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

Hepatic ischemia followed by reflow results in a myriad of metabolic and circulatory derangements that may eventually result in liver failure and death. In the present experiments we have used the technique of intravital fluorescence microscopy with fluoroscein isothiocyanate conjugated to bovine serum albumin as the intravascular fluorochrome to study the effects of ischemia and reperfusion on the hepatic microcirculation in vivo. Total hepatic ischemia was produced for 90 min to the left and median lobes of pentobarbital-anesthetized rats. After ischemia, reflow was allowed for 2 h. Three groups were studied: sham-ischemia controls and rats treated with either 1 ml saline or 12.5 mumol ATP-MgCl2 in 1-ml volume at the beginning of reflow. Although control rats exhibited stable microcirculation throughout the experiment, in saline-treated rats the number of perfused centrilobular areas and perfused sinusoids per unit area on the surface of the liver was decreased to approximately 50 and 40% of sham-ischemia controls, respectively. However, in rats treated with ATP-MgCl2 the density of perfused centrilobular areas and perfused sinusoids was 86 and 80% of sham-ischemia controls, respectively. From these results we conclude that intravital fluorescence microscopy is a potentially valuable method for the study of the hepatic microcirculation in vivo. Moreover, the results with ATP-MgCl2 treatment indicate that its effect on the microcirculation is a major factor in its beneficial effects on hepatic function after ischemia and reflow.
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PMID:Hepatic microcirculatory failure after ischemia and reperfusion: improvement with ATP-MgCl2 treatment. 392 42

Conformational changes in blood serum albumin under heart ischemia are found from the dispersion parameters of optical rotation and circular dichroism. It is also found that patients with myocardium infarction have a considerable amount of carbohydrate components in the modified albumin form.
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PMID:[Properties of human serum albumin in ischemic heart disease]. 671 66

To define relationships better between the duration of severe ischemia and microvascular functional integrity with an approach potentially applicable to studies in vivo, the effects of 30 and 60 minutes of global, no-flow ischemia on the coronary vasculature of isolated, perfused rabbit hearts were determined. Residue-detection data, analyzed with a two-compartment model, were used to estimate indices of microvascular function, including the mean-transit time (tBSA) of radiolabeled bovine serum albumin (125I-BSA), vascular into extravascular space clearance, and vascular and extravascular space volumes. It was shown that the Central Volume Principle of tracer kinetics does not hold when transport of label between vascular and extravascular spaces takes place convectively by solvent drag, and a more general expression for tBSA was derived and applied. Left ventricular end-diastolic pressure and left ventricular developed pressure were monitored with an isovolumic balloon. Aortic perfusion pressure, left ventricular end-diastolic pressure, left ventricular developed pressure and vascular space volume remained constant, while mean transit time, vascular into extravascular space clearance and extravascular space volumes increased gradually during 3-hour control perfusions. Perfusion pressure, mean transit time and extravascular space clearance increased significantly with reperfusion after 30 minutes of ischemia even though left ventricular end-diastolic and left ventricular-developed pressures returned to control levels. Vascular space volumes increased minimally, whereas extravascular space volumes increased 5-fold during reperfusion. These changes in 125I-BSA washout and permeation across endothelium with reperfusion after no-flow ischemia indicate that compromised vascular integrity is an early manifestation of ischemia with functional consequences that persist even after ischemia sufficiently brief to permit restoration of left ventricular performance.
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PMID:External detection of early microvascular dysfunction after no-flow ischemia followed by reperfusion in isolated rabbit hearts. 682 15

A male rhesus macaque was found to have what appeared to be numerous platelet-fibrin emboli in retinal vessels in the perimacular area. Indocyanine green (ICG) dye fluorescence and fluorescein angiograms of the fundus demonstrated leakage of fluorescein, but not ICG, from the involved arterioles. Histopathologic changes in the eyes included occlusion of retinal and choroidal vessels with platelet-fibrin emboli, inner retinal ischemia, ischemic injury to the parafoveal capillary bed distally to occlusion of precapillary arterioles, and retinal exudate limited to the regions of capillary damage. Differential leakage of fluorescein may be explained by the difference in binding affinities of the 2 dyes to blood protein: 20% to 40% of the circulating fluorescein is unbound, and 98% of ICG is bound to serum albumin. Simultaneously or serially performed angiograms with fluorescent probes of different sizes might be used to obtain a qualitative measure of vascular integrity in persons with embolism, diabetic retinopathy, sickle cell retinopathy, vasculitis, and other disorders known to produce focal retinal and choroidal vascular occlusion.
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PMID:Platelet-fibrin embolism in a rhesus macaque: angiographic and pathologic studies comparing fluorescein and indocyanine green. 688 77

After an initial perfusion using the Langendorff technique, rat hearts were perfused through the left atrium according to the working heart technique. Hearts were preloaded with l noradrenaline 3H (3H-NA) and the release of radioactivity and 3H-NA in the coronary effluent was evaluated. Coronary flow, cardiac output, myocardial oxygen consumption and the electrocardiogram were simultaneously recorded. The perfusion medium consisted of a modified Krebs Henseleit solution containing 3 mM potassium and 0.5 mM sodium palmitate complexed with serum albumin in a molar ratio of 6/1. 1. The addition of palmitate to the perfusion fluid during the Langendorff perfusion produced increases in coronary flow and oxygen consumption, but the release of 3H-NA was not significantly modified, and no irregularities in ventricular concentration were observed. Likewise, the working of the heart did not alter the rate of 3H-NA release. 2. Ischemia was induced on the working heart by left coronary artery ligation for 15 min. It resulted in a reduction in coronary flow and in a similar decrease in the rate of release of 3H-NA. During the first minutes of the occlusion period, there was a slight increase in the incidence of ventricular extrasystoles, but ventricular tachycardia or fibrillation were never encountered. 3. Re-perfusion was accompanied by the occurrence of ventricular tachycardia and fibrillation in all the hearts. These arrhythmias were almost uninterrupted during the first 3 min of re-perfusion, and lasted to a lesser extent up to the 9th minute. Re-perfusion resulted in a sudden release of 3H-NA which was multiplied by a factor 4 during the first 2 min, and then decreased progressively. 4. These results suggest that a release of NA from the myocardial ischemic zones plays a role in the genesis of cardiac arrhythmias following reperfusion.
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PMID:[Release of noradrenaline and ventricular arrhythmias in the isolated perfused working rat heart in the presence of fatty acids. Effect of coronary artery occlusion and re-perfusion (author's transl)]. 721 61

A radioisotope test using 131I-labelled serum albumin and venous occlusion plethysmography were performed simultaneously on the feet of normal individuals and patients with peripheral arterial disease during a period of reactive hyperemia. The radioisotope test includes a circulation time and a build-up curve reflecting a local clearance process which is characterized by the parameter M/2 -- delay. Between the parameter M/2 -- delay of the radioisotope test and the blood flow measured by the plethysmograph, the power relationship was found to be: M/2 -- delay = 74.01 F-0.74 with r = 0.69. The experimental data show that the plethysmographic blood flow measurement is an accurate method for the assessment of the peripheral circulation in normal individuals but is less suitable in patients with peripheral arterial disease. The radioisotope test appears to be more valuable than the plethysmographic blood flow measurement for the differentiation of normal individuals from patients with peripheral arterial disease and for the evaluation of the grade of ischemia.
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PMID:Relationship between the radioisotope test using 131I-labelled serum albumin and plethysmographic blood flow measurements in the study of the circulation in the foot. 732 9

Acute lesions of the gastroduodenal mucosa may result from gastric mucosal ischemia with subsequent cellular dysfunction, capillary leakage and increased susceptibility to mucosal damage. A new technique for measuring the effect of hypovolemic shock and gastric mucosal permeability is presented. Piglets were injected intravenously with human serum albumin labelled with 100 micro Ci of iodine-131 (131I-HSA). Serial blood and gastric samples were obtained for gamma counting during the control, hypovolemic shock and resuscitative periods. Increased gastric acid secretion and clearance of labelled serum albumin occurred after resuscitation from hypovolemic shock. The authors believe that increased capillary permeability and defective gastric mucosal cell function due to ischemia contribute to these changes.
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PMID:Radiotracer assessment of gastric mucosal permeability after hypovolemic shock. 736 60

In control rabbits, a renal ischemia of 60 min followed by 10 min of reperfusion resulted in an enhanced free radical production in cortical tissue, as assessed by a significant decrease of free glutathione (42%), protein-bound GSH (17%), and vitamin E (49%). In contrast, catalase or glutathione peroxidase activities were not affected by these experimental conditions. Free radical production in this model was also measured directly using electron spin resonance (ESR) spectroscopy associated with a PBN (alpha-phenyl N-tert-butyl-nitrone) spin trap agent in the venous blood arising from the ischemic kidney. The signal consisted of a triplet of doublets. In contrast, no signal could be detected in control blood samples taken prior to inducing ischemia. The burst of free radical production occurred in the early phase after restoration of flow in the kidneys rendered ischemic, as evidenced by a signal of weak intensity which generally appeared within the third minute after reperfusion and progressively increased to form a well-defined asymmetric signal following 10 min of reperfusion. The precise nature of free radicals trapped by the PBN agent remains, however, to be elucidated, but analysis of the coupling constants (aN = 14.5-15 G; a beta H = 2.5-3 G) and asymmetry of the central doublets suggests that the ESR signal may arise from a nitorxy-radical adduct resulting from the spin trapping by PBN of both oxygen- or carbon-centered radicals of lipid origin. As evidenced by both direct and indirect measurements, exchange of rabbit blood immediately after inducing renal ischemia with 30 ml/kg of Diaspirin Crosslinked Hemoglobin (7.5 g/dl in lactated electrolyte) or human serum albumin (7.5 g/dl in lactated electrolyte) did not exacerbate free radical production mediated by an ischemia reperfusion phenomenon, a typical situation found in a resuscitation setting.
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PMID:Diaspirin crosslinked hemoglobin (DCLHb): absence of increased free radical generation following administration in a rabbit model of renal ischemia and reperfusion. 763 50

Occlusion of the carotid arteries for 5 minutes in the Mongolian gerbil results in selective necrosis of CA1 pyramidal neurons. In the present experiments we studied whether intraventricular infusion of acidic fibroblast growth factor (aFGF) could attenuate this damage. Intraventricular infusions of bovine serum albumin (BSA-10 ng/h) or aFGF (1, 10 or 100 ng/h) were started 2 days prior to 5 minutes of bilateral carotid occlusion and continued for 5 days post-ischemia. The brains were perfused and fixed at 5 days post-ischemia and histological assessment of CA1 damage was made. Animals receiving intraventricular infusions of 10 or 100 ng/h aFGF showed a significant reduction of CA1 neuronal damage in comparison to no treatment ischemic controls (no treatment-8 +/- 1; aFGF 10 ng/h-147 +/- 28; aFGF 100 ng/h-168 +/- 35 cells/mm CA1; P < 0.05 for both aFGF groups). The results indicate that aFGF infusion can attenuate the severity of ischemic neuronal necrosis in the gerbil hippocampus.
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PMID:Acidic fibroblast growth factor infusion reduces ischemic CA1 hippocampal damage in the gerbil. 768 46

Ischemia in rat hind limbs followed by reperfusion results in local as well as remote organ (lung) injury characterized by increased vascular permeability (125I-labeled bovine serum albumin leakage) and hemorrhage (51Cr-labeled rat erythrocytes extravasation) in skeletal muscle and lung, together with an associated increased tissue content of myeloperoxidase, reflecting neutrophil accumulation. Within 60 minutes of reperfusion following ischemia, tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and IL-6 plasma levels increased significantly, reaching maximum levels after 2 hours of reperfusion. Polyclonal antibodies to TNF-alpha and IL-1 provided significant protection against vascular injury in both muscle and lung. These results were confirmed by the use of soluble TNF-alpha receptor and IL-1 receptor antagonist. In rat lungs following ischemia and reperfusion, there was immunohistochemical evidence of E-selectin expression in the lung vasculature; this expression was blocked by treatment of animals with anti-TNF-alpha. These data indicate that both local (hind limb) and remote (lung) organ injury after ischemia/reperfusion requires participation of TNF-alpha and IL-1. The cytokines may, in part, be involved in the up-regulation of endothelial adhesion molecules.
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PMID:Requirements for tumor necrosis factor-alpha and interleukin-1 in limb ischemia/reperfusion injury and associated lung injury. 768 84


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