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Results for “Microcirculation”

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At least 577 records · Page 32Linked to original sources

PubMed1976

Effect of ionizing radiation on liver microcirculation and oxygenation.

Platelet aggregation and adhesiveness, as well as TPO2 responses to hypoxia were measured as microcirculation parameters in beagle dogs subject to Co60 ionizing radiation to a dose of 4600 rads in 5 weeks. Simultaneously, changes in blood chemistry and coagulation were also determined. Marked changes in all studied parameters in the post radiation period lead to the conclusion that radiation liver damage is at least in part mediated through microcirculation disturbances.

Animals↗

PubMed1986

Hepatic microcirculation in Zucker fatty rats.

We have developed a microscopic analyzing system for studying in vivo hepatic microcirculation, and measured the sinusoidal erythrocyte flow velocity simultaneously in the various sinusoids. With this system and organ reflectance spectrophotometry, the pathophysiological role of microcirculation and of energy metabolism in Zucker fatty rats were studied. The results were as follows: The erythrocyte flow velocity in the predominant sinusoids in the fatty rats was similar to that of the control rats, but the intersinusoidal erythrocyte flow was undetected in the fatty liver. Index of regional hepatic blood volume, regional hepatic blood flow and oxygen saturation of Hb decreased significantly in the fatty rats. The estimated in vivo oxygen consumption was not changed in the fatty liver. From these data, it is concluded that in Zucker fatty rats a marked fatty infiltration causes a decreased hepatic tissue blood flow and volume, but relatively homogeneous erythrocyte flow with an increased extraction of oxygen compensated the decreased vascular beds and maintained normal energy metabolism.

Animals↗

PubMedDate not supplied

Prevention of ionizing radiation-induced liver microcirculation changes by the use of flow improvers.

Platelet aggregation and adhesiveness, as well as TpO2 responses to hypoxia were measured as microcirculation parameters in beagle dogs subject to Co60 ionizing radiation to a dose of 4600 rads in 5 weeks. Simultaneously, changes in blood chemistry and coagulation were also determined. Marked changes in all studied parameters in the post radiation period lead to the conclusion that the radiation liver damage, which is at least in part mediated through microcirculation disturbances, can be prevented with the flow improver, Rheomacrodex.

Animals↗

PubMed1996

Quantitative analysis of the microcirculation of xenogeneic haemoperfused rat livers by intravital microscopy.

Livers from male Sprague-Dawley rats were perfused with heparinised, unmodified isogeneic rat blood (n = 6) or xenogeneic human blood. The microcirculation of these livers, as the primary manifestation of hyperacute xenogeneic rejection, was directly observed and quantified by using fluorescence videomicroscopy. Bile flow and enzyme release of the isogeneic perfused livers were in the physiological range, whereas bile flow was significantly reduced and enzyme release increased during xenogeneic perfusion. In contrast to an almost physiological acinar (90.4%) and sinusoidal (93.6%) perfusion rate in the isogeneic group, a rapid breakdown of microcirculation with an acinar perfusion index of 47.5% and a sinusoidal perfusion rate of 67.1% were found in the xenogeneic group. This direct quantification of microcirculatory parameters is a step forward towards sensitive and early characterisation of the severity of the xenogeneic rejection of the liver.

Animals↗

PubMed1995

Volatile and intravenous anesthetics selectively attenuate the release of endothelium-derived hyperpolarizing factor elicited by bradykinin in the coronary microcirculation.

In addition to nitric oxide (NO) and prostacyclin (PGI2) another endothelium-derived factor, which hyperpolarizes vascular smooth muscle cell via activation of K+ channels, contributes to the vasorelaxant effect of bradykinin in different vascular beds. Preliminary findings suggest that this endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation is attenuated by both volatile and intravenous anesthetics. Since EDHF may play an important role in the coronary microcirculation, we investigated the effects of isoflurane (2 vol.% equivalent to approximately 250 microM), etomidate (30 and 100 microM), phenobarbital (100 microM) and thiopental (30 and 100 microM) on the EDHF-mediated dilator response to bradykinin and on the endothelium-independent dilatation evoked by sodium nitroprusside (SNP) in the isolated saline-perfused rat heart (Langendorff preparation). None of the anesthetics tested affected the dilator response to bradykinin or SNP under basal conditions. However, following inhibition of NO and PGI2 formation with NG-nitro-L-arginine (100 microM) and diclofenac (1 microM) respectively, isoflurane, etomidate and thiopental, but not phenobarbital, significantly attenuated the NO/PGI2-independent, i.e. EDHF-mediated dilator response to bradykinin, while the vasorelaxant effect of SNP remained unaffected. Isoflurane, etomidate and thiopental, but not phenobarbital, display cytochrome P450-inhibiting properties, suggesting that these anesthetics impair the cytochrome P450-dependent synthesis of EDHF in the coronary microcirculation.

Analysis of Variance↗

PubMed1993

Lack of short-term autoregulation in the cochlear microcirculation in guinea pigs.

To determine the relationship between the dynamics of mean arterial blood pressure (MABP) elevation and possible changes in the cochlear microcirculation the cochlear blood flow (CBF) was measured in guinea pigs by a laser Doppler method. The MABP was elevated at rates ranging from 0.02 mmHg/s to 4 mmHg/s by intravenous infusions of norepinephrine or epinephrine in various concentrations. A fall in MABP was induced by exsanguination of the animals. The purpose of the experiments was to record the time of onset and course of an expected autoregulation in the cochlea in response to slow or rapid changes in MABP. The data suggest that there is no short-term autoregulation in the cochlear microcirculation reflecting the increase of the MABP, but a slight compensation occurs when the MABP declines. These latter changes could be attributed to the high CO2 sensitivity of the cochlear blood vessels.

Animals↗

PubMed1990

[Disorders of microcirculation in colon anastomoses and their significance for the pathogenesis of suture dehiscence].

In this morphologic experimental study in the rabbit disturbances in the microcirculation at the site of colonic anastomoses were found in all suture techniques employed. They are caused by resection, intraoperative traumatization, the suture technique, and, secondarily, by abscess formation on the anastomosis. The suture-induced disturbances of the microcirculation lead to necroses of the mucosa, partial and complete necroses of the inverted cuff, and transmural necroses with destruction of the sero-serous contact zone. For the pathogenesis of anastomotic dehiscence only transmural and extensive complete necroses of the anastomotic bulge, including the serosal contact, are important. They result in transmural abscess formations which correspond to microscopic small secondary anastomotic leakages.

Abscess↗

PubMed1993

Role of thromboxane A2 in a microcirculation disorder of the rat inner ear.

Since thromboxane (TX) A2 causes vasoconstriction and platelet aggregation, we evaluation the effect of a TXA2 receptor antagonist (vapiprost) and a TXA2 synthetase inhibitor (Y-20811) on a microcirculation disorder in the rat inner ear that was induced by a photochemical reaction between an intravenous injection of rose bengal (RB) and green light. A gradual decrease of the cochlear action potential (CAP) to an 8 kHz sound stimulus was measured with an electrocochleogram and occurred after the RB injection. The CAP then disappeared 5 min after the injection of RB. Both vapiprost and Y-20811 significantly prolonged the time required to complete suppression of the CAP as compared with saline as control. These findings indicate that TXA2 may play an important role in microcirculation disorders in the rat inner ear.

Action Potentials↗

PubMed1996

The role of the microcirculation in multiple organ dysfunction syndrome (MODS): a review and perspective.

Major advances in intensive care medicine during the past two decades have altered the spectrum of disease encountered by intensive care physicians, anaesthesiologists, traumatologists and pathologists. One of the most important manifestations of severe trauma or infections is the multiple organ dysfunction syndrome (MODS), a life-threatening condition that often ends in multiple organ failure (MOF) and death. Evidence gathered from clinical and morphological observations in humans, taken together with experimental animal studies and a vast accumulation of in vitro data, clearly indicate that the microcirculation lies at the centre of this complex process, which results in peripheral vascular insufficiency, inadequate oxygen delivery to vital organs, and hence, severe organ dysfunction. The multifunctional nature of the endothelium makes it a prime candidate for study of the pathomechanisms of MODS. This paper reviews the evidence for the hypothesis that the microcirculation, and in particular its endothelial component, has a central role in the pathogenesis of MODS. The evidence is reviewed principally from the standpoints of classical morbid anatomy and cell pathobiology.

Animals↗

PubMed1989

Effects of Fusobacterium necrophorum on the mesenteric microcirculation of guinea pigs.

Thrombi formation was demonstrated in mesenteric microcirculation of guinea pigs inoculated with Fusobacterium necrophorum and the bacterial hemagglutinin (HA). The thrombi were initially observed in venules and later, in arterioles. Immunofluorescence study revealed that the HA bound to the thrombi in the microcirculation. These results indicate that thrombosis is an early step in the pathogenesis of necrosis.

Animals↗

PubMed1988

The effects of slip velocity at a membrane surface on blood flow in the microcirculation.

Closed-form solutions are presented for blood flow in the microcirculation by taking into account the influence of slip velocity at the membrane surface. In this study, the convective inertia force is neglected in comparison with that of blood viscosity on the basis of the smallness of the Reynolds number of the flow in microcirculation. The permeability property of the blood vessel is based on the well known Starling's hypothesis. The effects of slip coefficient on the velocity and pressure fields are clearly depicted.

Blood Flow Velocity↗

PubMed1987

An investigation of the microcirculation of the human tympanic membrane with laser-Doppler flowmetry.

The present investigation was performed to evaluate the use of laser-Doppler flowmetry as a means for measuring the blood flow of the microcirculation of the human tympanic membrane. The blood cell flux in the microvascular bed of the normal tympanic membrane was measured in healthy subjects. The laser-Doppler output signals continuously recorded showed a steady value ranging from 70 to about 120 V, as well as spontaneous oscillations (or rhythmical active vasomotion). Our findings show that the laser-Doppler instrument tested seems to be useful for evaluating blood flow changes in the microcirculation of the human tympanic membrane.

Adult↗

PubMed1993

Doxorubicin and local hyperthermia in the microcirculation of skeletal muscle.

Doxorubicin HCl (Doxo) is an established intercalating antitumor drug. Specific side effects of Doxo primarily affect the cardiac muscle tissue to cause cardiac arrhythmias and chronic cardiomyopathies. The mechanism of action of these side effects is incompletely understood. Thus, the first objective of the present study was to test whether Doxo might have a direct effect on the microcirculation of muscular tissue. We studied large and small arterioles and large venules in the cremaster muscle of rats before and after sequential infusion of 1 (low-dose) and 10 mg/kg (high-dose) Doxo. Large arterioles showed some constriction after low Doxo doses and pronounced constriction after high Doxo doses, whereas small arterioles showed a variable response to low Doxo doses. At high Doxo doses, small arterioles dilated almost maximally (80% of the maximal response to nitroprusside). The heart rate and the diameter of large venules did not change at high Doxo doses, although the blood pressure decreased. This indicates that Doxo directly affects skeletal muscle arterioles. The second purpose of this study was to determine whether local hyperthermia would influence the microcirculation of muscular tissue such that the systemic concentration of Doxo could be reduced. In this second series of experiments, we tested whether local hyperthermia would have an effect on the skeletal muscle microvasculature and whether Doxo would change that response. Local hyperthermia alone did not alter the diameter of small arterioles or large venules, but we observed constriction of large arterioles at temperatures above 37 degrees C and during continued (60-min) hyperthermia at 40 degrees C. The low dose of Doxo did not alter these microvascular diameters at 40 degrees C. However, local hyperthermia at 40 degrees C changed the response of small arterioles to low doxo doses (no vasodilation was observed). Large arterioles continued to constrict in response to Doxo during hyperthermia. These data suggest that large arteriolar responses could be partly responsible for the toxic effect of Doxo on cardiac muscle and that local hyperthermia potentiates that response.

Animals↗

PubMed1985

Lead-induced permeability changes in immature vessels of the developing cerebellar microcirculation.

The ultrastructure and microcirculatory permeability changes of lead encephalopathy were studied in an animal model using horseradish peroxidase as an intravascular tracer. The fine structure of capillary sprouts in the developing cerebellar microcirculation of lead-poisoned rats were described. Immature vessels, characterized by the presence of endothelial sprouts, were found to have focal areas of endothelial injury with degenerating endothelial cells. These disruptions of the microcirculatory endothelium had tracer extending from the vessel lumen to the surrounding neuropil. The degenerating endothelial cells were found as early as 24-28 h after the first administration of lead acetate by gastric lavage (2-3-day-old rats). The early injury to endothelial cells of immature vessels in the developing microcirculation is suggested as an important component of the vascular permeability changes which characterize lead encephalopathy. Older animals (5-10 days old) had microaneurysmal vascular dilatations which had a complex internal structure formed by endothelial cells. These microaneurysmally dilated vessels may represent an endothelial response to preceding endothelial injury of immature vessels.

Animals↗

PubMed1992

A new model of equilibrium dysfunction in the rat induced by photochemical damage to the inner ear's microcirculation.

A new photochemical method was employed to damage the inner ear microcirculation in the rat. Under pentobarbital anesthesia, the middle ear was exposed by a ventral approach and the tympanic membrane and the malleus and incus were removed. The vestibule was then illuminated by a filtered xenon light (wave length: 540 nm) while rose bengal was infused intravenously. Microscopic examination revealed disintegration of the hair cells in the vestibule. Changes could be prevented by pretreatment with intravenous acetylsalicylic acid (ASA) or heparin. Twenty-four hours after the completion of photo-illumination the rats exhibited nystagmus toward the intact ear and showed rolling during the swimming test, both signs of equilibrium dysfunction. These findings were inhibited by ASA or heparin pretreatment. Our present results indicate that our method causes a photochemically induced occlusion in the rat's inner ear microcirculation and may be useful for evaluating the various effects of drugs on the inner ear.

Animals↗

PubMed1985

[Hemorrhagic pancreatitis: effect of dextran 40 and plasma on microcirculation disorders of the pancreas].

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Continuous measurements of pancreatic blood flow, cardiac output, mean arterial blood pressure and pancreatic oxygen consumption were made under normal conditions and during acute pancreatitis. All animals received 100 ml of saline/h during the time of observation. Three methods of therapy then were instituted in the dogs starting 30 min after induction of pancreatitis. 10 dogs served as controls (saline 100 ml/h); in 6 dogs additionally 15 ml/kg plasma was infused over 45 min and 6 dogs received 1.5 ml/kg Dextran 40/h continuously. Hemorrhagic pancreatitis was characterized by a fall in cardiac output and mean arterial pressure and the development of severe impairment of the pancreatic microcirculation with early reduction of pancreatic blood flow followed by a fall in pancreatic oxygen consumption. Administration of plasma produced a significant increase in cardiac output; however, blood pressure and pancreatic blood flow remained low. Low-molecular weight Dextran has no influence on cardiac output, but significantly improved the blood pressure and leads to a normalization in pancreatic blood flow and oxygen consumption. These results suggest that low-molecular weight Dextran appears to reverse the impairment of microcirculation and hypoxia of the pancreas and limits the progression from edematous to hemorrhagic pancreatitis and irreversible pancreatic damage.

Animals↗

PubMed1993

In vivo effect of visible light on feline cortical microcirculation.

The present study was designed to test the hypothesis that prolonged illumination of the cerebral cortex, for instance during neurosurgical interventions, may affect the pial microcirculation. Experiments were performed with the closed window technique in cats. The cortical surface below the window was exposed to visible, cold light of 61,000 lumens/m2 (lux) over a period of 1 to 5 hours. Pial arterioles reacted with a slight initial dilatation to 106.8 +/- 2.6% of their resting diameter after switching to the high intensity light. Measurements of the cortical surface temperature showed an average temperature increase of 1.5 +/- 0.34 degrees C within the first 10 minutes of illumination. For assessment of pial vascular function, the responses to topical application of acetylcholine (ACh) were tested before and during the illumination period. The effect of sustained illumination on the cortical microcirculation consisted of abolition of the endothelium dependent relaxation due to ACh, and of intravascular thrombus formation, the latter, however, only in the presence of topically applied ACh. The suspected mechanism responsible for these functional alterations is light-induced generation of free oxygen radicals which are known to inactivate or destroy the endothelium-derived relaxing factor (EDRF). Further studies are recommended to elucidate the practical and clinical relevance of these findings to neurosurgical procedures.

Acetylcholine↗

PubMed1982

Effects of prolonged cold injury on the subcutaneous microcirculation of the hamster. I. Technique, morphology and tissue oxygenation.

An animal model is described allowing for direct measurements of local tissue PO2, microhemodynamics and vascular density in the event of a prolonged non freezing cold injury. The model consists of implanting a transparent skin fold chamber in the dorsal skin fold in hamsters and of inserting two permanent indwelling catheters in jugular vein and carotid artery, respectively. The microcirculation was studied using a Wild Photomacroscope for photography and a platinum multiwire electrode for measurements of local PO2 in the conscious animal. After 72 h of recovery from anesthesia and surgery, the experimental was started with the animal immobilized. The decrease of local s.c. temperature was achieved by perfusing a heat exchanger with distilled H2O and Isopropanol 70% (1:1) at a rate of 81/min with the heat exchanger located directly beneath the aluminium frame of the chamber. With this technique, a decrease in local tissue temperature from 28 degrees C to 15 degrees C could be obtained within 15 min and was kept constant for 60 min. After photography of the microcirculation and local PO2-measurements, the local temperature was further reduced to 5 degrees C with 15 min. Sixty minutes later, the area exposed was slowly rewarmed from a level of 5 degrees C within 30 min. This procedure was repeated in intervals of 24 h over a period of five days. During the course of the experiments, local PO2 values shifted toward hypoxic or even anoxic values. Intravital microscopic observation revealed aggregate formation, stasis and obstruction of capillary flow associated with pronounced tissue anoxia after five cold exposures. This event resulted inevitably in tissue necrosis and scar formation after seven consecutive exposures to cold. It is concluded that this model can be used to study the effects of local non freezing cold injury in a precisely reproducible manner.

Animals↗