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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluorescence emission of reduced nicotinamide adenine dinucleotide (NADH) from the surface of perfused rat hearts was photographed to provide a two-dimensional recording of NADH levels. Sodium Amytal inhibition of NADH oxidation resulted in a homogeneous increase in NADH fluorescence, while lowering perfusion pressure from 55 to 10 torr caused a heterogeneous increase in NADH fluorescence, reflecting the heterogeneous oxygen delivery at this low pressure. Local ischemia resulted in a well-defined region of high NADH fluorescence that corresponded to the region of ischemic inslut. The sharp transition between the ischemic and normoxic areas demonstrated that the hypoxic interface separating the two areas must be quite small.
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PMID:Ischemic areas in perfused rat hearts: measurement by NADH fluorescence photography. 18 43

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
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PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

Sodium meglumine calcium metrizoate was injected into isolated blood-perfused canine hearts to evaluate the effect of contrast agents containing calcium on normal and ischemic myocardium. Under normal perfusion pressure and mild ischemia, this contrast agent produced a positive inotropic effect, but during profound ischemia, this positive effect was followed by a period of myocardial depression. These findings indicate that the addition of an inotropic agent to contrast medium can produce a paradoxical depressant effect which can be deleterious to the ischemic myocardium.
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PMID:Differential effects of sodium meglumine calcium metrizoate on the inotropic state of normal and ischemic myocardium. 66 67

The mechanism of sodium retention by the kidney in rats with ligation of the common bile duct was studied with micropuncture techniques. 10-14 days after bile duct ligation, rats showed positive sodium balance and ascites formation. Measurements of renal blood flow and glomerular filtration rate yielded values that were not different from those in normal control animals. Likewise, single nephron filtration rte of surface nephrons was the same in the experimental rats as in the controls. Sodium reabsorption, however, was markedly increased in the proximal convoluted tubule, as well as in segments beyond the proximal convolutions. Single nephron filtration fraction, calculated from measurements of efferent arteriolar and arterial hematocrits, was significantly elevated in the cortical nephrons, even though whole kidney filtration fraction was the same as in normal rats. The calculated protein concentration of cortical peritubular blood was higher in the bile duct-ligated rats than in the normal controls. The observations are consistent with the view that sodium retention is the result of enhanced reabsorption primarily by cortical nephrons. The enhanced reabsorption can be accounted for by relative cortical ischemia due to efferent arteriolar vasoconstriction with the consequent elevation of peritubular colloid oncotic pressure.
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PMID:A micropuncture study of renal salt and water retention in chronic bile duct obstruction. 112 34

The limitation of a myocardial necrotic area by some energy-yielding compounds in rat coronary occlusion and their capacity to elevate the ischemia threshold in conscious rabbits were studied. Sodium malate, ascorbic acid and phosphoenolpyruvate were demonstrated to reduce the sizes of necrotic areas and increase the ischemia threshold, whereas cytochrome C and fructose-1,6-diphosphate were effective solely in limiting the infection area. It was concluded that the preventive antianginal effect of energy-yielding and electron-accepting compounds depended on their capacity to accumulate in intact cardiomyocytes.
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PMID:[A comparative evaluation of the cardioprotective and antianginal actions of energy-providing agents]. 145 76

Sodium spectroscopy and imaging sequences designed to emphasize fast T2 decay or the multiple quantum signal have previously demonstrated a high contrast between normal and pathologic tissue which may be due to changes in intracellular versus extracellular sodium distribution. Since alterations in the amount of signal with fast T2 decay have previously been shown to occur with changes in intracellular sodium content, this study investigated the fast T2 relaxation characteristics of extracellular sodium during pathologic interventions on nonsubmerged perfused rat hearts. T2 data on total sodium content were obtained while global ischemia (stopping all perfusate flow) and extracellular edema (due to long perfusion times) were induced in the heart. The data were fit to a biexponential, with Mf(T2f) the magnitude (time constant) of the fast component of decay. Mf increased significantly in both pathologies (to 319 +/- 26%, n = 3, of baseline for ischemia and to 527 +/- 284%, n = 3, of baseline for edema); the increase with edema was demonstrated to be due to extracellular sodium by intermittently perfusing the heart for a short period with shift reagent. When shift reagent was not used until the conclusion of the edema experiment, Mf increased to 169 +/- 35% of baseline, also due mainly to extracellular sodium. T2f did not exhibit any trends with these experiments, with values ranging from 1.7 to 5.5 ms. We believe that these results indicate that compartmental sodium content will most likely not be quantifiable in pathologic states in the heart with relaxation-based techniques. However, correlations between the pathologic state of the tissue and the sodium NMR signal obtained with pulse sequences or images that emphasize a particular aspect of relaxation may prove to be useful.
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PMID:Characteristics of extracellular sodium relaxation in perfused hearts with pathologic interventions. 146 Nov 13

Spinal trauma can originate from internal or external sources. Injuries to the spinal cord can be classified as either concussive or compressive and concussive. The pathophysiologic events surrounding spinal cord injury include the primary injury (compression, concussion) and numerous secondary injury mechanisms (vascular, biochemical, electrolyte), which are mediated by excessive oxygen free radicles, neurotransmitter and electrolyte alterations in cell membrane permeability, excitotoxic amino acids, and various other biochemical factors that collectively result in reduced SCBF, ischemia, and eventual necrosis of the gray and white matter. Management of acute spinal cord injuries includes the use of a high-dose corticosteroid regimen within the initial 8 hours after trauma. Sodium prednisolone and methylprednisolone, at recommended doses, act as oxygen radical scavengers and are anti-inflammatory. Additional considerations are the stability of the vertebral column, other conditions associated with trauma (i.e., pneumothorax), and the presence or absence of spinal cord compression, which may warrant surgical therapy. Vertebral fractures or luxations can occur in any area of the spine but most commonly occur at the junction of mobile and immobile segments. Dorsal and dorsolateral surgical approaches are applicable to the lumbosacral and thoracolumbar spine and dorsal and ventral approaches to the cervical spine. Indications for surgical intervention include spinal cord compression and vertebral instability. Instability can be determined from the type of fracture, how many of the three compartments of the vertebrae are disrupted, and on occasion, by carefully positioned stress studies of fluoroscopy. Decompression (dorsal laminectomy, hemilaminectomy, or ventral cervical slot) is employed when compression of the spinal cord exists. The hemilaminectomy (unilateral or bilateral) causes less instability than dorsal laminectomy and therefore should be used when practical. The preferred approach for atlantoaxial subluxation is ventral, and the cross pinning, vertebral fusion technique is used for stabilization. Fracture luxations of C-2 are repaired with small plates on the ventral vertebral body. The thoracic and upper lumbar spine is stabilized with dorsal fixation techniques or combined dorsal spinal plate/vertebral body plate fixation. Several methods of fixation can be used with lower lumbar or lumbosacral fractures, including the modified segmental technique and the combined dorsal spinal plate/Kirschner-Ehmer technique.
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PMID:Spinal trauma. Pathophysiology and management of traumatic spinal injuries. 164 21

Sodium transport in the early postischemic period was studied using Mongolian gerbils with right common carotid artery ligation. [22Na]sodium chloride ([22Na]NaCl) was infused immediately after, 10 minutes before, and 4 hours before carotid ligation, and the 22Na distribution was measured in symptomatic animals by autoradiography 1 hour after ischemia. Regional cerebral blood flow was determined by [14C]iodoantipyrine autoradiography. The specific gravity of the brain was measured in symptomatic gerbils 1 and 2 hours after carotid ligation by a gradient column. There was a low uptake of 22Na in the ischemic core and a high uptake in the ischemic periphery when the tracer was given 10 minutes before or immediately after ischemia. In contrast, tracer given 4 hours before ischemia showed an increased radioactivity in both the ischemic core and periphery. It is suggested that increased sodium in the ischemic core is due to a decreased sodium clearance rate and increased sodium in the ischemic periphery is due to some active transport process.
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PMID:Relationship between 22Na distribution and cerebral blood flow in ischemic gerbil brain. 171 59

The following study was performed to determine whether calcium channel blockers, delivered before or after an ischemic insult, were effective at reducing cyclosporine-induced exacerbation of renal ischemic injury. When cyclosporine (5 mg/kg) was administered intravenously to rats after 30 min of renal ischemia, GFR fell by 60% compared with values observed in rats subjected to ischemia alone (190 +/- 30 vs. 330 +/- 40 microliters/min/100 g; P less than 0.05). Pretreatment with verapamil (10 micrograms/kg/min delivered intravenously) prevented the fall in GFR (320 +/- 70 microliters/min 100 g), as did pretreatment with nitrendipine, 1 micrograms/kg/min (460 +/- 90 microliters/min/100 g). Verapamil was less effective if given after the ischemia-cyclosporine insult (GFR 260 +/- 90 microliters/min/100 g), and nitrendipine given at this time had no beneficial effect at all (GFR 180 +/- 10 microliters/min/100 g). The doses of calcium channel blockers used had no protective effect on renal ischemic injury alone. Blood pressure during study ranged between 105 and 119 mm Hg with minor differences between groups. Sodium and potassium excretion and urinary flow rates were similar in all groups, except for a slight increase in sodium excretion in verapamil-treated rats. These values demonstrate that calcium channel blockers ameliorate the exacerbation or renal ischemic injury induced by cyclosporine if given before but not after the ischemia-cyclosporine insult. The protective effect of these agents, used preischemia in cyclosporine-treated rats, is observed with intravenous use of the drugs at doses that have no protective effect on renal ischemic injury alone.
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PMID:Evidence that calcium channel blockade prevents cyclosporine-induced exacerbation of renal ischemic injury. 184 48

The potassium channel activators cromakalim and pinacidil were recently shown to have anti-ischemic properties in isolated globally ischemic rat hearts. The effects of two reported blockers of ATP-sensitive potassium channels, glibenclamide (glyburide) and sodium 5-hydroxydecanoate, on the anti-ischemic efficacy of cromakalim were determined in this model. Buffer-perfused rat hearts were subjected to 25 minutes of ischemia followed by 30 minutes of reperfusion. Pretreatment of these hearts with 60 microM cromakalim significantly decreased indexes of contractile function but caused a significant improvement of postreperfusion function and a significant decrease in release of lactate dehydroxygenase and in end-diastolic pressure. Pretreatment with glibenclamide at concentrations that reversed the preischemic effects of cromakalim (0.05 and 1.0 microM) also significantly reversed its postischemic protective effects. Sodium 5-hydroxydecanoate (100 and 300 microM) had no effect on the preischemic (negative inotropic) effects of cromakalim but completely reversed its cardioprotective effects. Sodium 5-hydroxydecanoate did not reverse the cardioprotective effects of the calcium entry blocker diltiazem. In phenylephrine-contracted rat aorta, glibenclamide (0.1-10 microM) inhibited cromakalim-induced relaxation, whereas sodium 5-hydroxydecanoate (10-1,000 microM) had no effect. Similarly, the ability of cromakalim to shorten cardiac action potential duration in guinea pig papillary muscle and to increase outward whole-cell potassium currents in isolated myocytes was inhibited by glibenclamide, whereas sodium 5-hydroxydecanoate was without effect. Thus, both glibenclamide and sodium 5-hydroxydecanoate inhibited the effects of cromakalim after reperfusion; however, sodium 5-hydroxydecanoate, unlike glibenclamide, had no effect in nonischemic preparations. These results suggest that sodium 5-hydroxydecanoate is an ischemia-selective inhibitor of ATP-sensitive potassium channels.
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PMID:Specific block of the anti-ischemic actions of cromakalim by sodium 5-hydroxydecanoate. 193 46


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