome P450 inhibitor SKF525a (3 microM, 6 +/- 1% decrease in CPP, n = 6, P < 0.01). 5. Tetrabutylammonium, quinacrine or SKF 525a did not affect the endothelium-independent dilator response to sodium nitroprusside (1 nmol), indicating that these compounds did not affect smooth muscle relaxation in a non-specific manner.6. These findings suggest that in the coronary microcirculation bradykinin stimulates the release of a cytochrome P450-derived arachidonic acid metabolite, which exhibits the characteristic features of EDHF.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2005

In vivo imaging of human pancreatic microcirculation and pancreatic tissue injury in clinical pancreas transplantation.

Pancreatitis remains to be a major complication following clinical pancreas transplantation. We performed orthogonal polarized spectral (OPS) imaging for direct in vivo visualization and quantification of human pancreatic microcirculation in six healthy donors for living donor liver transplantation and 13 patients undergoing simultaneous pancreas-kidney transplantation. We further determined the impact of microvascular dysfunction during early reperfusion on pancreatic graft injury. Exocrine and endocrine pancreatic impairment was determined by analysis of serum lipase, amylase and C-peptide levels. Compared to normal pancreas in liver donors (homogeneous acinar perfusion) functional capillary density (FCD) and capillary red blood flow velocity of reperfused grafts were significantly decreased. Elevated CRP concentrations on day 2 post-transplant and serum lipase and amylase levels determined on days 4-5 significantly correlated with microvascular dysfunction during the first 30 min of graft reperfusion. Post-transplant serum C-peptide also correlated significantly with pancreatic capillary perfusion. OPS imaging allows to intra-operatively assess physiologic pancreatic microcirculation and to determine microcirculatory impairment during early graft reperfusion. This impairment correlated with the manifestation of post-transplant dysfunction of both exocrine and endocrine pancreatic tissue. OPS imaging may be used clinically to determine the efficacy of interventions, aiming at attenuating microcirculatory impairment during the acute post-transplant reperfusion phase.

Adult↗

PubMed2006

Angiotensin II attenuates endothelium-dependent responses in the cerebral microcirculation through nox-2-derived radicals.

OBJECTIVE: Angiotensin II (Ang II) exerts deleterious effect on the cerebral circulation through production of reactive oxygen species (ROS). However, the enzymatic source of the ROS has not been defined. We tested the hypothesis that Ang II impairs endothelium-dependent responses in the cerebral microcirculation through ROS generated in cerebrovascular cells by the enzyme NADPH oxidase. METHODS AND RESULTS: Cerebral blood flow (CBF) was monitored by laser Doppler flowmetry in anesthetized mice equipped with a cranial window. Ang II (0.25+/-0.02 microg/kg per minute for 30 to 45 minutes) attenuated the CBF increase produced by the endothelium-dependent vasodilators acetylcholine (-42+/-5%; P<0.05), bradykinin (-53+/-5%; P<0.05), and A23187 (-43+/-4%; P<0.05), and induced cerebrovascular ROS production, assessed by hydroethidine fluoromicrography. These actions of Ang II were prevented by losartan, by the ROS scavenger Mn(III) tetrakis (4-benzoic acid) porphyrin chloride (100 micromol/L), or by the NADPH oxidase peptide inhibitor gp91ds-tat (1 micromol/L), and were not observed in mice lacking the NADPH oxidase subunit gp91phox (nox-2). CONCLUSIONS: Ang II impairs the endothelial regulation of the cerebral microcirculation through AT1 receptor-mediated cerebrovascular oxidative stress. The source of the ROS is a nox-2-containing NADPH oxidase. These effects of Ang II could threaten the cerebral blood supply and contribute to the increased susceptibility to stroke and dementia associated with hypertension.

Acetylcholine↗

PubMed2000

Microbubble persistence in the microcirculation during ischemia/reperfusion and inflammation is caused by integrin- and complement-mediated adherence to activated leukocytes.

BACKGROUND: Albumin microbubbles that are used for contrast echocardiography persist within the myocardial microcirculation after ischemia/reperfusion (I-R). The mechanism responsible for this phenomenon is unknown. METHODS AND RESULTS: Intravital microscopy of the microcirculation of exteriorized cremaster muscle was performed in 12 wild-type mice during intravenous injections of fluorescein-labeled microbubbles composed of albumin, anionic lipids, or cationic lipids. Injections were performed at baseline and after 30 to 90 minutes of I-R in 8 mice and 2 hours after intrascrotal tumor necrosis factor-alpha (TNF-alpha) in 4 mice. Microbubble adherence at baseline was uncommon (<2/50 high-power fields). After I-R, adherence increased (P<0.05) to 9+/-5 and 5+/-4 per 50 high-power fields for albumin and anionic lipid microbubbles, respectively, due to their attachment to leukocytes adherent to the venular endothelium. TNF-alpha produced even greater microbubble binding, regardless of the microbubble shell composition. The degree of microbubble attachment correlated (r=0.84 to 0.91) with the number of adhered leukocytes. Flow cytometry revealed that microbubbles preferentially attached to activated leukocytes. Albumin microbubble attachment was inhibited by blocking the leukocyte beta(2)-integrin Mac-1, whereas lipid microbubble binding was inhibited when incubations were performed in complement-depleted or heat-inactivated serum rather than control serum. CONCLUSIONS: Microvascular attachment of albumin and lipid microbubbles in the setting of I-R and TNF-alpha-induced inflammation is due to their beta(2)-integrin- and complement-mediated binding to activated leukocytes adherent to the venular wall. Thus, microbubble persistence on contrast ultrasonography may be useful for the detection and monitoring of leukocyte adhesion in inflammatory diseases.

Albumins↗

PubMed2005

Carbon monoxide from heme oxygenase-2 Is a tonic regulator against NO-dependent vasodilatation in the adult rat cerebral microcirculation.

Although the brain generates NO and carbon monoxide (CO), it is unknown how these gases and their enzyme systems interact with each other to regulate cerebrovascular function. We examined whether CO produced by heme oxygenase (HO) modulates generation and action of constitutive NO in the rat pial microcirculation. Immunohistochemical analyses indicated that HO-2 occurred in neurons and arachnoid trabecular cells, where NO synthase 1 (NOS1) was detectable, and also in vascular endothelium-expressing NOS3, suggesting colocalization of CO- and NO-generating sites. Intravital microscopy using a closed cranial window preparation revealed that blockade of the HO activity by zinc protoporphyrin IX significantly dilates arterioles. This vasodilatation depended on local NOS activities and was abolished by CO supplementation, suggesting that the gas derived from HO-2 tonically regulates NO-mediated vasodilatory response. Bioimaging of NO by laser-confocal microfluorography of diaminofluorescein indicated detectable amounts of NO at the microvascular wall, the subdural mesothelial cells, and arachnoid trabecular cells, which express NOS in and around the pial microvasculature. On CO inhibition by the HO inhibitor, regional NO formation was augmented in these cells. Such a pattern of accelerated NO formation depended on NOS activities and was again attenuated by the local CO supplementation. Studies using cultured porcine aortic endothelial cells suggested that the inhibitory action of CO on NOS could result from the photo-reversible gas binding to the prosthetic heme. Collectively, CO derived from HO-2 appears to serve as a tonic vasoregulator antagonizing NO-mediated vasodilatation in the rat cerebral microcirculation.

Animals↗

PubMed1999

Integrative physiology of coronary microcirculation.

Coronary microvessels play a crucial role for mechanoenergetic interaction between blood flow and myocardial function, which is not uniform transmurally. Thus, highly organized vascular regulations are required for matching local blood flow with myocardial energy requirement. Recently, new technologies to investigate in vivo coronary microcirculation with new knowledge of the signaling molecules for vascular regulation have revolutionized our abilities to understand the integrative regulation of coronary microcirculation. In this review, the mechanical aspects of the interaction between coronary blood flow and myocardium, coronary arte-rial tree and its roles in myocardial blood flow regulation, hierarchical and dynamic control of coronary flow, capillary network and function, function of venous drainage system, and molecular and cellular aspects of integrative coronary blood flow regulation are discussed, focusing on their integrational roles in maintaining coronary microvascular function and cell signaling.

Animals↗

PubMed1994

Gastric mucosal injury: microcirculation and Helicobacter pylori.

The integrity of gastric mucosa is well-balanced by an array of defensive mechanisms which protect the mucosa against external aggressive factors. When excessive stimulation of autonomic nervous system (irritation) is induced, microcirculatory disturbances easily lead to the gastric mucosal damage due to the formation of vasoactive mediators and oxygen radicals. In this review, our discussion has been focused on the co-ordinating function of the autonomic nervous system as well as the microcirculation as an important defense bastion. In this context, Helicobacter pylori represents an important pathogenic factor. In particular, we have discussed the contribution of monochloramine, and active oxidant, which is formed by neutrophils in the presence of ammonia derived from H. pylori to the gastric mucosal injury. Microcirculatory disturbances may be also involved in the pathogenesis of H. pylori-induced mucosal injury. On the basis of these considerations, we should not depend solely on the use of anti-acid secretory drugs for the treatment of gastric mucosal injury, but also should be aware of beneficial effect of mucosal protective drugs which may act on microcirculation and the autonomic nervous system.

Animals↗

PubMed2005

Two alternative models concerning the perialveolar microcirculation in mammalian lungs.

Despite the fact that the concept of sheet-flow in the pulmonary microcirculation of mammals was introduced more than three decades ago, the capillary circulatory model still prevails in the physiological literature. Since cardiac output is identical in the systemic and in pulmonary circulations, it is noteworthy that in the former, the resulting arterial pressure is five times higher than that of the latter, which means that the corresponding microcirculations must be radically different. The present study addresses this problem from both morphological and physiological perspectives.

Animals↗

PubMed1999

Radiation-induced leukocyte entrapment in the rat retinal microcirculation.

PURPOSE: To evaluate the effects of irradiation on leukocyte dynamics in the rat retinal microcirculation. METHODS: Thirty-five Brown-Norway rats received a dose of 10 Gy irradiation in one fraction. Leukocyte dynamics were studied with acridine orange digital fluorography, in which a nuclear fluorescent dye of acridine orange is used and examined by scanning laser ophthalmoscope. This technique allowed visualization of fluorescent leukocytes in vivo. The leukocyte dynamics were evaluated at 0, 4, 7, 14, 30, and 60 days after the irradiation. RESULTS: Mean leukocyte velocity in the retinal capillaries decreased immediately. It partially recovered on day 4 but then gradually decreased up to the 2-month mark. Low-dose irradiation induced entrapment of leukocytes in the retinal microcirculation. The number of entrapped leukocytes gradually increased with time. The major retinal vessels significantly constricted immediately after irradiation. The diameter was reduced by 76% in arteries and 75% in veins, 2 months after irradiation. CONCLUSIONS: Entrapped leukocytes may be activated and exacerbate vascular injury and microinfarction and thus may participate in the pathogenesis of radiation retinopathy.

Acridine Orange↗

PubMed1975

[Morphologic changes in the lymph microcirculation of serous membranes in rheumatism and systemic lupus erythematosus].

Microcirculation consists of two elements--hemomicrocirculation and lymphomicrocirculation, the both being closely interrelated with each other. Lymphomicrocirculation was studied on the serous membranes taken from dead people who had died of rheumatism and systemic lupus erythematosus (SLE). The microcirculatory bed in the serous membranes was identified by V. V. Kupriyanov's method. The results of the studies showed that in serous membranes in rheumatism there occurred gradual emptying of lymphomicrocirculation and at the same time--compensatory-adaptive and regeneratory processes, the latter being manifested in formation of blind projections of capillaries, in broadening of the lumen. In SLE the lymphatic link actively participated in elimination of metabolism products and underwent a continuous rearrangement with formation of closed and communicant cysterns. Moreover, there was noted a new formation of lymphatic capillaries, which should be considered as a compensatory-adaptive process. Hemo- and lymphomicrocirculation elements are intimately connected due to close contacts between capillaries of the two elements of microcirculation, however, without formation of connecting fistulas. Hemo- and lymphomicrocirculation is an integrate, and under conditions of pathology there developed therein compensatory-adaptive and regenerative processes aimed at the maintenance of tissue metabolic and hemodynamic homeostasis.

Adolescent↗

PubMed2003

[Morphodynamic analysis of the role of leukocytes in the microcirculation disorder of the cerebral cortex].

The aim of this work was to establish the reasons for the disturbances of microcirculation (no reflow) during various kinds of oxygen starvation of the brain. Using contact optics and video-recording, direct observations were performed and leukocyte and erythrocyte displacement was monitored in the blood vessels of rat cerebral cortex in vivo in normoxia, during the development of various kinds of oxygen deficiency up to the terminal periods of life of an organism. In normoxia leukocytes were shown to decelerate erythrocyte movement in capillaries and to cause the irregularity of the capillary blood flow. Using the color videofilm recording it was shown that at deep stages of brain oxygen deficiency the disturbances of microcirculation up to its complete cessation were explained by the occlusion of venous microvessels as a result of massive adhesion of leukocytes to the inner surface of venules and the smallest veins. The co-adhesion of leukocytes was also found to take place. The latter leads to the formation of large leukocyte aggregates in venous vessels, results in "no reflow" effect. Leukocyte aggregates in veins block the venous outflow from the brain and may become the immediate cause of organism death as a result of disruption of circulation and oxygen deficiency.

Animals↗

PubMed1978

Pharmacological factors influencing permeability of the bronchial microcirculation.

The bronchial microcirculation is organized as a network of interconnected superficial and deep small blood vessels that extend throughout the bronchial tree. The close proximity of the bronchial venules to the origin of the pulmonary lymphatics suggests a role in fluid balance in the lung. The responsiveness of the venous segment of this network to agents influencing permeability clearly indicates a role in the genesis of certain types of noncardiogenic interstitial edema. The responsiveness of the venous segment of the bronchial circulation to neural and humoral stimuli raises the possibility of a significant role in the distribution of blood flow between the mucosa and peribronchial space. Such control may play a significant role in heat and water exchange between blood and air. Thus, these observations indicate that the bronchial microcirculation is involved with aspects of pulmonary function other than the nutrition of the bronchi, nerves, pleura, and large pulmonary blood vessels.

Animals↗