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 role of the inflammatory process in the onset of sickle cell crisis has not been fully elucidated, although there is evidence for leukocytosis and enhanced leukocyte to endothelium adhesion. The elevated LEA typical of inflammation may impede recovery from transient ischemic episodes by increasing the resistance to blood flow, which in the case of sickle cell disease may exacerbate the "vicious cycle" of HbS deoxygenation which leads to microvascular stasis. Recent studies on the mechanics of white blood cell margination and adhesion in postcapillary venules of laboratory animals, either in the low-flow state or following tissue exposure to chemoattractants, reveal a marked rise in intravascular resistance with LEA. Such increases may be as great as twofold with as few as 6 WBCs adhering per 100 microns of venule length. In human subjects, leukocytosis attendant to crisis has been correlated with increased time to recover from induced periods of ischemia in skin capillaries. Thus, further definition of the role of the inflammatory process in crisis is needed in light of microvessel obstruction in the low-flow state.
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PMID:Role of leukocyte-endothelium adhesion in affecting recovery from ischemic episodes. 247 65

Patients in sickle cell crisis may complain of unilateral or bilateral hearing loss which is typically a mild to moderate high-frequency sensorineural hearing loss in the affected ear(s). Auditory acuity can return to precrisis levels. A literature review suggests that the etiology is cochlear ischemia. A review of the literature, case study, and discussion will be presented.
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PMID:Sickle cell crisis and sensorineural hearing loss: case report and discussion. 267 Jul 95

This prospective study was designed to examine the relationship between serial serum nitric oxide (NO) levels and pain during the emergency department (ED) treatment of acute vasoocclusive sickle cell crisis (SCC). 102 patient visits, age > or =18 years of age, presenting to the ED with uncomplicated, typical SCC pain had serum NO levels obtained at 2-hr intervals during treatment of pain and were measured using an NO-specific chemiluminesence technique. Pain was measured prior to each NO measurement using a 10 cm visual analog scale (VAS), and subjects were divided into a persistent pain group and an improved pain group. Patients with persistent pain had significantly low initial NO levels (11.51 microM +/- 2.8, P < 0.05) while those with pain improvement had higher initial NO levels (18.1 microM +/- 3.08, P < 0.05). There was no significant correlation between changes in NO and changes in pain scores. These results suggest that the initial NO level may serve as a marker for the severity of tissue ischemia. Sequential NO levels do not appear useful in predicting the course of SCC.
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PMID:Sequential nitric oxide measurements during the emergency department treatment of acute vasoocclusive sickle cell crisis. 1081 82

We report a case of an adolescent who had sickle cell disease and previous evidence of myocardial damage and presented with abdominal pain and rapid progression to cardiogenic shock and subsequent development of myocardial infarction. To our knowledge, this represents only the second report of a case of acute myocardial ischemia and subsequent infarction resulting transient ventricular dysfunction reported in a child with sickle cell disease successfully treated with exchange transfusion. The pathophysiology of this complication remains unclear, and cardiac complications may remain undetected as lung, bone, and brain infarcts are more common and the pain associated with sickle cell crisis may mask the ischemic symptoms. Multiple factors may contribute to ischemia in addition to the presence of a vaso-occlusive crisis or infection. Acute or chronic myocardial ischemia are probably more prevalent than currently known.
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PMID:Myocardial infarction and transient ventricular dysfunction in an adolescent with sickle cell disease. 1256 93

The majority of patients in pain clinics are treated for muscle pain yet methods to study it in animals are relatively weak compared to methods to study skin pain. Here we describe an in vitro muscle-nerve preparation and model of muscle ischemia and contractile fatigue in mice. Timed muscle contraction is electrically evoked, while single unit activity of muscle sensory neurons and muscle contractile force are simultaneously recorded. The muscle is placed in a small (<1 mL) chamber where oxygen levels can be manipulated, drugs can be applied, and the extracellular milieu can be highly controlled. We demonstrate that we can record from sensory afferents that have the properties expected of ischemic nociceptors. This method serves for studying the neuronal and molecular mechanisms underlying ischemic pains such as angina, intermittent claudication, and sickle cell crisis.
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PMID:A novel mouse skeletal muscle-nerve preparation and in vitro model of ischemia. 1695 26

The painful crisis accounts for the majority of sickle cell disease (SCD) related hospital admissions. The prototypic long pentraxin 3 (PTX3), an acute phase protein, is elevated in patients with inflammatory and ischemic states. As the sickle cell painful crisis is associated with both inflammation and tissue ischemia, we questioned whether plasma PTX3 levels are increased during and associated with painful crisis severity. Furthermore, since PTX3 up-regulates endothelial expression of tissue factor we studied PTX levels in relation to markers of endothelial and coagulation activation. Plasma levels of PTX3, ultra-sensitive C-reactive protein (US-CRP), prothrombin fragment 1+2, thrombin-antithrombin (TAT) complexes, von Willebrand Factor antigen and soluble vascular adhesion molecule-1 were determined in 105 asymptomatic sickle cell patients, 33 patients during painful crisis and 30 race matched healthy controls. Plasma PTX3 levels were comparable between patients in asymptomatic state and healthy controls, but significantly higher during painful crisis (P<0.01). US-CRP levels were higher in asymptomatic patients compared to controls (P<0.0001) and increased further during painful crisis (P<0.0001). PTX3 levels at presentation with painful crisis correlated significantly with the duration of subsequent hospital admission (r(s) = 0.43; P = 0.013), whereas US-CRP levels did not. PTX3 levels did not correlate with markers of hypercoagulability. The increase of PTX3 levels during painful crisis and their relation to the duration of subsequent hospital stay suggest that PTX3 might serve both as a diagnostic and severity marker of the painful sickle cell crisis.
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PMID:Plasma levels of pentraxin-3, an acute phase protein, are increased during sickle cell painful crisis. 2125 76

The hemoglobin S is a consequence of the substitution of valine for glutamic acid at position 6 of beta globin chain. The problem arises when some individuals with Hb S is moved to the mountains and exposed to hypoxia. The decrease in oxygen saturation distorts the red blood cell with HbS-shaped crescent (sickle cell). Sickle cell (rigid and fragile) tends to adhere to the other red blood cells, generating a series of intravascular alterations that can lead to tissue ischemia or infarction. The spleen by type of movement and lack of lateral communications between the branches of the splenic artery was the most susceptible to sickle cell crisis. Splenic infarction at altitude corresponding to different circumstances can evolve in three stages: a) Acute (focal, uncomplicated), b) massive attack (more than 50% of parenchyma) and c) spontaneous rupture.Early diagnosis is crucial, allowing the quick and timely introduction of various measures, including adequate hydration and oxygenation continues until its evacuation to lower altitude locations. These measures would reduce the phenomenon of sickle and some patients may overcome this acute trance without major complications. The delay in diagnosis leads to action that can exacerbate tissue hypoxia and cause ischemia or infarction of various organs. A large population of black and mixed race of African descent living in the Peruvian coast, 10% and 2% respectively have hemoglobin S; Caucasian subjects with Mediterranean ancestry this hemoglobin also can carry. It is therefore essential to disseminate within the clinicians working in regions of high status and to thus prevent potentially fatal complications in patients with Hb S; is also essential to promote preventive measures for individuals with African or Mediterranean ancestry know their sickle cell status before traveling to places above 2,500 m.
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PMID:[Spleen infarction and S hemoglobinopathies S in the high altitude lands]. 2247 81

Poloxamer 188 (P188) is a non-ionic amphiphilic copolymer with hemorheologic, antithrombotic, anti-inflammatory, and cytoprotective properties. It potentially has clinical utility in diverse diseases, such as acute myocardial infarction, acute limb ischemia, shock, acute stroke, heart failure, and sickle cell crisis. P188 is available as an excipient-grade product, manufactured to National Formulary specifications, which we refer to as P188-NF. During synthesis of P188-NF, polymerization of its polyoxyethylene and polyoxypropylene components generates undesirable low molecular weight (LMW) substances, such as truncated polymers and glycols. In early clinical studies, P188-NF yielded unexpected renal dysfunction. Here, we explore the nature of the renal dysfunction associated with P188-NF and use a purified (more homogenous) form of P188-NF (P188-P) to show that removal of LMW substances is associated with substantially less renal dysfunction. In both a remnant-kidney animal model and in clinical studies, P188-P demonstrates a substantially improved renal safety profile.
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PMID:Differential effects of commercial-grade and purified poloxamer 188 on renal function. 2472 48

Sickle cell trait (SCT), a benign hematological condition affecting approximately 300 million individuals globally, is associated with an increased risk of vaso-occlusive disease. However, the risks related to surgery employing cardiopulmonary bypass in patients with SCT are not well established. Herein, we report the case of a 27-year-old African American man with SCT who underwent an emergency aortic repair for acute Stanford type A aortic dissection using hypothermic circulatory arrest. The patient developed a sickle cell crisis, which was followed by spontaneous splenic infarction and rupture, nonocclusive mesenteric ischemia, and spinal infarction.
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PMID:Spontaneous splenic rupture, mesenteric ischemia and spinal infarction after aortic repair for acute type A dissection in a patient with sickle cell trait. 3309 Mar 64