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)

Propranolol has been shown to be effective for as long as 5 days in massively burned children to reduce heart rate and cardiac work. This article describes the use of propranolol given for 10 days to burned children to test whether the drug remains effective and safe in reducing heart rate and cardiac work for longer periods. We prospectively studied 22 children, 1 to 10 years of age with burns covering > or = 40% of their total body surface area. These children were treated with 0.5 to 1.0 mg/kg propranolol given orally or intravenously every 8 hours for 10 days. In both septic and nonseptic patients, propranolol significantly decreased their daily average heart rate (between 10% and 13%, p < 0.05) and rate-pressure product (between 10% and 16%, p < 0.05) compared with their 24-hour mean before propranolol treatment. No significant change in mean arterial blood pressure, or plasma urea nitrogen creatinine or glucose levels could be shown. No hypotension, hypothermia, azotemia, hyperglycemia or hypoglycemia, arrhythmia, bronchospasm, or peripheral ischemia was noted during or after treatment. Whereas propranolol lowered heart rate more per milligram per kilogram body weight when given intravenously, both routes were safe and effective. From these data, we conclude that propranolol can be given to decrease the work of the heart safely and effectively for > or = 10 days.
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PMID:Prolonged use of propranolol safely decreases cardiac work in burned children. 916 45

This is the first confirmed report of exertional rhabdomyolysis in a non-human primate. The monkey was singly housed and presented with anorexia and reluctance to move. There was no external evidence of trauma. Clinicopathologic findings included mild azotemia, marked elevation in serum creatine phosphokinase (CPK), alanine aminotransferase, aspartate aminotransferase, and myoglobinuria. Two days post-incident, the peripheral skeletal muscle had marked multifocal myonecrosis and fibrillar disruption without an inflammatory reaction. Treatment included diuresis and pain relief, and urinary output was monitored. The monkey recovered over the next two weeks. The major significance of skeletal muscle damage is the potential of released myoglobin to cause acute renal failure in the presence of other co-factors such as hypovolemia, acidosis, or ischemia. CPK levels can be highly variable and are inconsistent with the degree of muscle damage; however, CPK is thought to be the most sensitive enzyme marker for muscle necrosis. Because of the potential life-threatening sequelae, exertional rhabdomyolysis should be included as a differential diagnosis when similar clinical and pathological signs are observed.
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PMID:Review of exertional rhabdomyolysis and a case in a rhesus monkey (Macaca mulatta). 1020 11

We studied the activity of some enzymes directly involved in the endogenous antioxidative defense system: glutathione-peroxidase (GPX), glutathione s-transferase (GST) and superoxide dismutase (SOD). We have investigated the effects of selenium and vitamin E diet supplementation, in form of selenium-vitamin E enriched yeast, in Wistar rats that were undergone to surgical right nephrectomy and 30 minutes of hypoxia. Blood samples were tested for several parameters as glucose, cholesterol, etc. to assess the general health conditions. The protocol consisted of 3 groups of 25 Wistar rats: a control group, a pre-fed group and a post-fed group. The results showed a significative difference in the behaviour of azotemia, proteins and cholesterol. In the control group the activity rapidly increased, then the values decreased slowly and differently for each substance. The pre and post-fed group showed a pronounced increase after 48 h but the normal values are reached more rapidly. We observed an increase in the activity of the GPX and GST after surgical operation and ischemia, but the GPX in pre-fed group reached the normal value before the other groups.
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PMID:[Oxidative stress in kidney failure: an experimental study]. 1136 28

Transcatheter endovascular procedures are increasingly used to treat symptomatic peripheral atherosclerosis. This two-part review identifies the existing evidence supportive of the application of transcatheter treatments for peripheral atherosclerotic lesions. The first part addresses the treatment of obstructive lesions that cause limb claudication and critical ischemia, renovascular hypertension and azotemia, and mesenteric ischemia. Studies were identified via a search of MEDLINE (January 1993 through April 1999) and reference lists of identified articles. When multicenter prospective randomized trials or other high-quality studies were unavailable, a preference was given to studies with at least 50 patients per treated group and a minimum mean follow-up duration of 6 months. Data presented in tables are proportionally weighted averages from included studies. For each application, the authors assessed the quality of evidence (QOE; efficacy, safety, and, where available, cost-effectiveness) and made recommendations with appropriate caveats. There is higher QOE supporting the more established treatments such as lower limb percutaneous transluminal angioplasty (PTA) with stent placement and thrombolysis. Treatments such as renal artery PTA and stent placement and mesenteric and brachiocephalic PTA are in wide use, but high QOE supporting general application is lacking. Blanket recommendations based on established efficacy and cost-effectiveness cannot be made. However, the use of transcatheter therapies can be supported in specific circumstances based on an expected reduction in procedure-related morbidity and/or mortality rates. It is hoped that the identification of deficiencies in the literature will inform and inspire critically needed research in this area.
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PMID:Transcatheter interventions for the treatment of peripheral atherosclerotic lesions: part I. 1138 19

Acute renal failure (ARF) is a serious damage of renal function induced by various nephrotoxic drugs, ischemia, bilateral urethral obstruction, trauma and unilateral nephrectomy. Dramatic clinical syndrome, azotemia, develops as a result of hypovolemia, oliguria, reduced glomerular filtration and acidosis. In addition to classic medications recent studies give more attention to beneficial effect of natural plant products as bioflavonoids. We have studied the influence of bioflavonoid, quercetin, on hepatic urea production in glycerol induced ARF in the rats. Male Sprague Dawley rats were used in the experiment. The value of urea production in the liver was determined by measuring of liver arginase activity, the terminal enzyme of urea cycle. Arginase activity was increased (p < 0.01) as well as urea level (p < 0.001) 48 h after glycerol administration. Pretreatment by quercetin suppressed the arginase activity in the liver (p < 0.05) and plasma levels of urea (p < 0.01). So, we have concluded that quercetin may be beneficial in glycerol induced ARF.
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PMID:Role of quercetin on hepatic urea production in acute renal failure. 1273 22

Acute thrombotic thrombocytopenic purpura (TTP) is a life-threatening disorder that has previously been described associated with various types of surgery. An association between total abdominal hysterectomy (TAH) and TTP has never been reported. Thrombotic thrombocytopenic purpura is classically characterized by thrombocytopenia, microangiopathic hemolytic anemia, fever, azotemia and neurological manifestations. Atypical manifestations of TTP include hepatitis, pancreatitis, acute respiratory distress syndrome, non-occlusive mesenteric ischemia and peripheral digital ischemia. This case report describes the occurrence of acute TTP following TAH and bilateral salpingo-oopherectomy, which manifested with typical and atypical features (i.e. hepatitis, pancreatitis). Plasma exchange therapy resulted in the complete resolution of the process.
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PMID:A case report of total abdominal hysterectomy resulting in acute thrombotic thrombocytopenic purpura with pancreatitis and hepatitis: complete resolution with plasma exchange therapy. 1292 16

Neutrophil gelatinase-associated lipocalin (Ngal), also known as siderocalin, forms a complex with iron-binding siderophores (Ngal:siderophore:Fe). This complex converts renal progenitors into epithelial tubules. In this study, we tested the hypothesis that Ngal:siderophore:Fe protects adult kidney epithelial cells or accelerates their recovery from damage. Using a mouse model of severe renal failure, ischemia-reperfusion injury, we show that a single dose of Ngal (10 microg), introduced during the initial phase of the disease, dramatically protects the kidney and mitigates azotemia. Ngal activity depends on delivery of the protein and its siderophore to the proximal tubule. Iron must also be delivered, since blockade of the siderophore with gallium inhibits the rescue from ischemia. The Ngal:siderophore:Fe complex upregulates heme oxygenase-1, a protective enzyme, preserves proximal tubule N-cadherin, and inhibits cell death. Because mouse urine contains an Ngal-dependent siderophore-like activity, endogenous Ngal might also play a protective role. Indeed, Ngal is highly accumulated in the human kidney cortical tubules and in the blood and urine after nephrotoxic and ischemic injury. We reveal what we believe to be a novel pathway of iron traffic that is activated in human and mouse renal diseases, and it provides a unique method for their treatment.
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PMID:Endocytic delivery of lipocalin-siderophore-iron complex rescues the kidney from ischemia-reperfusion injury. 1571 40

Urinary exosomes containing apical membrane and intracellular fluid are normally secreted into the urine from all nephron segments, and may carry protein markers of renal dysfunction and structural injury. We aimed to discover biomarkers in urinary exosomes to detect acute kidney injury (AKI), which has a high mortality and morbidity. Animals were injected with cisplatin. Urinary exosomes were isolated by differential centrifugation. Protein changes were evaluated by two-dimensional difference in gel electrophoresis and changed proteins were identified by mass spectrometry. The identified candidate biomarkers were validated by Western blotting in individual urine samples from rats subjected to cisplatin injection; bilateral ischemia and reperfusion (I/R); volume depletion; and intensive care unit (ICU) patients with and without AKI. We identified 18 proteins that were increased and nine proteins that were decreased 8 h after cisplatin injection. Most of the candidates could not be validated by Western blotting. However, exosomal Fetuin-A increased 52.5-fold at day 2 (1 day before serum creatinine increase and tubule damage) and remained elevated 51.5-fold at day 5 (peak renal injury) after cisplatin injection. By immunoelectron microscopy and elution studies, Fetuin-A was located inside urinary exosomes. Urinary Fetuin-A was increased 31.6-fold in the early phase (2-8 h) of I/R, but not in prerenal azotemia. Urinary exosomal Fetuin-A also increased in three ICU patients with AKI compared to the patients without AKI. We conclude that (1) proteomic analysis of urinary exosomes can provide biomarker candidates for the diagnosis of AKI and (2) urinary Fetuin-A might be a predictive biomarker of structural renal injury.
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PMID:Exosomal Fetuin-A identified by proteomics: a novel urinary biomarker for detecting acute kidney injury. 1702 8

Urine chemical analysis can extend "beyond the dipstick" with an understanding of renal physiology and expected changes in electrolyte and solute handling. Urine electrolytes, such as sodium and chloride, can be helpful in discerning prerenal azotemia from acute renal tubular damage, which occur secondary to nephrotoxins or ischemia. Urine osmolality also is essential in determining appropriate antidiuretic hormone action and renal water handling. Urine solutes, such as albumin and brush border enzymes, may be more sensitive than plasma markers for early renal dysfunction. This article reviews these topics and the use of "extended" urine indices in veterinary medicine.
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PMID:Urinary electrolytes, solutes, and osmolality. 1840 77

Apoptosis of tubular epithelial cells is a hallmark of acute kidney injury (AKI), but the cellular events preceding apoptosis in this setting are incompletely understood. Because matrix metalloproteinase 9 (MMP9) degrades matrix components involved in cell survival, we studied the role of MMP9 in AKI. In the mouse model of folic acid-induced AKI, we observed a marked increase of MMP9 activity in the S3 segment of the proximal tubule (S3PT), correlating with the apoptotic phase. MMP9 deficiency increased apoptosis and the severity of renal lesions and substantially delayed recovery of renal function. MMP9-/- mice exhibited significant apoptosis in the S3PT and the intercalated cells of the collecting duct (I-CD), whereas wild-type mice exhibited none in these segments. Stem cell factor (SCF), an MMP9 substrate, was identified in the S3PT, and its receptor, c-Kit, was expressed in both the S3PT and I-CD. MMP9 released the soluble form of SCF (sSCF) from kidney cells in vivo and in vitro. In addition, SCF inhibited apoptosis of tubular cells in vitro, rescued MMP9-/- S3PT and I-CD from apoptosis in vivo, and improved renal function. An ischemia-reperfusion model of AKI produced similar results. In patients with AKI, urinary sSCF increased with acute tubular necrosis but not with prerenal azotemia. In conclusion, these data show that MMP9 protects the S3 segment of the proximal tubule and the I-CD from apoptosis in AKI, most likely by releasing sSCF.
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PMID:MMP9 and SCF protect from apoptosis in acute kidney injury. 1932 63


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