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)

The parathyroid hormone-related peptide (PTHrP) was initially identified in the early eighties, as the humoral mediator causing hypercalcaemia associated with malignancy. However, recently PTHrP was also shown to mediate a wide range of local paracrine/autocrine and intracrine functions in various tissues under physiological and pathological conditions. Indeed, PTHrP is a polyhormone, which can act through different receptors, including the type 1 parathyroid hormone (PTH) receptor 1 (PTH-1R). In the cardiovascular system, PTHrP appears to have potent effects on vascular smooth muscle cells and cardiomyocytes, where it participates in different pathological conditions, such as ischemia and heart failure. Therefore, it is conceivable that further studies on the regulation of PTHrP expression, characterization of its autocrine/paracrine/intracrine functions and definition of its intracellular signal transduction pathways in cardiomyocytes and cardiac vascular smooth muscle cells can elucidate the potential role of PTHrP in cardiovascular pathophysiology.
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PMID:Parathyroid hormone-related peptide and cardiovascular system. 1459 5

The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications.
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PMID:Occurrence of "J waves" in 12-lead ECG as a marker of acute ischemia and their cellular basis. 1754 22

Microsurgical procedures such as free tissue transfer or replantations of amputated digits involve an obligatory ischemic period leading to regional tissue oedema, rhabdomyolysis, systemic acidosis, hypercalcemia and multiple organ dysfunction syndrome reflecting ischemia-reperfusion (I/R) injury. Since nitroxide stable radicals act as antioxidants their potential protective effects were tested. Anaesthetized Sabra rats were subjected to regional ischemia of the hind limb for 2 h using a tourniquet. Upon reperfusion rats were injected with 4-OH-2,2,6,6-tetramethylpiperidine-1-oxyl (TPL). Systemic I/R-induced damage was assessed by sampling blood for differential count, lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) serum levels. Regional injury was evaluated by analysing excised muscle samples for oedema (tissue water content) and inflammatory infiltrate (number of cell nuclei in histomorphometric analysis). I/R-induced changes of biomarkers reflecting systemic damage peaked about 8 h following the start of reperfusion and fully disappeared as the biomarkers relaxed to their pre-ischemic values after 24 h. TPL facilitated the recovery of some of these parameters and partially affected release of cellular CPK and LDH. The parameters of I/R-induced regional tissue injury did not demonstrate any recovery and were not inhibited by TPL.
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PMID:The effect of a nitroxide antioxidant on ischemia-reperfusion injury in the rat in vivo hind limb model. 1829 4

Acute pancreatitis is a relatively common disease that affects about 300,000 patients per annum in America with a mortality of about 7%. About 75% of pancreatitis is caused by gallstones or alcohol. Other important causes include hypertriglyceridemia, medication toxicity, trauma from endoscopic retrograde cholangiopancreatography, hypercalcemia, abdominal trauma, various infections, autoimmune, ischemia, and hereditary causes. In about 15% of cases the cause remains unknown after thorough investigation. This article discusses the causes, diagnosis, imaging findings, therapy, and complications of acute pancreatitis.
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PMID:Acute pancreatitis: etiology, clinical presentation, diagnosis, and therapy. 1857 Sep 47

Rhabdomyolysis is a syndrome of skeletal muscle cell damage that leads to the release of toxic intracellular material into the systemic circulation. The pathogenesis of rhabdomyolysis is based on an increase in free ionized calcium in the cytoplasm. Its main complications include (a) acute renal failure, which is triggered by renal vasoconstriction and ischemia, (b) myoglobin cast formation in the distal convoluted tubules, and (c) direct renal toxic effect of myoglobin on the epithelial cells of proximal convoluted tubules. Other major complications include electrolyte disorders, such as hyperkalemia, which may cause cardiac arrhythmias, metabolic acidosis, hyperphosphatemia, early hypocalcemia, and late hypercalcemia. Compartmental syndrome and disseminated intravascular coagulopathy may also emerge. The management of myoglobinuric acute renal failure includes aggressive fluid administration to restore the hypovolemia and urine alkalization. The concomitant electrolyte and metabolic disorders should also be treated appropriately; hemodialysis should be considered when life-threatening hyperkalemia and metabolic acidosis exist. In the case of compartmental syndrome, it is important to monitor the intra-compartmental pressure and to perform fasciotomy, if required. When diagnosed early and if the appropriate treatment is initiated promptly, the complications of rhabdomyolysis are preventable and the syndrome has a good prognosis.
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PMID:The syndrome of rhabdomyolysis: complications and treatment. 1904 20

Ischaemia significantly affects the cellular homeostasis (sodium and calcium overload, intracellular acidosis, swelling, cytoskeleton injuries, mitochondrial hypercalcaemia and others). If reperfusion of an organ in ischaemia is essential for its viability and its functional recovery, the arrival of blood oxygen will cause a series of lesions; this is known as the phenomenon of ischaemia-reperfusion. Vasomotricity and the endothelial functions are significantly affected by it. Endothelium-dependent vasodilatation is more affected by ischaemia-reperfusion injuries than vasoconstriction and endothelial-independent vasodilatation. Reactive oxygen species and tumour necrosis factor-alpha seem to play a major role in this perturbation. Reperfusion also induces an important inflammatory response, characterized by a massive production of free radicals and by the activation of the complement and leucocyte neutrophils. A narrow interaction between activated endothelium and neutrophils will result in a significant concentration of neutrophils activated in the interstitium, where they release many oxygen radicals and many kinds of proteases, which destroy cells and extracellular matrix. This transfer of neutrophils from the intravascular bed to the intestitium involves several families of proteins such as selectins (P-selectin and L-selectin), integrines (intercellular adhesion molecule-1) and immunoglobulins (platelet-endothelial cell adhesion molecule-1). Last, oxidative stress, the production of cytokines and the secondary mitochondrial lesions that occur with reperfusion will induce apoptosis on the level of the parenchyma and the vascular structures. According to the stage of the vascular system considered (small arteries, capillaries or postcapillary veins), the repercussions of ischaemia-reperfusion are identical, but the clinical pictures differ. The proinflammatory state induced by reperfusion continues for several days and can affect the patient's prognosis.
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PMID:The impact of ischaemia-reperfusion on the blood vessel. 1941 12

Bisphosphonate-related osteonecrosis of the jaws (BRONJ) is a newly emerging condition in a long-term administration of mainly intravenous bisphosphonates for the treatment of hypercalcemia associated with malignancy, multiple myeloma, and metastatic breast and prostate cancers. The incidence of BRONJ is not so high, but it is very refractory to ordinary dental treatments, and the bone exposure, a typical symptom, continues for several months. Although many cases of BRONJ have been reported worldwide, the precise pathogenesis remains obscure. Diabetes mellitus (DM) is one of the systemic risk factors contributing in the development of BRONJ. DM is generally associated with microvascular ischemia of the bone, endothelial cell dysfunction, decreased bone turnover and remodeling, resulting in a delayed wound healing and easy to infection. In this issue, the relation of DM as a systemic risk factor with development of BRONJ as well as the incidence, clinical manifestations and prevention and treatment of BRONJ are described.
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PMID:[Diabetes mellitus and bisphosphonate-related osteonecrosis of the jaws]. 1972 Dec 6

Calciphylaxis is a rare disease associated with thrombotic cutaneous ischemia and necrosis. Lesions are usually located on the lower extremities, buttocks and the abdomen. Calciphylaxis is recognized by medial calcification, inflammation and subintimal fibrosis of cutaneous arterioles. Calcification, thrombus formation and occlusion occur sequential before tissue necrosis. The disease is usually observed in patients with end-stage renal disease and hyperparathyroidism. In end-stage renal disease, an elevated parathyroid hormone level, hypercalcemia and hyperphosphatemia direct to vascular mineralization. Calciphylaxis affects about 4% of hemodialysis patients. The clinical syndrome is characterized by a high mortality rate. The most important measure is an active multidisciplinary management approach, with intention to wound care and prevention of sepsis.
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PMID:[Calciphylaxis. Pathogenesis and therapy]. 2168 45

Mithramycin A (MTM) is an antibiotic used for the treatment of hypercalcemia and several types of cancer. We have reported previously that MTM protects against endoplasmic reticulum (ER) stress-induced neuronal death in organotypic hippocampal slice cultures. In the present study, the neuroprotective effect of MTM against ischemia/reperfusion-induced neuronal injury was evaluated in the hippocampus in mice. Neuronal damage was apparent in area CA1 of the hippocampus after transient global ischemia/reperfusion. The expression of C/EBP homologous protein (CHOP), a key transcription factor for ER stress-induced neuronal death, showed a pronounced increase in area CA1 in these mice. Treatment of the mice with MTM significantly decreased both the number of neurons stained with Fluoro-Jade B and the level of CHOP expression in the hippocampus. MTM did not affect the increase of 78-kDa glucose-regulated protein induced by ischemia/reperfusion. MTM also restored the ischemia/reperfusion-induced impairment of long-term potentiation in the hippocampus, without any change in paired pulse facilitation. These results suggest that administration of MTM protects hippocampal neurons against injury induced by transient global ischemia/reperfusion through attenuation of ER stress-associated signals, and ameliorates neuronal injury induced by ischemia/reperfusion in the hippocampus.
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PMID:Protective action of mithramycin against neurodegeneration and impairment of synaptic plasticity in the hippocampal CA1 area after transient global ischemia. 2210 May 65

We report the case of a 78-year-old male who developed acute pancreatitis related to quetiapine that was administered for the treatment of delirium. No evidence of hypertriglyceridemia, infection, ischemia, chololithiasis or hypercalcemia could be documented.Clinicians should be alerted when treating critical care patients with antipsychotics, as risks might present and potentially lead to hazardous results.
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PMID:Quetiapine-associated pancreatitis in a geriatric critical care patient with delirium. 2293 21


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