Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic causes of leg edema include idiopathic cyclic edema, heart failure, cirrhosis, nephrosis and other hypoproteinemic states. Lymphedema may be primary, or secondary to neoplasm, lymphangitis, retroperitoneal fibrosis and, rarely (in the U.S.), filariasis. Thrombophlebitis and chronic venous insufficiency are not uncommon causes. Finally, infection, ischemia, lipedema, vascular anomalies, tumors and trauma can be responsible for the swollen leg.
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PMID:The swollen leg. 18 30

The autopsy and biopsy materials were used for clinico-anatomical comparisons, and three types of changes were distinguished in transplants of cadaver kidneys of man in insufficiency of the function developing in the first 2 months after transplantation: I type--necrotic changes, II--changes resembling the picture of acute renal insufficiency in circulatory shock with retention of the signs of cortical bloodflow and filtration; III--osmotic nephrosis. The nature of the initial function of the transplant reflects not only the features of the rejection reaction but also the degree of ischemia of nonimmune character suffered by the kidney which determines the rate of restoration of its function as well as sensitivity to the rejection reaction and the effect of some therapeutic factors.
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PMID:[Morphological manifestations of graft functional insufficiency in the 1st 2 months after a human cadaver kidney transplant]. 36 30

Rats were anesthetized and their lift kidneys were made ischemic for 1 h by clamping of the aorta just above the left renal artery. Mannitol (2.5 g/kg), Dextran 70 (0.6 g/kg), methylprednisolone (50 and 100 mg/kg), and allopurinol (100 mg/kg body weight) were administered before, during, or after the ischemia period in order to test the effect of each of these drugs upon this model of renal injury. At 24 h after the release of the aortic clamp the left kidneys of the drug treated animals wwere perfusion fixed and processed for light and electron microscopy. Dextran administration to animals with ischemic kidneys gave rise to a pronounced vacuolization ("osmotic nephrosis"), in the entire proximal tubule and especially in the pars recta. This was in contrast to dextran administration to rats with nonischemic kidenys, which showed no or very mild "osmotic nephrosis." This demonstrates that ischemia makes rat kidneys more susceptible to the development of "osmotic nephrosis." In controls (no drug treatment) one hour of renal ischemia gave partial necrosis of pars recta of the proximal tubule, while the pars convoluta tubule survived. Mannitol treatment significantly reduced the amount of necrosis of the pars recta, whereas dextran, methylprednisolone, and allopurinol had no or a negative effect on the survival of the cells of the pars recta segment. It is suggested that mannitol protects against the development of necrosis by increasing medullary blood flow in combination with a counteractive influence on the cellular swelling, which is known to occur in ischemia.
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PMID:Effect of mannitol, dextran (macrodex), allopurinol, and methylprednisolone on the morphology of the proximal tubule of the rat kidney made ischemic in vivo. 40 53

This report consists of an analysis of 256 consecutive patients with a total of 260 arterial emboli to the upper limbs treated in the Spasokukotsky Surgical Department of the Second Moscow Pirogov Medical Institute during the 35 year period from 1939 through 1974. Cardiac diseases were the causes of embolism in 92.58 percent of these patients. Mild ischemia of the limbs was revealed only in 33.82 percent of the patients. Severe ischemia accompanied by significant restriction or full absence of active movements in the joints of affected extremities was observed in 55.94 percent of the patients. Acute ischemia with a muscular edema and partial or total contracture was observed in 9.88 percent of the patients. Forty-seven patients were treated conservatively. Arteriectomy was performed in three patients. Embolectomy was carried out on 206 patients, 101 of whom were operated on by means of the approach outside the cubital fossa and 105 by means of the antecubital approach. The best results were obtained when embolectomy was performed with the use of the Fogarty catheter by means of the antecubital approach. This method achieved full restoration of circulation in 91.59 percent of our patients. The mortality rate was approximately equal in all groups of patients. The over-all hospital mortality rate was 21.1 percent. Recurrent embolism of cerebral and mesenteric arteries was the main cause of death. Fatal postischemic complications led to the death of two patients who were operated on with a total ischemic contracture of a limb. Autopsy revealed a pulmonary microembolism in one case and a myoglobinuric nephrosis in the other.
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PMID:Artery embolism of the upper limbs. 84 43

The kidney function was studied in postischemia period in 80 patients with acute arterial occlusion,using the methods of radioisotope renography and effective renal blood flow. For the purpose of prophylaxis agains renal complications in addition to regional perfusion and venesection the method of regional inhibition of toxic products in the ischemia focus is suggested. In increased myoglobinuiea the stimulation of diuresis, alkalization of the organism would be a necessity. Renal complications were observed in 13 of 80 patients (16.25%). In 6 patients myoglobinuric tubular nephrosis was noted with lethal issues; in the remaining 7 patients due to early establishment of the diagnosis and intensive therapy myoglobinuria showed an abortive character.
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PMID:[Study of the changes in kidney function in acute obstruction of the arteries of the extremities]. 85 33

Revascularization syndrome is one of the dangerous postoperative complications which results sometimes in loss of a limb, renal shutdown and death due to myoglobin-nephrosis and hyperkalemia. During the past 3 years, 2 cases of revascularization syndrome were experienced in 16 cases of thrombo-embolectomies for acute peripheral arterial occlusion. One patient died from hyperkalemia 100 minutes after revascularization. Another patient suffered from a renal shutdown, and was treated with hemodialysis and thigh amputation. It is sometimes very difficult to predict whether the revascularization syndrome will occur or not. When revascularization is performed within 12 hours after an onset of acute occlusion and when the amount of ischemic muscle is not large, the syndrome may not occur. When the time-interval between the onset of ischemia and revascularization is longer than 24 hours and when the mass of ischemic muscle is large, the syndrome will occur. Preoperative serum creatinine and urea nitrogen level are important parameters predicting the prognosis.
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PMID:[Pathogenesis and prevention of the revascularization syndrome]. 667 83

Studies were carried out on the changes in the electrocardiogram, the content of sodium and potassium in the plasma and erythrocytes, and the morphology of the viscera of sheep spontaneously intoxicated with monensin. It was found that in the initial phases of poisoning the plasma level of Na and K strongly rose--410 +/- 12.57 mg% and 36.28 +/- 1.99 mg%, respectively, while after the tenth day it showed a trend of coming back to normal. The electrocardiogram of the poisoned sheep was inevitably deprived of the P deflection, while the QRST complex showed deformations characteristic of ischemia and degeneration of the myocardium. Morphologically, there were catarrhal abomasoenteritis, edomatized and fragile kidneys and liver, enlarged mucous membrane of the gallbladder, showing hyperemia and nodules, hemorrhages in the heart, and hyperemia and edema of the lungs. Histologically, there were dystrophic and necrotic nephrosis and focal glomerulonephritis, granular and fatty dystrophy and necroses of the liver, cholecystitis, granular and hyaline dystrophy of the myocardium, hyperemia, hemorrhages, and edema of the lungs as well as degenerative changes in the ganglion cells of the brain. The cadavers of animals that were ill for seven to ten days and died had multiple hemosiderosis in the kidneys, liver, lungs, and heart.
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PMID:[Biochemical, electrocardiographic and pathomorphological studies the monensin poisoning of sheep]. 734 29

The importance of analyzing the kinetics of reactive oxygen species or related substances in vivo is increasing. Electron paramagnetic resonance (EPR) is currently a powerful method for in vivo, non-invasive analysis of oxidative stress. We have applied EPR imaging for murine renal ischemia-reperfusion injury, as a model of acute renal damage, and NF-E2-related factor 2 (Nrf2)-deficient mice, a model for chronic progressive renal disease. In the ischemia-reperfusion model, EPR imaging revealed that the renal radical-reducing activity showed only partial recovery when serum creatinine and BUN have recovered. In the Nrf2-deficient mice, we have revealed that the impaired antioxidant activity is brought by both Nrf2 deficiency and the aging process and may play a key role in the onset of autoimmune nephritis in this model. In addition, EPR imaging is recently being applied to the redox analysis of several nephrosis models, hypertensive rats and streptozotocin-induced diabetic rats. This article summarizes the nephrological application of EPR imaging and in vivo EPR.
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PMID:Electron paramagnetic resonance imaging of oxidative stress in renal disease. 1654 59

Tetramethylpyrazine (TMP), a compound purified from Rhizoma Ligustici, is a widely used active ingredient in Chinese herbal medicine to treat cardiovascular diseases on account of its vasodilatory actions and antiplatelet activity. Studies have shown that TMP can remove oxygen free radicals and protect rat kidney from ischemia-reperfusion injury. In addition, adriamycin-induced nephrosis in rats is commonly used in pharmacological studies of human chronic renal diseases. Apoptosis of renal tubular cells has been reported in adriamycin-treated rats. To examine the therapeutic potential of TMP on chronic progressive renal diseases, adriamycin-induced injury in rat renal tubular cells NRK-52E has been used to monitor its protective effect. In TUNEL staining, TMP showed a dose-dependent protective effect against adriamycin-induced apoptosis in NRK-52E cells. Pretreatment of the cells with 10 or 100 microM of TMP effectively decreased the reactive oxygen species (ROS) formation induced by adriamycin, as measured in fluorescent assays. TMP was found to reduce the adriamycin-stimulated activities of caspase-3, caspase-8 and caspase-9, inhibit adriamycin-induced release of cytochrome C, and elevate the expression of Bcl-x (L). TMP was also able to inhibit the death receptor signaling pathway and suppress the activation of transcription factor NF-kappaB in adriamycin-treated NRK-52E cells. Based on the results of this study, we suggest that TMP can attenuate adriamycin-induced oxidative stress and apoptotic injury in NRK-52E cells, and that it may have therapeutic potential for patients with renal diseases. TMP: tetramethylpyrazine LDH: lactate dehydrogenase ROS: reactive oxygen species DCF: 2',7'-dichlorofluorescein TNF-alpha: tumor necrosis factor-alpha TUNEL: terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling.
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PMID:Tetramethylpyrazine attenuates adriamycin-induced apoptotic injury in rat renal tubular cells NRK-52E. 1690 63

The pathophysiology of contrast-induced AKI (CIAKI) is incompletely understood due to the lack of an appropriate in vivo model that demonstrates reduced kidney function before administration of radiocontrast media (RCM). Here, we examine the effects of CIAKI in vitro and introduce a murine ischemia/reperfusion injury (IRI)-based approach that allows induction of CIAKI by a single intravenous application of standard RCM after injury for in vivo studies. Whereas murine renal tubular cells and freshly isolated renal tubules rapidly absorbed RCM, plasma membrane integrity and cell viability remained preserved in vitro and ex vivo, indicating that RCM do not induce apoptosis or regulated necrosis of renal tubular cells. In vivo, the IRI-based CIAKI model exhibited typical features of clinical CIAKI, including RCM-induced osmotic nephrosis and increased serum levels of urea and creatinine that were not altered by inhibition of apoptosis. Direct evaluation of renal morphology by intravital microscopy revealed dilation of renal tubules and peritubular capillaries within 20 minutes of RCM application in uninjured mice and similar, but less dramatic, responses after IRI pretreatment. Necrostatin-1 (Nec-1), a specific inhibitor of the receptor-interacting protein 1 (RIP1) kinase domain, prevented osmotic nephrosis and CIAKI, whereas an inactive Nec-1 derivate (Nec-1i) or the pan-caspase inhibitor zVAD did not. In addition, Nec-1 prevented RCM-induced dilation of peritubular capillaries, suggesting a novel role unrelated to cell death for the RIP1 kinase domain in the regulation of microvascular hemodynamics and pathophysiology of CIAKI.
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PMID:The RIP1-kinase inhibitor necrostatin-1 prevents osmotic nephrosis and contrast-induced AKI in mice. 2383 61


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