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)

Cerebral intraventricular hemorrhage (IVH), a problem widely recognized in premature infants, was found in six older infants, ages 2 weeks to 3 months. IVH was often initially misdiagnosed as subarachnoid hemorrhage or meningits with a traumatic lumbar tap. IVH occurred primarily in infants with hypoxemia, acidosis, ischemia, and/or hypernatremia, conditions found in association with IVH in premature infants, but also occurred spontaneously. Computerized tomography scans were the most valuable diagnostic procedure for detection of IVH.
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PMID:Cerebral intraventricular hemorrhages in infants: a widening age spectrum. 735 33

Chronic nitric oxide (NO) inhibition promotes hypertension and ischemic glomerular injury with only minor glomerulosclerosis (GS). We evaluated the effect of superimposed salt overload, which has been shown to aggravate GS in other models. Fifteen days of treatment with the NO inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) promoted marked arterial and glomerular hypertension, hyporeninemia, and slight renal interstitial expansion, but no glomerular injury. Salt overload slightly exacerbated systemic and glomerular hypertension, promoted albuminuria, interstitial expansion, and glomerular ischemia, and paradoxically reversed hyporeninemia. The angiotensin II inhibitor losartan attenuated glomerular and systemic hypertension and prevented renal injury in these rats. Thirty days of treatment with L-NAME resulted in marked hypertension, hyperreninemia, interstitial expansion, and glomerular ischemia. Concomitant salt overload exacerbated hypertension, interstitial expansion, and ischemia and promoted massive albuminuria, GS, and creatinine retention. Losartan attenuated these effects. Sodium overload aggravates the renal and systemic consequences of chronic NO inhibition by mechanisms that may include paradoxical activation of renin secretion. Interstitial expansion and glomerular ischemia, rather than GS, constitute the chief modalities of renal injury in this model.
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PMID:Sodium excess aggravates hypertension and renal parenchymal injury in rats with chronic NO inhibition. 820 52

The use of marginal donors has become very common in many liver transplantation units due to the increase in the number of possible recipients. Experience has shown that previous donor protocols were too restrictive. Meanwhile, formerly unknown factors influence current donor evaluation. Different donor factors affecting the outcome of transplantation have been studied. Current absolute contraindications are severe macrosteatosis, long ischemia, sepsis, some viral infections and extra-CNS malignancy. Old age, mild to moderate steatosis, long ICU stay, altered liver function tests, hypernatremia, hypotension and pressors, moderately prolonged ischemia and sex mismatch are usually considered relative contraindications. The result of this wider acceptance policy has been an increasing number of usable livers without deleterious influences on graft and patients survival.
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PMID:Marginal donors in liver transplantation. 1069 Jun 18

Axonal degeneration is a prominent pathological feature in multiple sclerosis observed over a century ago. The gradual loss of axons is thought to underlie irreversible clinical deficits in this disease. The precise mechanisms of axonopathy are poorly understood, but likely involve excess accumulation of Ca ions. In healthy fibers, ATP-dependent pumps support homeostasis of ionic gradients. When energy supply is limited, either due to inadequate delivery (e.g., ischemia, mitochondrial dysfunction) and/or excessive utilization (e.g., conduction along demyelinated axons), ion gradients break down, unleashing a variety of aberrant cascades, ultimately leading to Ca overload. During Na pump dysfunction, Na can enter axons through non-inactivating Na channels, promoting axonal Na overload and depolarization by allowing K egress. This will gate voltage-sensitive Ca channels and stimulate reverse Na-Ca exchange, leading to further Ca entry. Energy failure will also promote Ca release from intracellular stores. Neurotransmitters such as glutamate can be released by reverse operation of Na-dependent transporters, in turn activating a variety of ionotropic and metabotropic receptors, further exacerbating overload of cellular Ca. Together, this Ca overload will inappropriately stimulate a variety of Ca-dependent enzyme systems (e.g., calpains, phospholipases), leading to structural and functional axonal injury. Pharmacological interruption at key points in these interrelated injury cascades (e.g., at voltage-gated Na channels or AMPA receptors) may confer significant neuroprotection to compromised central axons and supporting glia. Such agents may represent attractive adjuncts to currently available immunomodulatory therapies.
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PMID:General mechanisms of axonal damage and its prevention. 1589 99

Despite the use of well-accepted protocols for donor maintenance, the severe electrolytic disorders are not infrequent with deleterious consequences to the organs. The objective of our survey was to determine the incidence of episodes of electrolyte disorders among brain-dead patients (despite of rigid protocols of maintenance) and the rate of anaerobic metabolism in these patients (suggestive of an occult systemic hypoperfusion). The study group of 50 brain-dead patients underwent therapy to maintain normal arterial pressure, urine output, and body temperature. Standard monitoring for brain-dead patients was followed, except for a frequent evaluation of electrolytes, including glucose, sodium, potassium, phosphorus, osmolality, base excess, and lactate plasma levels. Our results demonstrate that with frequent determinations of electrolytes, despite following strict protocols of maintenance, there was a high incidence of hyperglycemia, hypophosphotemia, hypokaemia, and hyperosmolality. Interesting findings were the high incidence of elevated lactate, and the relationship between lactate levels and bases deficit as well as hypernatremia. It can be concluded that, even following rigid protocols, the maintenance of brain-dead patients demands a close evaluation of electrolyte levels. Our results also suggest that the inclusion in the monitoring protocol of anerobic metabolism data including lactate levels can help to avoid occult ischemia of organs, and consequently improve their quality for transplantation.
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PMID:Electrolytic disorders, hyperosmolar states, and lactic acidosis in brain-dead patients. 1596 19

To expand the donor pool, clinicians are continually modifying criteria to accept organs, particularly those in the so-called expanded or marginal donor pool. The concept and definition of a marginal donors continues to evolve. The impact of their use is the result of a combination of donor and recipient factors. Most clinicians accept steatosis above 30%, donor age over 60 years, prolonged ischemia time, prolonged intensive care unit stay, hypernatremia, previous cardiac arrest, prolonged episodes of hypotension, large use of inotrope drugs, and elevated liver function tests as criteria for designation of a marginal organ. In June 2003, we started to use marginal donors each year tripling the number of transplants per year at our center.
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PMID:Acceptance of marginal liver donors increases the volume of liver transplant: early results of a single-center experience. 1618 45

The serum- and glucocorticoid-inducible kinase-1 (SGK1) is ubiquitously expressed and under genomic control by cell stress (including cell shrinkage) and hormones (including gluco- and mineralocorticoids). Similar to its isoforms SGK2 and SGK3, SGK1 is activated by insulin and growth factors via phosphatidylinositol 3-kinase and the 3-phosphoinositide-dependent kinase PDK1. SGKs activate ion channels (e.g., ENaC, TRPV5, ROMK, Kv1.3, KCNE1/KCNQ1, GluR1, GluR6), carriers (e.g., NHE3, GLUT1, SGLT1, EAAT1-5), and the Na+-K+-ATPase. They regulate the activity of enzymes (e.g., glycogen synthase kinase-3, ubiquitin ligase Nedd4-2, phosphomannose mutase-2) and transcription factors (e.g., forkhead transcription factor FKHRL1, beta-catenin, nuclear factor kappaB). SGKs participate in the regulation of transport, hormone release, neuroexcitability, cell proliferation, and apoptosis. SGK1 contributes to Na+ retention and K+ elimination of the kidney, mineralocorticoid stimulation of salt appetite, glucocorticoid stimulation of intestinal Na+/H+ exchanger and nutrient transport, insulin-dependent salt sensitivity of blood pressure and salt sensitivity of peripheral glucose uptake, memory consolidation, and cardiac repolarization. A common ( approximately 5% prevalence) SGK1 gene variant is associated with increased blood pressure and body weight. SGK1 may thus contribute to metabolic syndrome. SGK1 may further participate in tumor growth, neurodegeneration, fibrosing disease, and the sequelae of ischemia. SGK3 is required for adequate hair growth and maintenance of intestinal nutrient transport and influences locomotive behavior. In conclusion, the SGKs cover a wide variety of physiological functions and may play an active role in a multitude of pathophysiological conditions. There is little doubt that further targets will be identified that are modulated by the SGK isoforms and that further SGK-dependent in vivo physiological functions and pathophysiological conditions will be defined.
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PMID:(Patho)physiological significance of the serum- and glucocorticoid-inducible kinase isoforms. 1701 87

Rhabdomyolysis is a clinical and biochemical syndrome occurring when skeletal muscle cells erupt and result in release of creatine phosphokinase (CPK), lactate dehydrogenase (LDH) and myoglobin into the interstitial space and plasma. Mechanical trauma, compression, excessive muscle activity and ischemia are frequent causes, but non-traumatic rhabdomyolysis is usually caused by a toxic reaction to drugs. In this study, 181 patients suspected of rhabdomyolysis were admitted to the poisoning center of Loghman-Hakim Hospital in Tehran during one year (September 2004 to September 2005) were studied. Patients were included on the basis of physical examination and blood analysis for CPK and LDH. Rhabdomyolysis was confirmed if CPK level has been greater than 975 U/L. Out of 181 patients, 64 were female and 117 were male with an age range between 13-78 years. One-hundred and forty-three (79%) patients had CPK greater than 975 U/L. In 6% of the cases, multiple drug poisoning were observed. Two patients (1.1%) had muscle pain, five patients (2.8%) had rigidity and five patients (2.8%) had muscle inflammation. One-hundred and nineteen patients (65.7%) were febrile. The most common cause of rhabdomyolysis was opium. Blood ALT showed an increase in 109 patients (60.9%), AST in 80 patients (44.7%), and LDH in 144 patients (79.6%). Fifty patients (28.2%) had higher blood direct bilirubin and 64 patients (36.4%) showed higher total bilirubin. Six percent of patients had been diagnosed as ARF by indication of creatinine greater than 1.4 mg/dL. Five percent of patients had hypernatremia and 1.1% of patients had hyperkalemia. It is concluded that rhabdomyolysis is a matter of concern in human poisonings and needs special approach to attend.
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PMID:Rhabdomyolysis among acute human poisoning cases. 1788 58

Previous studies have shown that donor hypernatremia and possibly recipient hyponatremia negatively impact graft function after orthotopic liver transplant (OLT). The purpose of this retrospective investigation was to determine whether measured differences in serum sodium values between cadaveric donors and OLT recipients (DeltaNa(+)) influence immediate postoperative allograft function and short-term patient outcomes. Two hundred and fifty patients that underwent OLT from January 2001 to December 2005 were included in this study. The DeltaNa(+) for each donor recipient pair was correlated with standard postoperative liver function tests as well as recipient length of intensive care unit stay (LOICUS), length of hospital stay (LOHS) and recipient survival. The relationship between donor hypernatremia (serum sodium >or= 155 mEq/mL), recipient hyponatremia (serum sodium level <or= 130 mEq/mL), and postoperative outcomes were analyzed as well. Adjustments were made for baseline potential confounders, including model for end-stage liver disease (MELD) score, preservation solution used (HTK vs. UW), recipient and donor demographics and cold ischemia time (CIT). DeltaNa(+) as well as donor hypernatremia and recipient hyponatremia were not found to be associated with immediate postoperative allograft function, intraoperative blood product usage, LOICUS, LOHS or short-term patient survival. However, both the preoperative MELD score and HTK preservation solution used were significantly associated with several patient outcomes. A higher MELD score was associated with both increased red blood cell (RBC) (P < 0.001) and fresh frozen plasma (FFP) usage (P = 0.002), elevated postoperative total bilirubin levels (P < 0.001), increased LOHS (P = 0.04), and a higher 30-day post transplant mortality (P = 0.02). The use of HTK preservation solution was associated with higher mean postoperative aspartate aminotransferase levels (P = 0.02) and decreased mean RBC (P < 0.001) and FFP usage (P = 0.009) compared to UW preservation solution use.
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PMID:Association between donor-recipient serum sodium differences and orthotopic liver transplant graft function. 1816 40

Donor hypernatremia is known to be associated with initial graft dysfunction in liver transplantation. Controversial data exist regarding the impact of sodium dysregulation on patient survival after heart transplantation (HTX). The aim of this study was to investigate the influence of donor sodium levels on survival in a large cohort of heart transplant recipients from the Eurotransplant registry. From 1997 to 2005, all consecutive adult HTX performed in the Eurotransplant region were included into this study (n = 4641 patients). Multivariate analysis was applied to investigate possible clinical predictors for 1-year post-transplant survival after cardiac transplantation (donor sodium levels, donor age, donor cause of death, recipient age, primary disease, urgency status, cold ischemia time). In multivariate analysis, recipients receiving a donor heart with serum sodium level lower than 130 mmol/l or higher than 170 mmol/l had a 1.25-fold higher risk for 1-year post-transplant mortality than patients with normal donor sodium ranges (P = 0.007). Other independent risk factors for impaired 1-year survival were recipient age, the indication for transplantation and the urgency status of the recipient. Our study demonstrates that hyponatremia as well as hypernatremia show a strong U-shaped correlation with poor survival after cardiac transplantation. Accurate donor management to avoid electrolyte disorder seems to be crucial for ensuring good quality of donor hearts.
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PMID:Donor hypo- and hypernatremia are predictors for increased 1-year mortality after cardiac transplantation. 2000 30


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