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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to determine the effect of coronary reperfusion on (1) myocardial infarct size and (2) the accuracy of previously reported methods for estimation of infarct size serum creatine phosphokinase (CPK) values. Thirty mongrel dogs, chronically prepared, were studied in the awake state, and were divided into four groups according to the period or left circumflex coronary artery (LCCA) occlusion. Group 1: permanent occlusion (24 h) in nine dogs; group 2: 45 min occlusion (eight dogs); group 3: 1 h occlusion (five dogs); and group 4: 3 h occlusion (eight dogs). Serial blood samples were drawn for 24 h following the beginning of occlusion and were used to determine total and isoenzyme levels of CPK, and lactic dehydrogenase isoenzymes. All dogs were sacrified 24 h after the beginning of occlusion and were anatomically examined. The extent of anatomical myocardial infarction was determined and compared with the extent of myocardial infarction as estimated from serial serum CPK values. Total serum CPK increased significantly in all groups and was associated with the appearance of CPK-MB isoenzyme and an increase in LDH1,2 (LDH1 greater than LDH2) in most dogs. Total serum CPK increased within an hour after reperfusion and the mean values in groups 2, 3, and 4 were significantly high (P less than 0.05) than serum CPK values in group 1 in the period from 110 min to 4 after occlusion. These data demonstrate that reperfusion after 45 min to 3 h of coronary occlusion results in an earlier appearance of total serum CPK. The anatomical infarction in group 1 averaged 28% +/- 3% (SEM) of the total heart and was significantly larger than infarct size in all groups with reperfusion. In contrast, estimated infarction calculated from total CPK in group 1 was not significantly different from the reperfused groups. Although there was correlation between estimated and anatomical infarction, the data in each group showed that anatomical infarct size could not be accurately estimated from total serum CPK.
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PMID:Effect of reperfusion on myocardial infarct, and the accuracy of estimating infarct size from serum creatine phosphokinase in the dog. 93 92

Cerebrospinal fluid and serum were obtained from 16 clinically normal adult cows (11 dairy, 5 beef). Sodium, potassium, magnesium, total protein, and albumin concentrations, osmolality, and lactate dehydrogenase and creatine kinase activities, were quantified in CSF and serum. Total and differential cell counting, protein electrophoresis, and IgG quantification were performed on CSF. Statistical analyses of these variables, including mean, SEM, range, and 95% confidence intervals, were performed. Effects of blood contamination were evaluated, and were found to be negligible for all measured constituents. Correction factors for CSF creatine kinase and lactate dehydrogenase activities accounting for cellular contamination were developed. Total nucleated cell count was similar to counts in CSF of other species, but higher than values in healthy people. Differential leukocyte count in CSF was similar to that reported in CSF of other domestic animals: mostly lymphocytes, fewer monocytoid cells, and scant neutrophils. Cerebrospinal fluid protein concentration was higher than concentration reported for dogs, goats, and people, but was similar to values reported for horses. Beef cows had higher CSF total protein concentration than did dairy cows; also, beef cows had higher CSF gamma-globulin concentration. The concentration of sodium in CSF was slightly higher than the value in serum, and potassium concentration was lower than the value in serum. In contrast to studies of human beings, CSF osmolality was generally less than serum osmolality in the cows studied. Reference values for CSF electrolyte concentrations and osmolality are useful for diagnosis of salt poisoning and for assessment of the effects of fluid therapy. Magnesium concentration was lower in CSF, compared with serum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Composition and analysis of cerebrospinal fluid in clinically normal adult cattle. 146 1

The effects of the calcium antagonists, chlorpromazine (CPZ), nisoldipine (NIS), trifluoperazine (TFP), and nicardipine (NIC) were compared in rat livers following either 20- or 30-hr ice storage in sodium lactobionate sucrose solution (SLS). Survivals beyond 7 days after orthotopic liver transplantation following 20-hr cold storage were 1/14 in the University of Wisconsin solution, 4/14 in SLS, 4/8 in UW+CPZ, 7/8 in SLS+CPZ. Survivals beyond 7 days after OLT following 30-hr cold storage were 3/8 in SLS+CPZ, 3/8 in SLS+NIS, 2/8 in SLS+TFP, 0/8 in SLS+NIC, and 0/8 in SLS alone. Survival rates were significantly (P less than 0.05) better in both SLS+CPZ and SLS+NIS than in UW and SLS alone. The effluent lactate dehydrogenase (LDH) levels and pH changes were measured at the time of OLT. After 20 hr, LDH levels were 525 +/- 78 IU/L (mean +/- SEM) in UW, 492 +/- 44 in SLS, 322 +/- 35 in UW+CPZ, and 290 +/- 39 in SLS+CPZ. After 30 hr, LDH values were 416 +/- 40 in SLS+CPZ, 450 +/- 25 in SLS+NIS, 448 +/- 21 in SLS+TFP, 573 +/- 18 in SLS+NIC, and 614 +/- 68 in SLS. The LDH levels for SLS+CPZ and SLS+NIS were significantly lower than those of SLS and UW (P less than 0.01). The pH changes in the effluent were significantly less in both the CPZ and NIS groups (P less than 0.01). This study demonstrated improved liver preservation by the use of a simplified colloid-free lactobionate solution containing sodium as the principal cation. The addition of CPZ or NIS to the solution demonstrated the same potency for significant improvement in efficacy of this solution, while NIC was ineffective.
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PMID:Calcium antagonists in sodium lactobionate sucrose solution for rat liver preservation. 156 35

Cytosolic free adenosine diphosphate (ADP) concentration in remnant rabbit liver 24 hours after 70% hepatectomy was calculated from the measured components of the glyceraldehyde-3-phosphate dehydrogenase:3-phosphoglycerate kinase/lactate dehydrogenase reaction. The concentration of free cytoplasmic ADP of the remnant liver increased from the control value of 76.9 +/- 6.0 mumol/L to 208.8 +/- 31.9 mumol/L (mean +/- SEM) at 24 hours after hepatectomy. The calculated free ADP provides the following three interpretations with respect to mitochondrial respiration acceleration as a result of liver regeneration. First, the Michaelis-Menten equation for physiologic respiration relative to maximal respiration gave 1.16 as the value of acceleration. Next, the classical thermodynamic theory showed that the logarithm of [adenosine triphosphate]/[free ADP] [free inorganic phosphate], which is reciprocally correlated with mitochondrial respiration, was decreased by a factor of 0.78 after hepatectomy. Finally, the irreversible thermodynamic theory indicated that chemical affinity, which is linearly correlated to mitochondrial respiration, was increased 1.36 times. These interpretations suggest that the rate of mitochondrial respiration is accelerated after major hepatectomy.
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PMID:A role of cytoplasmic free adenosine diphosphate in regenerating rabbit liver. 158 84

To study the effect of the inflammatory mediator hydrogen peroxide (H2O2) on airway ciliary activity, we measured ciliary beat frequency (CBF) in cultured tracheal explants from sheep. Addition of H2O2 (10(-8) to 10(-4) M) produced a concentration-dependent mean (+/- SEM) decrease in CBF between 11.1 +/- 0.4% (P less than 0.01) and 100 +/- 0% (P less than 0.001); at each concentration, the maximal effect was reached by 20 to 25 min. Between 10(-8) and 10(-6) M H2O2, the decrease in CBF was reversible, lactate dehydrogenase (LDH) release was not significantly increased, and major morphologic lesions were not seen. At higher concentrations of H2O2, incomplete recovery of CBF (10(-5) M) or irreversible ciliostasis (10(-4) M) developed, and a significant increase in LDH and morphologic lesions were present. Catalase (2,000 U/ml) and H-7 (10(-5) M), a protein kinase inhibitor, abolished cilioinhibition produced by H2O2 at 10(-6) M and lower concentrations but not at 10(-5) M and higher concentrations. Phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, caused a dose-dependent (10(-11) to 10(-5) M), reversible decrease in CBF; this effect was abolished by H-7. We suggest that at nonlethal concentrations, H2O2 inhibits the beat frequency of airway epithelial cilia reversibly, through the activation of second messengers, including protein kinase C. This mechanism might contribute to the previously demonstrated impairment of mucociliary clearance in airway inflammation.
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PMID:Mechanism of hydrogen peroxide-induced inhibition of sheep airway cilia. 159 Oct 15

A method is described for the measurement and on-line monitoring of muscular extracellular lactate concentration in both anaesthetized and freely moving rats. This method is based on microdialysis sampling and lactic dehydrogenase-catalysed nicotinamide adenine dinucleotide, reduced (NADH)-fluorescence detection techniques. In vivo calibration revealed a resting extracellular lactate concentration of 1.92 +/- 0.13 mmol/l (+/- SEM) in the gastrocnemius muscle of adult male Wistar rats (n = 6), while the average whole-blood lactate level was 0.76 +/- 0.12 mmol/l (+/- SEM). This measured extracellular lactate concentration was 1.73-times higher than that deduced from the arterial lactate concentration. Blocking glycolysis with iodoacetate reduced the extracellular lactate concentration to 52 +/- 6% (+/- SEM, n = 4) of the resting level. The extracellular lactate concentration in rat gastrocnemius muscle had increased to significantly (P less than or equal to 0.05) different levels, 2.4 +/- 0.03 (+/- SEM) or 4.0 +/- 0.55 (+/- SEM) times the control value, 1 h after aortic clamping (n = 3) or cardiac arrest (n = 3), respectively. Stimulation of the sciatic nerve induced elevations of the extracellular lactate concentration in the tibialis anterior muscle which were linearly related to the recorded isometric force-time integral. We also monitored on-line the changes in extracellular lactate concentration in the tibialis anterior muscle of a swimming rat. Our results indicate that microdialysis lactate reflects also intracellular metabolism. Lactography may be a useful alternative to biopsies and nuclear magnetic resonance spectroscopy in clinical medicine and physiology for the monitoring of metabolism in vivo.
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PMID:Continuous monitoring of extracellular lactate concentration by microdialysis lactography for the study of rat muscle metabolism in vivo. 194 55

The purpose of this study was to compare the degree of ischemic and hypoxic injury in normal versus hypertrophied rat hearts to investigate basic mechanisms responsible for irreversible myocardial ischemic injury. Hearts from rats with bands placed on the aortic arch at 23 days of age (BAND) and sham-operated rats (SHAM, 8 weeks postoperative) were isolated, perfused with Krebs buffer, and had a left ventricular balloon to measure developed pressure. Hearts were made globally ischemic until they developed peak ischemic contracture and were reperfused for 30 minutes. Additional hearts were perfused for 15 minutes with glucose-free hypoxic buffer followed by 20 minutes of oxygenated perfusion. There was an 87% increase in heart weight of BAND compared with SHAM (p less than 0.01). During ischemia, lactate levels increased faster in BAND compared with SHAM, ischemic contracture occurred earlier in BAND than in SHAM despite no difference in ATP levels, and postischemic recovery of left ventricular pressure was less in BAND (26.8 +/- 5.6% of control left ventricular pressure, mean +/- SEM) compared with SHAM (40 +/- 4.6%, p less than 0.05). During hypoxic perfusion, lactate release was greater in BAND than in SHAM (48.8 +/- 1.2 versus 26.6 +/- 0.97 mumols/g, p less than 0.01), and with reoxygenation, lactate dehydrogenase release was less in BAND than in SHAM (13.2 +/- 0.7 versus 19.5 +/- 0.2 IU/g, p less than 0.01). After hypoxia and reoxygenation, left ventricular pressure recovery was greater in BAND than in SHAM (93 +/- 8.4% versus 66 +/- 5.3%, p less than 0.01). Thus, this study suggests that hypertrophied hearts have a greater potential for glycolytic metabolism, resulting in an increased rate of by-product accumulation during ischemia, which may be responsible for the increased susceptibility of hypertrophied hearts to ischemic injury.
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PMID:Increased ischemic injury but decreased hypoxic injury in hypertrophied rat hearts. 214 92

The adverse effects of administration of gentamicin (5 mg/kg of body weight, IM, q 12 h) for 7 days were studied in healthy scarlet macaws (Ara macao) and galahs (Eolophus roseicapillus; cockatoos). Polydipsia and polyuria developed in each species, but were greater and persisted longer in the cockatoos. Peak water intake in the cockatoos more than quadrupled, and remained increased for 23 days after cessation of gentamicin administration. Plasma aspartate transaminase activity increased significantly (P less than 0.05) after treatment in the macaws, and plasma aspartate transaminase and lactate dehydrogenase activities increased in the cockatoos. Single IM administration of gentamicin (5 mg/kg) resulted in mean (+/- SEM) plasma concentration of 20.6 (+/- 1.85) micrograms/ml at 0.5 hour for either species of birds. There were no significant differences between mean plasma gentamicin concentrations for cockatoos and macaws at any time after drug administration, except at 12 hours, when values for cockatoos were significantly (P less than 0.05) greater than those for macaws. The elimination half-life for gentamicin after IM administration of 5 and 10 mg/kg was 1.17 and 1.07 hours, respectively, for macaws and 1.23 and 1.44 hours, respectively, for cockatoos. Correlation between drug disposition and adverse side effects could not be detected.
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PMID:Adverse effects of gentamicin in scarlet macaws and galahs. 231 18

Alveolar macrophages (AM) were retrieved by bronchoalveolar lavage from 20 patients. Following AM purification by glass adherence, the effect of bleomycin on hydrogen peroxide and lactic dehydrogenase release was assessed by colorimetric methods. All AM from nine nonsmokers had no detectable spontaneous release of hydrogen peroxide. The AM did not release hydrogen peroxide when stimulated with bleomycin (25 mU/mL). AM from all eleven smokers spontaneously released hydrogen peroxide (36 +/- 5.3 nm/10(6) AM, mean +/- SEM). AM from eight of the eleven smokers released more hydrogen peroxide when incubated with bleomycin (smokers 55 +/- 6.8 nm/10(6) AM, p less than 0.05). There was no difference in the amount of lactic dehydrogenase released by AM spontaneously or when incubated with bleomycin at 25 mU/mL, suggesting that this dose of bleomycin was not directly toxic to the AM. Results from this study further support the premise that bleomycin pulmonary toxicity may result from the generation of reactive oxygen metabolites and that cigarette smoking may predispose to bleomycin pulmonary toxicity.
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PMID:Bleomycin causes alveolar macrophages from cigarette smokers to release hydrogen peroxide. 245 24

Neutrophils which ingest particles (serum-treated zymosan, monosodium urate crystals) or are exposed to calcium ionophore A23187 generate leukotriene B4 (LTB4). Earlier work has shown that cells exposed to colchicine before exposure to monosodium urate crystals produce less LTB4; the formation of 5-HETE is unaffected. To determine whether inhibition by colchicine of LTB4 generation was stimulus-specific and was mediated by microtubule integrity, the effects of colchicine (10 microM, 60 min) on the release of lipoxygenase products from neutrophils exposed to ionophore A23187 (10 microM, 5 min) were examined. In the presence of exogenous arachidonic acid (100 microM, 15 min), colchicine decreased LTB4 to 48% +/- 11.7 of control and 5-HETE to 60.5% +/- 5.7 of control (mean +/- SEM); 15-HETE was also decreased to 61% +/- 10.3 of control. In the absence of exogenous arachidonate, LTB4 was decreased to 22.2% +/- 11.7 of control and 5-HETE to 13% +/- 4.8 of control. Lumicolchicine did not significantly affect formation of 5-HETE or LTB4. However, vinblastine sulfate (20 microM, 60 min), another microtubule-disruptive agent, decreased the formation of both 5-lipoxygenase products. The effects of colchicine and vinblastine were not due to impairment of cell viability because the release of cytoplasmic lactic dehydrogenase was unaffected. Ultrastructural analysis of centriolar microtubules showed that decrements in microtubule numbers of colchicine- and vinblastine-treated cells paralleled decrements in 5-lipoxygenase products. These pharmacologic manipulations suggested that functional microtubules might be required for optimal lipoxygenase activity. Consequently, we prepared neutrophil-derived cytoplasts, devoid of an intact microtubule system. No significant decreases in the 5- or 15-lipoxygenase products were found when cytoplasts were exposed to colchicine in the presence of exogenous arachidonate and A23187. The data show that colchicine inhibits the formation of lipoxygenase products from neutrophils stimulated with A23187, most likely via its effect on microtubules, the integrity of which appears necessary for full expression of 5- and 15-lipoxygenases.
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PMID:Colchicine inhibits ionophore-induced formation of leukotriene B4 by human neutrophils: the role of microtubules. 300 Nov 84


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