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)

We studied the effects of superfusion of canine heart muscle tissue with a solution that mimicks hypoxia, acidosis and hyperkalemia (altered Tyrode's solution). Contracture (rise in resting tension) develops much sooner (5.2 +/- 0.8 vs. 30-40 min in 5 mM dextrose) in the absence of dextrose. High dextrose (55 mM) stabilizes the rise in tonic tension and protects against the action potential shortening during such superfusion. Presence of verapamil (1-1.5 microM) during altered Tyrode's superfusion considerably lessens the magnitude of the increase in tonic tension (31.7 +/- 8.6 vs. 129.5 +/- 32.6 mg in the control). Presence of high magnesium (5 mM) during altered Tyrode's superfusion also offers some protection against tonic tension increase (12.6 +/- 3.6 mg rise in tonic tension vs. 129.5 +/- 3.2 mg in the control), action potential shortening, and amplitude decrease. These results suggest that (a) magnesium and verapamil both have significant effects on the cellular calcium uptake, and (b) anaerobic metabolism utilizing either glycogen or exogenous glucose is capable of preventing contracture during ischemia.
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PMID:Effects of dextrose, verapamil and magnesium during hypoxia in myocardial tissue. 262 58

The purpose of this study is to investigate whether isolated hearts perfused with cardioplegic solution release inflammatory mediators such as neutrophil chemotactic factors (NCF). Three conditions were tested, including: (1) perfusion of rabbit hearts with crystalloid cardioplegic solution (4 degree C) saturated with air (95% oxygen) and containing dextrose (i.e. complete system), (2) perfusion of rabbit hearts with non-oxygenated cardioplegic solution, containing dextrose (i.e. minus oxygen system), and (3) perfusion of hearts with cold cardioplegic solution saturated with air in the absence of dextrose (i.e. minus dextrose system). At various time intervals (5 min, 1, 2, 3 and 4 h) samples of circulated perfusate were removed and assayed for the presence of NCF using modified Boyden chambers. Rabbit peritoneal neutrophils were the indicator cells. The standard chemoattractant, f-Met-Leu-Phe (f-MLP) was the positive control. High levels of neutrophil chemotactic activity were detected in perfusate of all above described hearts perfused for 4 h (i.e. 194 +/- 22% of f-MLP control--complete system, 126 +/- 13%--minus oxygen and 136 +/- 10%-minus dextrose). Histological evaluation of these hearts showed evidence of global ischemia. We also detected significant levels of NCF in effluent of hearts perfused for 5 min, 1, 2 and 3 h. Similar to perfused hearts, isolated rabbit hearts incubated for 4 h with non-oxygenated cardioplegic solution (in presence and absence of dextrose) released high levels of NCF (132 +/- 18%-intact heart; and 100 +/- 6% myocardial segments). Standard checkerboard analysis revealed that the observed activity released from these hearts is chemotactic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac derived neutrophil chemotactic factors; preliminary biochemical characterization. 267 54

This study examines the effects of complement activation and of complement-induced oxygen radical production on the principal determinant of hepatic function, i.e., effective hepatic blood flow (EHBF). Female Sprague-Dawley rats received cobra venom factor, 40 units/kg, in two divided doses at 30-minute intervals. At t = 2 hours, thermodilution cardiac output, mean arterial pressure, heart rate, hematocrit, and EHBF by galactose clearance were determined. Complement activation produced a significant depression in EHBF independent of changes in systemic perfusion. To determine whether oxygen radicals participated in the insult, additional animals were pretreated with superoxide dismutase, 6 mg/kg, plus catalase, 15 mg/kg, immediately before complement activation. Concomitant treatment with the oxygen radical scavengers attenuated the degree of complement-induced hepatic ischemia, again independent of effects on systemic perfusion. This study suggests that the reduction in hepatic blood flow that accompanies animal models of trauma and sepsis may result, in part, from the sequelae of complement activation with oxygen radicals as secondary mediators.
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PMID:Contribution of toxic oxygen intermediates to complement-induced reductions in effective hepatic blood flow. 284 55

The effects of acute moderate hyperglycemia on local cerebral pH (LCpH) and local cerebral blood flow (LCBF) were studied in rats infused with glucose before middle cerebral artery (MCA) occlusion, and compared with findings in MCA occlusion alone. The effects of nimodipine infusion on LCBF and LCpH in MCA-occluded hyperglycemic rats were also studied. LCpH and LCBF were determined simultaneously by a double-label autoradiographic technique. Hyperglycemia was induced by an intraperitoneal injection of 2 g/kg D-glucose before MCA occlusion. Nimodipine-treated rats received the drug as an intravenous infusion of 0.5 micrograms/kg/min starting 15 min after occlusion, and ending at decapitation 4 h postocclusion. Cortical LCpH of five structures in the MCA territory of hyperglycemic rats varied between 6.64 +/- 0.04 and 6.72 +/- 0.02 (mean +/- SEM). These values were significantly lower than LCpH in the same ischemic structures in the control rats, which varied between 6.76 +/- 0.04 and 6.82 +/- 0.03 (p less than 0.05 for four of five structures). Cortical LCpH of hyperglycemic nimodipine-treated rats ranged between 6.94 +/- 0.02 and 7.05 +/- 0.02, indicating significant elevations in LCpH (p less than 0.001) compared with the untreated ischemic hyperglycemic animals. LCBF in the ischemic structures was not modified by hyperglycemia or nimodipine treatment. This suggests that nimodipine, by mechanisms other than improvement in blood flow, can prevent the enhanced cerebral tissue acidosis produced by hyperglycemia before incomplete focal ischemia.
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PMID:Nimodipine prevents hyperglycemia-induced cerebral acidosis in middle cerebral artery occluded rats. 291 Aug 98

The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia was examined in New Zealand white rabbits. Spinal cord ischemia was produced by infrarenal balloon occlusion of the aorta in unanesthetized animals. Animals were observed for 3 days for neurologic evaluation. Fasted animals received intravenous dextrose, 0.5 g.kg-1, or placebo before a period spinal cord ischemia. The dextrose was administered as either a bolus of a 50% solution (D50) 15 min before ischemia or as an infusion of a 5% solution (D5W) over 90 min before ischemia. With either mode of administration, preocclusion plasma glucose level was moderately increased as compared with that in animals that received lactated Ringer's solution in equivalent volume, i.e., for the D50 bolus: 291 +/- 82 (SD) versus 166 +/- 67 mg.dl-1 (P less than 0.005); and for D5W infusion: 177 +/- 38 versus 137 +/- 13 mg.dl-1 (P less than 0.01). With either mode of administration, neurologic outcome was poorer (P less than 0.025) at 72 h in the animals that had received dextrose. For example, of the 10 animals that received D5W by infusion, nine were paraplegic (unable to walk) 72 h after ischemia, whereas only three of 10 control animals were paraplegic. The adverse effect of an increased blood glucose level has been demonstrated previously for cerebral ischemia. The present results are the first demonstration that increased plasma glucose may result in a worsened neurologic outcome after spinal cord ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia in the rabbit. 291 17

Some human and experimental neuropathies are characterized by endoneurial edema and increased intercapillary distance (ICD). This may potentially produce chronic endoneurial ischemia. To examine the relationship between nerve blood flow (NBF) and ICD we measured NBF in rats with experimental galactose neuropathy (EGN), a model where ICD is known to be increased. Simultaneous measurements of NBF in the center and subperineurial region were made in normal and edematous tibial nerves using hydrogen-sensitive microelectrodes and hydrogen polarography. NBF was significantly reduced in rats with EGN when compared with controls. A second finding was that in half the rats with EGN there was a greater reduction in NBF in the subperineurial region, a site of maximal ICD increase. In contrast, NBF was similar in central and peripheral regions in control rats. These findings support the hypothesis that an increase in ICD produces a reduction in NBF. Further support for the hypothesis is derived from a computer model of the effect of changes in ICD on endoneurial oxygen tension. We conclude that a chronic reduction in NBF may participate in the pathogenesis of edematous neuropathies.
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PMID:Relationship between nerve blood flow and intercapillary distance in peripheral nerve edema. 301 93

Warm ischemia (WI) has been shown to be detrimental to organ function following transplantation. We investigated the effect of increasing warm ischemic time (WIT) on islet isolation in rats and dogs. Rat isolations were performed by collagenase digestion and Ficoll purification after increasing periods of WI. Dog isolations were performed after similarly increasing periods of WI by ductal perfusion with collagenase, counts being performed on unpurified tissue. Viability studies were performed on isolated purified rat islets by in vitro perifusion. Islet counts decreased as WIT increased such that after 45 min WI islet counts were only 45.7% of those at 0 WIT (P less than 0.001) in rats and 52.5% in dogs (P less than 0.002). Islet volumes decreased to 47.0% in rats (P less than 0.001) in rats and 52.5% in dogs (P less than 0.002). period. After 90 min WIT islet counts were down to 15.6% (P less than 0.001) in rats and 23.9% in dogs (P less than 0.001) and volumes were down to 16.0% (P less than 0.001) in rats and 10.9% (P less than 0.001) in dogs. The increased release of insulin in response to dextrose stimulation was abolished after only 30 min WIT as assessed by perifusion. This work suggests that if successful islet isolation is to be performed for clinical transplantation, WI during donor pancreatectomy must be minimized, or techniques must be developed to prevent or reverse the ensuing effects.
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PMID:The effect of pancreatic warm ischemia on islet isolation in rats and dogs. 305 26

Although hyperglycemia is known to exacerbate neuronal injury in the setting of reversible brain ischemia, its effect on irreversible thrombotic infarction is less well understood. In this study, unilateral thrombotic infarction was induced photochemically in the parietal cortex of Wistar rats. Seven days later, brains were perfusion-fixed for light microscopy. Infarct areas were measured by computer-assisted planimetry on multiple coronal sections at 250-micron intervals; these data were integrated to yield infarct volumes. Fasted, normoglycemic rats were compared with hyperglycemic rats that had received 1.2-1.5 ml of 50% dextrose i.p. 15 minutes prior to the induction of infarction. Infarct volume averaged 12.5 +/- 4.0 mm3 (mean +/- SD) in rats (n = 14) with plasma glucose levels of 72-184 mg/dl; this differed statistically from the average volume of 9.3 +/- 3.3 mm3 observed in rats (n = 13) with elevated plasma glucose (range 264-607 mg/dl). Spearman rank correlation analysis confirmed a significant correlation of larger infarct volumes with lower plasma glucose levels. In contrast, rats receiving mannitol i.p. to produce an osmotic load comparable with that of the dextrose-pretreated animals showed larger infarct volumes than saline-treated controls. The small but definite beneficial effect of hyperglycemia in this end-arteriolar thrombotic infarction model is possibly attributable to improved local energy metabolism at the periphery of the lesion during the early period of lesion expansion.
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PMID:Hyperglycemia reduces the extent of cerebral infarction in rats. 310 78

Regional myocardial perfusion and glucose metabolism were assessed in six normal volunteers and 29 patients with coronary heart disease and stable or unstable angina using rubidium-82 (Rb-82) and F-18 fluoro 2-deoxy-D-glucose (FDG) with positron emission tomography. All normals and patients were studied following overnight fasting, at rest, with no angina or electrocardiographic signs of acute myocardial ischemia or necrosis. Rb-82 myocardial cross-sectional images were obtained employing the continuous infusion technique, while dynamic FDG imaging was employed after intravenous tracer bolus injection. Regional Rb-82 and FDG myocardial concentrations were then calculated by drawing regions of interest over the interventricular septum, anterior and lateral wall of the left ventricle. The mean Rb-82 uptake for each left ventricular region analyzed was found to be similar between both groups of patients and normal volunteers. The mean myocardial glucose utilization was found to be similar in normal volunteers and patients with stable angina (0.023 +/- 0.032 vs. 0.012 +/- 0.008 microns ml/min p less than 0.42). However, myocardial glucose utilization was found to be significantly higher in patients with unstable angina compared with both normals and patients with stable angina (0.048 +/- 0.047 microM/ml/min p less than 0.001 for both comparisons). Thus, in patients with severe coronary artery disease and unstable angina, myocardial glucose utilization was enhanced in spite of the absence of clinical, electrocardiographic, or detectable perfusion evidence of acute ischemia.
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PMID:Abnormalities in myocardial metabolism in patients with unstable angina as assessed by positron emission tomography. 315 93

Complement, activated during infection and injury, has been implicated as a mediator of microvascular injury and obstruction. This study examines how two potent activators of complement, zymosan, and cobra venom factor (CVF), affect systemic and visceral perfusion. Rats were injected with either saline (1 ml/kg), zymosan (5 mg/kg) or CVF (5 units/kg) at t = 0 and 30 minutes. Thermodilution cardiac output, mean arterial pressure, heart rate, systemic vascular resistance, and hematocrit were determined at t = 2 hours. Effective hepatic and renal blood flows, by clearance of galactose and p-aminohippurate respectively, were determined over the next hour. The per cent change in total hemolytic complement from t = 0 to t = 3 hours was determined by immune hemolysis of sheep erythrocytes. There was no difference in systemic hemodynamic parameters between the three groups. Hepatic blood flow was depressed in both the zymosan (3.83 +/- 0.23 ml/min/100 g) and CVF (3.72 +/- 0.20 ml/min/100 g) groups compared with controls (4.62 +/- 0.19 ml/min/100 g, P less than 0.05). Renal blood flow in the zymosan-treated group (6.40 +/- 0.24 ml/min/100 g) increased over control (4.80 +/- 0.40 ml/min/100 g, P less than 0.05) but was unchanged in the CVF group (5.06 +/- 0.23 ml/min/100 g). The amount of complement activated correlated with the change in hepatic (r = -0.419, P less than 0.05) but not renal (r = -0.008, P = 0.917) flow. Complement activation may occupy a proximal position in the pathogenesis of hepatic ischemia associated with trauma and sepsis.
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PMID:Visceral perfusion abnormalities following complement activation. Clues to the mediators of organ ischemia in trauma and sepsis. First place winner: Conrad Jobst Award. 319 44


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