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)

Spontaneous intraperitoneal rupture of the bladder (also called unsuspected, idiopathic, or non-traumatic rupture of the bladder) is a well defined but rare condition which has not been universally recognized in the past. We are reporting four cases and emphasizing its clinical picture so it might be better recognized and diagnosed early on in the process, and so that its management be planned appropriately in order to reduce its morbidity and its mortality. A review of the literature is provided to help achieve this end. Spontaneous intraperitoneal vesical rupture is almost always a surprise at laparotomy. A high degree of suspicion, the finding of urea in the ascitic fluid, and cystography may help in the diagnosis. Symptoms include abdominal pain, difficulty in micturition, hematuria and renal failure with elevation of the blood urea and acidosis. The etiology seems to be varied and somehow confused. We discuss four groups of etiological factors: dulled sensorium, weakening of the bladder wall, increased intra-vesical pressure (with or without bladder outlet obstruction) and vascular lesions (radiotherapy, arterial embolism and vesical infarction); and we try to discern common denominators for these four groups of etiological factors: an increase in intravesical pressure along with a weakening of the bladder wall. Finally the new concept of vesical infarction following ischemia due to overdistention of the bladder is introduced and discussed.
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PMID:Spontaneous intraperitoneal rupture of the bladder. 762 49

The possible protective effect of heat-shock proteins (HSPs) on ischemic injury to renal cells was assessed in two different experimental models: ischemia-reflow in intact rats and medullary hypoxic injury as seen in the isolated perfused rat kidney. Heat shock was induced by raising the core temperature of rats to 42 degrees C for 15 minutes. Following this, Northern blots showed enhanced gene expression of HSP70, HSP60 and ubiquitin at one hour and reaching a maximum by six hours after heat shock in all regions of the kidney, but most prominently in medulla and papilla. The HSP70 protein in the kidney, estimated by immunohistochemical means, was detectable 24 hours following heat shock and further increased at 48 hours following heat shock. In the first set of experiments, the animals underwent uninephrectomy followed by cross clamping of the remaining renal artery for 40 minutes prior to reflow. Serum creatinine and urea nitrogen rose to 3.15 +/- 0.98 and 126.4 +/- 62.5 mg/dl at 24 hours. No significant differences were observed at 24, 48 and 72 hours after reflow between these values in control rats and rats pretreated with heat shock 48 hours earlier. Severe morphological damage to proximal tubules of the renal cortex was observed to the same extent in both groups. In a second set of experiments, the right kidney was removed either 24 or 48 hours after heat shock and perfused in isolation for 90 minutes. Functional and morphological parameters were compared with those of isolated perfused kidneys obtained from animals that had not been subjected to heat shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of heat-shock proteins does not prevent renal tubular injury following ischemia. 764 46

This study investigates the role of verapamil, a calcium channel blocker, combined with allopurinol, a xanthine-oxidase inhibitor, when given at reperfusion after severe renal ischemia injury in the rat. Male Sprague-Dawley rats were subjected to 60 minutes of warm ischemia by cross clamping the whole left renal pedicle (artery and vein). At the end of ischemia, the clamps were removed and a contralateral nephrectomy was performed. The animals (n = 40 per group) were divided into five groups; Group 1, ischemic control (IC) receiving lactated Ringer's; Group 2, allopurinol (A) 100 mg/kg; Group 3, verapamil (V) 1.25 mg/kg; Group 4, receiving a combination of A + V at the same concentrations; and Group 5, sham group. Each drug was given intravenously at the end of the ischemic period at reperfusion. Survival was evaluated at 7 days. Renal damage was assessed by kidney function tests (serum creatinine and blood urea nitrogen, or BUN), light histology. Lipid peroxidation was measured in renal tissue using the TBA (thiobarbituric acid) assay. The best survival rate was seen in the combination group of A + V (70% at 7 days; p < .01 vs. control). Single drugs were not as effective as the combination when compared to the IC. Serum creatinine at 24 and 48 hours showed a significant difference between the IC and treatment groups. At 72 hours there were no differences among the treated groups. Histological damage was more pronounced in the IC (Grade 4.0) than in the allopurinol (3.4 +/- 0.8), verapamil (3.0), or A + V (2.2 +/- 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Protective effect of combined allopurinol and verapamil given at reperfusion in severe renal ischemia. 773 32

Aiming at investigating biochemical markers of Primary Graft Nonfunction (PNF) in Orthotopic Liver Transplantation (OLT) an experimental work is made on 21 Large-White pigs randomly distributed in three groups of seven, and two additional groups of seven donors each. In Group I the supra and infrahepatic cava, the portal vein and the hepatic artery were clamped. After 30 minutes the caval and portal clamps were released and 30 minutes later the arterial clamp was also removed. In Group II (viable), OLT was performed. The Collins solution was used as preservation fluid, keeping the cold ischemia time under 2 hours. In Group III (Non-Viable), an OLT was carried out 24 hours of cold ischemia with Collins solution. Blood samples are taken in 8 different moments along the procedure to determinate the values of AST, ALT, LDH, FA, Bilirubin, Uric Acid, Cholesterol, Triglycerides, Urea, Creatinine, Glucose, Total Protein, Calcium, Phosphorus, CPK and Aldolase. The last 5 samples were drawn after reperfusion. In the Group III we found, in the samples drawn after reperfusion of the graft, significant increases in 5 of these parameters, AST, ALT LDH, Aldolase and Uric Acid. We consider that these 5 parameters may be of value in the early diagnosis of PNF of the graft, being the AST and ALT the most reliable, with the higher specificity for the same sensitivity.
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PMID:[Biochemical indicators of primary graft dysfunction in experimental orthotopic liver transplantation]. 776 81

Recent studies have indicated that ammonia is involved in the pathophysiology of Helicobacter pylori-associated gastric mucosal damage. Helicobacter pylori-associated chronic active gastritis is characterized by an invasion of neutrophils. We investigated the interrelationship among hypochlorous acid (oxidant produced by neutrophil), ammonia (product of Helicobacter pylori urease), and monochloramine (product of ammonia and hypochlorous acid) in the development of gastric mucosal damage in rats. Gastric mucosal lesions were produced by exposure of the gastric mucosa to ammonia, urea with urease, or urea with Helicobacter pylori in rats subjected to ischemia. Pretreatment with taurine (scavenger of hypochlorous acid) or antineutrophil serum significantly attenuated gastric mucosal lesions induced by the above test agents. Ammonia-induced gastric mucosal lesions were exacerbated in the presence of hypochlorous acid with concomitant generation of monochloramine. These results suggest that the ammonia, hypochlorous acid, and monochloramine triad may be important in Helicobacter pylori-mediated gastric mucosal damage.
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PMID:Products of neutrophil metabolism increase ammonia-induced gastric mucosal damage. 785 Nov 88

In the present work, we analyze the effects produced by cold ischemia on the liver using Eurocollins solution (EC). This evaluates the function of slices obtained from preserved livers in EC (livers from adult female Wistar rats were used), which were perfused with Krebs-Henseleit solution (KH) for 10 min. and then with cold EC. These livers were stored at 4 degrees C in EC for 7, 24 and 48 hours. At the end of each period of preservation, the livers were sliced and they were incubated 1 hour at 37 degrees C in KH. The following parameters were determined: tissular water distribution and electrolytes content (K+ and Na+), LDH release at the incubation medium, thiobarbituric acid reactive substances (TBARS) and urea synthesis. The slices obtained from preserved livers (7 hours), showed an increase of tissular water, expressed by the expansion of the extracellular space, a progressive diminution of tissular K+ content and an increase in TBARS and the LDH release with the increment of the preservation time. No changes in ureogenesis rate were observed. These results suggest that the cold ischemia in EC, in periods that exceed 5 hours, cause, changes in the membrane permeability and severely affects the mechanism of regulation of the tissular volume and may compromise the functional viability of the organ to be transplanted.
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PMID:[Hypothermic preservation of the liver. Evaluation of Eurocollins solution using rats liver slices]. 785 88

1. We investigated the effect of efonidipine hydrochloride (NZ-105) against acute renal failure (ARF) in male Wistar rats. ARF was produced by ischemia or glycerol. 2. Ischemia-induced ARF was produced by right nephrectomy and clamping of the left renal artery for 60 min, followed by reperfusion. NZ-105 (20 mg/kg) was orally administered twice a day for 3 days before ARF. The plasma creatinine and urea nitrogen concentrations were markedly elevated in the ischemia ARF group on the 1st day, but the elevation was significantly suppressed by NZ-105 treatment. 3. Glycerol-induced ARF was produced by intramuscular injection of 50% (v/v) glycerol (10 ml/kg) in rats which were restricted to drinking water for 24 hr. NZ-105 (20 mg/kg) was orally administered twice a day for 3 days before ARF. NZ-105 significantly attenuated the severe impairment of creatinine and urea nitrogen clearances and the elevated fractional sodium excretion (FENa) caused by ARF. 4. In the kidney homogenate, NZ-105 (10(-6)-10(-4) M) inhibited lipid peroxidation induced by ascorbic acid and Fe or by NADPH and the inhibitory effect of NZ-105 was stronger than alpha-tocopherol, an antioxidant agent. NZ-105 (10(-5)-10(-3) M) showed radical scavenging action against diphenyl-p-picrylhydrazyl and galvinoxyl induced radicals. 5. These findings suggest that NZ-105 prevents the renal damage caused by the two kinds of ARF. Moreover, the inhibitory effects of NZ-105 against lipid peroxidation and radical formation may be one of the mechanisms involved in the prevention of ARF.
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PMID:Effects of efonidipine hydrochloride (NZ-105), a new calcium antagonist, against acute renal failure in rats. 789 60

Renal glutamine uptake and subsequent urinary ammonia excretion could be an important alternative pathway of ammonia disposal from the body during liver failure (diminished urea synthesis), but this pathway has received little attention. Therefore, we investigated renal glutamine and ammonia metabolism in midly hyperammonemic, portacaval shunted rats and severely hyperammonemic rats with acute liver ischemia compared to their respective controls, to investigate whether renal ammonia disposal from the body is enhanced during hyperammonemia and to explore the limits of the pathway. Renal fluxes, urinary excretion, and renal tissue concentrations of amino acids and ammonia were measured 24 h after portacaval shunting, and 2, 4, and 6 h after liver ischemia induction and in the appropriate controls. Arterial ammonia increased to 247 +/- 22 microM after portacaval shunting compared to controls (51 +/- 8 microM) (P < 0.001) and increased to 934 +/- 54 microM during liver ischemia (P < 0.001). Arterial glutamine increased to 697 +/- 93 microM after portacaval shunting compared to controls (513 +/- 40 microM) (P < 0.01) and further increased to 3781 +/- 248 microM during liver ischemia (P < 0.001). In contrast to controls, in portacaval shunted rats the kidney net disposed ammonia from the body by diminishing renal venous ammonia release (from 267 +/- 33 to -49 +/- 59 nmol/100 g body wt per min) and enhancing urinary ammonia excretion from 113 +/- 24 to 305 +/- 52 nmol/100 g body wt per min (both P < 0.01). Renal glutamine uptake diminished in portacaval shunted rats compared to controls (-107 +/- 33 vs. -322 +/- 41 nmol/100 g body wt per min) (P < 0.01). However, during liver ischemia, net renal ammonia disposal from the body did not further increase (294 +/- 88 vs. 144 +/- 101 nmol/100 g body wt per min during portacaval shunting versus liver ischemia). Renal glutamine uptake was comparable in both hyperammonemic models. These results indicate that the rat kidney plays an important role in ammonia disposal during mild hyperammonemia. However, during severe liver insufficiency induced-hyperammonemia, ammonia disposal capacity appears to be exceeded.
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PMID:Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat. 790 48

The effects of glycerol and mannitol, as well as urea, on delayed neuronal death (DND) in the gerbil hippocampus were investigated. 20% solution of glycerol, mannitol and urea were prepared, and 6.5 ml/kg of each agent, or saline, was administered to male Mongolian gerbils intraperitoneally 30 min before ischemia. The animals were subjected to transient forebrain ischemia for 5 min. Seven days after the ischemic insult, the brains were fixed and stained for histopathological analysis. The number of normal neurons (neuronal density, ND) in a 1 mm linear length of hippocampal CA1 region was counted. ND of sham-operated group (n = 6) was 275.3 +/- 16.7 (mean +/- SD). ND in the saline-treated group (n = 6) was 14.8 +/- 5.0. ND of groups treated with glycerol (n = 6), mannitol (n = 6) and urea (n = 4) was 68.2 +/- 56.7 (p < 0.01), 52.8 +/- 54.4 (p < 0.01) and 12.0 +/- 2.5 (NS), respectively. The present study demonstrates that glycerol and mannitol have some protective effects against DND in the gerbil hippocampus, whereas urea has no effect.
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PMID:Comparison of the effects of glycerol, mannitol, and urea on ischemic hippocampal damage in gerbils. 797 79

This paper examines the nature of tissue metabolites collected in thermally induced sweat following the application of different loading regimes on the soft tissues of able-bodied subjects. Loading was produced by 1) external application on the forearm via both a tourniquet and a uniaxial indenter system, and 2) ischial support on a wheelchair and sacral support on an examination bed. In each case sweat pads were attached to the tissue areas of a group of able-bodied subjects and interface pressures were recorded. After a prescribed period, the pads were removed and a quantitative analysis of a range of metabolites was performed. Results indicated that tissues subjected to pressure ischemia produced a general increase in concentrations of lactate, chloride, urea, and urate associated with a decreased sweat rate. In the reperfusion phase, some of these metabolites returned to unloaded levels. It is proposed that specific metabolites may be used as an indicator of soft tissue damage.
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PMID:Analysis of sweat during soft tissue breakdown following pressure ischaemia. 803 53


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