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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purposes of this study were to develop an in vivo model of skeletal muscle ischemia--reperfusion to assess the patterns of microvascular injury, to evaluate a scoring system that permits quantitation of this injury, and to determine in vivo the extent of white blood cell adhesion within the microcirculation during the acute postreperfusion period. Syrian golden hamsters underwent 3.0 or 4.5 hr of lower extremity ischemia without anticoagulation. The microcirculation of the tibialis anterior muscle was visualized by fluorescent intravital microscopy (700X). During the first 1.5 hr of reperfusion the microvascular injury was scored by a grading system based upon the extent of extravasation of fluorescein-labeled albumin and the degree and level of microvessel obstruction. To correlate the observed changes in the microcirculation to changes in the whole muscle, in a separate group of animals, pH changes in the tibialis anterior muscle were measured at the same time intervals under identical experimental conditions as the microvascular measurements. White blood cells were transiently fluoresced at 1.5 hr after reperfusion by intravenous acridine red and the number of white blood cells rolling (rollers) or sticking (stickers) to the endothelium during a 30-sec observation period was recorded. Two distinct patterns of microvascular injury were seen: after 3.0 hr of ischemia there was a progressive extravasation, some capillary but no arteriolar or venular obstruction, flow velocities increased over time; after 4.5 hr of ischemia there was a greater heterogeneity of injury, primary "no reflow," extensive capillary, arteriolar, and venular obstruction, as well as a progressive decline in flow velocities. Thrombosis of microvessels was rare. There was no inflow vessel thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo assessment of acute microvascular injury after reperfusion of ischemic tibialis anterior muscle of the hamster. 236 24

The effect of hypervolemic hemodilution and hyperoncotic infusions on the reactive hyperemic volume flow rates during the initial minutes of post-ischemic reperfusion in the rat's tibialis anterior muscle after 1, 2 and 3 hours of tourniquet ischemia was studied using the 133Xenon clearance technique. Median maximal hyperemic peak reflow rates in muscle of non-infused, control animals upon release of a tourniquet were 56.5, 43.6 and 7.5 ml.min-1 x 100 g-1 respectively, demonstrating the development of a post-ischemic reperfusion impairment, a no-reflow phenomenon, that increased with the duration of the preceding period of ischemia. Rapid infusions of isotonic saline solutions over the last five minutes of tourniquet ischemia, aiming at increasing the circulating blood volume of the animals at start of the ischemic leg reperfusion by 2.0, 4.5, and 9.5 ml respectively, or by approximately 10%, 25% and 50%, gave no significant improvement in post-ischemic reperfusion, except in that following 3 hours of leg ischemia and after the two largest volumes. Rapid infusions of solutions of human albumin in a concentration of 200 mg.ml-1 to an amount approximately equalling 0.15, 0.40 and 0.75 g.kg-1 bodyweight till the moment the reperfusion was started, aiming to increase circulating albumin until the start of reperfusion by about 10%, 20% and 40%, significantly improved immediate peak hyperemic reperfusion in proportion to dose and more than doubled post-ischemic peak hyperemic reperfusion rates after the largest dose to 129.6, 102.6 and 39.1 ml.min-1 x 100 g-1 respectively. This improvement in initial post-ischemic hyperemia by hyperoncotic reperfusion may be of importance for achieving a rapid post-ischemic tissue oxygenation and for preventing tissue edema.
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PMID:The effect of hypervolemic hemodilution and hyperoncotic infusions on the immediate reperfusion impairment in skeletal muscle of the rat after prolonged total ischemia. 239 48

Effects of diltiazem on coronary vascular functional integrity were assessed in isolated rabbit hearts during reperfusion after 30 min of global, no-flow ischemia. External detection of radiolabeled albumin, [125I]bovine serum albumin ([125I]BSA), and compartmental-model analysis were used to estimate the mean transit time of [125I]BSA (tBSA), vascular volume (V1), and vascular into extravascular space clearance (F21) for [125I]BSA. Perfusion pressure, left ventricular (LV) end-diastolic pressure, LV developed pressure, maximum +dP/dt, and V1 remained constant during 5 h of continuous perfusion, while tBSA and F21 gradually increased (1.5 and 2.4 times baseline, respectively). Diltiazem, 4 microM, increased total water content (8.5%) and decreased perfusion pressure (11%), LV developed pressure (22%), and +dP/dt (24%) in nonischemic control experiments, but did not significantly affect estimates of V1, extracellular space, tBSA, or albumin permeation. During reperfusion after 30 min of ischemia, V1 increased 40% and perfusion pressure increased 60%, while tBSA and F21 increased three and eight times baseline, respectively. LV developed pressure and +dP/dt returned to control levels, even though the water content and extracellular space of ischemic hearts were increased significantly. Diltiazem, 4 microM, blocked ischemia-reperfusion-induced increases in water content, extracellular space, vascular resistance, V1, and vascular permeability to [125I]BSA, without reducing LV developed pressure or +dP/dt relative to nonischemic diltiazem controls. These results suggest that protection of ischemic myocardium by diltiazem is mediated, at least in part, by preservation of vascular functional integrity.
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PMID:Coronary vascular hemodynamic and permeability changes during reperfusion after no-flow ischemia in isolated, diltiazem-treated rabbit hearts. 241 Jun 70

Acute pancreatitis was initiated in the isolated ex vivo, perfused canine pancreas preparation by exposing the gland to a 2 hour period of ischemia before a 4 hour perfusion period. The pancreatitis was manifested by edema formation, weight gain, and hyperamylasemia. When the osmotically active agent albumin was added to the perfusate at the end of the ischemic period, virtually no edema developed, weight gain was minimal, and the amylase level remained within normal limits during the subsequent 4 hour perfusion period. This suggests that a change in capillary permeability may be an early step in the pathogenesis of ischemia-induced pancreatitis in this experimental model.
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PMID:Experimental ischemic pancreatitis: treatment with albumin. 241 56

Tritiated thymidine autoradiography was used to measure cellular proliferation after ischemic injury in gerbil brain. Gerbils were subjected to bilateral occlusion of the common carotid arteries which resulted in areas of necrosis, or infarcts, in the posterior thalamus or midbrain. From 12 h to 10 days following the ischemia, gerbils were injected with 3H thymidine, sacrificed 4 h later, and the brains sectioned. In order to identify astrocytes and monocytes/macrophages, immunocytochemistry was performed prior to autoradiography, using antisera against glial fibrillary acidic protein and endothelial-monocyte reticuloendothelial antigen, respectively. Immunocytochemistry was also used to visualize microvessel laminin, myelin, and leakage of serum albumin. Lastly, a histochemical procedure for acid phosphatase activity was employed to verify cellular phagocytic activity in the wound. A reproducible sequence of reactions took place during the first 10 days after ischemia. Early changes included leakage of albumin and myelin breakdown, followed by arrival of monocytes at 2 days and their differentiation into macrophages by 5 days. These cells exhibited intense proliferation from 2 to 6 days post-ischemia. Microvessel endothelial cells were maximally labeled at 4 days post-ischemia. Hypertrophied astrocytes were apparent at 2 days and proliferated from 3 to 7 days post-ischemia, and by 10 days the wound was replaced by a "glial scar".
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PMID:Cell proliferation after ischemic injury in gerbil brain. An immunocytochemical and autoradiographic study. 241 99

Recent studies suggest that polymorphonuclear leukocytes (PMNs) may cause additional myocyte injury during reperfusion of ischemic myocardium. The present study was done to investigate whether PMNs accumulate in myocardium during early reperfusion after reversible or irreversible ischemic injury. Open-chest anesthetized dogs underwent circumflex coronary occlusions for 12 min (n = 5), 40 min (n = 8), or 90 min (n = 8), followed by 1 h of reperfusion. Autologous PMNs were radiolabeled with 111In and reinjected to quantitate myocardial PMN influx during reflow. 125I-labeled albumin was injected simultaneously to correct for 111In associated with plasma proteins in myocardial tissue. The number of PMNs was determined in the inner, middle, and outer one-third of nonischemic and ischemic-reperfused myocardium. In the 12-min group, 40% fewer PMNs were present in the reperfused than in the nonischemic control tissue. In contrast, in both the 40- and 90-min groups, PMN accumulation was two- to sixfold greater in the ischemic-reperfused than nonischemic myocardium, with a transmural gradient of PMN influx increasing from the outer to inner layers. Collateral blood flow, measured with radioactive microspheres, was not significantly different among the three groups. The failure of PMNs to accumulate during reperfusion after 12 min of ischemia does not support the hypothesis that PMNs contribute to postischemic dysfunction of reversibly injured myocytes. Whether PMNs caused cell death during early reperfusion after longer ischemic episodes remains unknown; however, the rapidity of PMN accumulation in the zones of predicted infarction is consistent with this possibility.
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PMID:Myocardial neutrophil accumulation during reperfusion after reversible or irreversible ischemic injury. 246 Oct 99

Whether and how lidocaine reduced infarct size in a canine model of ischemia and reperfusion was investigated. Twenty dogs underwent a 90-min left anterior descending artery ligation and 300 min of reperfusion. Infarct size was measured by triphenyl tetrazolium chloride and the region at risk by 99Tc-labeled albumin microspheres injected during ischemia. In 10 dogs, lidocaine (70 micrograms/kg/min i.v.) was infused 90 min prior to and during ischemia and reperfusion, while 10 dogs were untreated. The ratio of infarct to risk area was 35.2 +/- 3.4% (SEM) in lidocaine dogs vs. 48.5 +/- 5.3% in untreated dogs (p less than 0.05). Lidocaine did not reduce neutrophil accumulation in ischemic and reperfused myocardium at 5 h of reperfusion, inhibit stimulated neutrophil superoxide production, or scavenge superoxide in vitro. However, during early reperfusion, lidocaine reduced coronary sinus levels of a lipid peroxidation product (conjugated dienes). Thus, clinically relevant lidocaine infusion rates reduced myocardial infarct size when given prior to and during ischemia and reperfusion. This protective effect may be due to lidocaine's membrane stabilizing effects, which could have protected the myocardial cell membrane from lipid peroxidation.
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PMID:Lidocaine reduces canine infarct size and decreases release of a lipid peroxidation product. 248 84

Because it is postulated that compartment syndrome developing secondary to an acute arterial occlusion may be due to reperfusion injury, oxygen-derived free radicals have been implicated in its genesis. To assess the possible beneficial effect of free radical scavengers in this setting, we used a previously established in vivo canine model of compartment syndrome to compare four groups: group I, no treatment; group II, prophylactic fasciotomy; group III, intravenous albumin conjugated superoxide dismutase (SOD); group IV, intravenous mannitol (hydroxyl radical scavenger). Both hind limbs were completely devascularized at the popliteal level except for an isolated pedicle to the anterior compartment. The right limb served as the nonischemic control, whereas the left underwent 8 hours of ischemia followed by reperfusion. Continuous monitoring of transfascial oxygen tension (tfPO2) demonstrated severe ischemia during occlusion (tfPO2 5.7 +/- 5.1 mm Hg) and restoration of blood flow with reperfusion (mean tfPO2 50 to 60 mm Hg). Measurements of compartment pressure were significantly higher after reperfusion in groups I, III, and IV when compared with those of group II (p less than 0.001, groups I and II; p less than 0.01, group IV). Extent of muscle necrosis assessed by technetium pyrophosphate scanning and expressed as a ratio of left to right legs was as follows: group I, 8.9 +/- 5.0; group II, 2.6 +/- 0.5; group III, 2.8 +/- 0.8; group IV, 1.8 +/- 0.6. Muscle contraction studies 16 hours after reperfusion indicated abnormal findings in all but group II. In conclusion, administration of free radical scavengers did not preserve normal neuromuscular function despite a significant reduction in muscle damage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Are free radical scavengers beneficial in the treatment of compartment syndrome after acute arterial ischemia? 249 3

Perturbation of the cerebral circulation by occlusion of the vertebral arteries and a carotid artery can be visualized by using MR imaging and the intravascular contrast agent Gd-DTPA complexed to albumin. This tracer consistently reduced the T1 relaxation time in the brain and blood. The difference between hemispheres was revealed by less T1 reduction in the occluded hemisphere and by an adjustment in the display contrast of images that revealed the territory of decreased perfusion. These results were confirmed by comparing them with cerebral blood flow using radioactive microspheres and the intravascular blood volume tracer 51Cr-EDTA. This method, combined with high-resolution MR imaging, can be applied to serial noninvasive studies of cerebral blood volume in ischemia and other conditions.
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PMID:Cerebral blood volume in a rat model of ischemia by MR imaging at 4.7 T. 249 53

The total time-controlled ischemia (up to 45 min) was studied for its effect on the Na,K-ATPase activity, content of nonesterified fatty acids (NEFA) and intensity of lipid peroxidation (LP) in sarcolemmal (SL) preparations and soluble fractions (SF) from the rat and guinea-pig left ventricles. A strong correlation between Na, K-ATPase inhibition and NEFA accumulation was revealed in the SF. On the contrary, changes in the NEFA content and LP level both in SL and SF did not correlate with a decrease in the enzymic activity. Pretreatment with albumin (0.5 mg/ml) induced equally small increase both in the control and in the ischemic SL preparations. It is suggested that the Na,K-ATPase activity during a short period of myocardial ischemia (up to 45 min) may be due to the NEFA accumulation in the cytosolic and/or extracellular space, but not in SL.
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PMID:[Na,K-ATPase activity in the myocardial sarcolemma in ischemia]. 255 47


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