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Biomedical subjects

M Ashraf

Publications and source records attributed to M Ashraf.

At least 127 records · Page 7Linked to original sources
PubMed1988

Cytochrome C, a potent oxygen free radical scavenger against the calcium paradox injury in the myocardium.

The calcium paradox was induced by perfusion of hearts with a calcium-free medium for 10 mins followed by calcium-containing medium for 20 mins (group A). During calcium depletion, myocytes were preserved but vascular endothelial cells underwent prominent morphological changes and their plasma membranes were disrupted and transformed to myelin-like whorls. Calcium repletion induced severe myocyte necrosis, massive release of creatine phosphokinase (CPK) and calcium accumulation. The effect of ferricytochrome C on the calcium paradox injury was investigated in groups of hearts; ferricytochrome C (75 microM) was given either during calcium repletion only (group B), during calcium depletion only (group C), or both during calcium depletion and repletion (group D). There was no protection by cytochrome C in group B with no reduction in release of CPK, calcium accumulation or cell damage. However, cytochrome C was very protective when given during calcium depletion (groups C and D). CPK was significantly reduced in groups C and D compared to group A (P less than 0.03) and less calcium accumulation was observed in groups C and D (6.0 +/- 0.8, 12.5 +/- 1.25 mumol) compared to group A (P less than 0.03). Moreover, a significant number of cells was preserved in group C (84%) and group D (80%), compared to group A (2%). This was associated with prevention of vascular damage caused by calcium depletion. The data provide strong evidence that cytochrome C is a potent protective agent against the calcium paradox injury that may be caused by oxygen-derived radicals.

Animals↗
PubMed1987

Analysis of detomidine in horse blood, plasma and urine samples utilizing a sensitive gas chromatography-mass spectrometry method.

Chemical ionization- and electron impact ionization-selective ion monitoring provided a simple and sensitive method for measuring detomidine (Domosedan), a potent sedative-analgesic drug for horses and cattle. Chemical ionization was at least 10 times more sensitive than electron impact ionization. By using propranolol as an internal standard, we found that the recovery of detomidine from the extraction procedure used in this study was greater than 75% for plasma, whole blood, or urine samples. Approximately 68% of detomidine was bound to plasma protein and 53% was bound to red blood cells.

Analgesics↗
PubMed1987

Oxygen derived radicals related injury in the heart during calcium paradox.

The effects of oxygen-derived radical scavengers (ODRS) on the heart was investigated during the calcium paradox. Perfusion with Ca2+-free medium caused cell separation at the intercalated discs and changes in the endothelial cells. Upon Ca2+ reintroduction, a massive cell damage occurred. The cytosolic enzyme, creatine phosphokinase (CPK), was released in large amounts (p less than 0.001). The tissue adenosine triphosphate (ATP) was reduced to 3.7 mumol/g dry weight from the control value of 21.6 mumol/g dry weight and tissue Ca2+ content was increased threefold. The treatment with superoxide dismutase (SOD) and catalase (CAT) increased percentage of normal cells (62.2%) compared to nontreated Ca2+ paradox group (0.2%) and caused negligible leakage of CPK. Tissue ATP was preserved (p less than 0.03), and Ca2+ content was also reduced in the hearts treated with SOD and CAT (p less than 0.03). The cell membranes and vascular endothelium were well preserved in the hearts treated with SOD and CAT. Boiled SOD and CAT administered were totally ineffective. It is suggested that oxygen-active species may have a role in the Ca2+ paradox injury.

Adenosine Triphosphate↗
PubMed1987

Moderating effect of low doses of ethanol on reoxygenation injury in the anoxic myocardium.

We have investigated the action of ethanol on the reoxygenation injury in isolated rat hearts. Perfusion of the anoxic Krebs-Henseleit medium for 40 minutes followed by 30 minutes of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mMol), in both anoxic and aerobic perfusion media resulted in a marked reduction of cell injury and inhibition of creatine kinase. Contraction band necrosis was reduced to 0.25 as compared to 1.14 per field in the nontreated hearts. The tissue Ca++ was decreased to 8.2 as compared to 12.12 mumol/g/dry weight in the non-treated hearts and tissue ATP was increased by 50% in the treated tissue (9.33 mumol/g/dry wt) as compared to the non-treated anoxic tissue (5.5 mumol). Thus, ethanol appears to lessen myofibrilar contraction bands and preserve plasma membrane integrity during anoxia and reoxygenation. This suggests a scavenging role of free radicals which include hydroxy radicals or closely related species, in the pathogenesis of anoxic cell injury and beneficial effect of ethanol in low doses on the post anoxic reoxygenation injury.

Adenosine Triphosphate↗
PubMed1987

Uncombable-hair syndrome.

Four children had short, unmanageable, pale blond hair. They had no associated abnormalities and no family histories of abnormal hair. Light microscopy of the hair was normal in three patients, with pili torti present in the fourth. Electron microscopy of hairs from all four children revealed longitudinal grooves in the hair shaft, diagnostic of uncombable-hair syndrome.

Child↗
PubMed1987

Role of ONO-3144, a new cardioplegic agent, in the reoxygenation injury in the anoxic myocardium.

We have investigated the effect of ONO-3144 (2-aminomethyl-4-tert-butyl-6-propionylphenol), which facilitates the conversion of prostaglandin G2 to H2 and acts as a scavenger of free radicals, on the reoxygenation injury in the anoxic heart. Rat hearts were perfused retrogradely with Krebs-Henseleit (KH) medium for 30 min (n = 8) in Group I. In Group II, the hearts which were perfused with anoxic KH medium for 40 min were reoxygenated for 30 min (n = 8). Group III hearts were similar to those in Group II except that 4 mg ONO-3144/liter was added to both anoxic and reoxygenation media (n = 8). Coronary effluent was collected for creatine kinase (CK) loss. Four rats hearts in each group were fixed for electron microscopic study and the remaining hearts were frozen in liquid nitrogen for measurement of adenosine triphosphate (ATP). A six-fold increase in CK leakage, observed after reoxygenation of anoxic heart, was prevented by ONO-3144. Tissue ATP was reduced from 22.2 +/- 0.9 mumol/g dry weight (Group I) to 5.5 +/- 1.1 mumol/g dry weight (Group II). A significant amount of ATP (9.05 +/- 1.22 mumol/g dry weight) was preserved in the treated Group III. The number of normal cells obtained by morphometrical analysis increased significantly from 56.7 +/- 7.8% (Group II) to 86.2 +/- 1.0% (Group III) and moderately injured cells were reduced to 3% in Group III as compared to 16% in the untreated Group I. Injury to the severely injured cells was not prevented by the drug treatment. At electron microscopic level, the cellular membranes, mitochondria and glycogen deposits were well preserved in Group III. Thus, ONO-3144 treatment provides a protection against reoxygenation injury in the anoxic myocardium by scavenging. .OH or other closely related species of free radicals. Therefore, free radicals generated through the conversion of prostaglandin G2 to H2 might play an important role in the reoxygenation injury of the anoxic myocardium.

Adenosine Triphosphate↗
PubMed1986

Analysis of organophosphorus insecticides in biological samples by selective ion monitoring gas chromatography-mass spectrometry.

Gas chromatography with chemical ionization or electron impact mass spectrometry and selected ion monitoring provided a simple and sensitive method for measuring organophosphorus insecticides. Chemical ionization produced higher-mass ions which might increase the selectivity and sensitivity of the assay. The recovery of organophosphates from saline and urine was greater than 75%. The recovery of these compounds from plasma was less than the saline because of the binding of insecticides to plasma protein. Insecticides with lower LD50 values showed lower recovery from plasma than organophosphates with higher LD50 values.

Gas Chromatography-Mass Spectrometry↗
PubMed1986

Preparation of 99mTc-tin-phosphate polyvinyl pyrollidone stabilized colloid and distribution in bone marrow.

Technetium-99m-Sn-phosphate colloid was prepared in the presence of polyvinylpyrollidone(PVP), molecular weight 44,000, for bone marrow imaging. Size of the colloidal particles, as determined by coulter counter, microphotographic and electron microscopic studies was 15-35 nm. The colloid preparation was checked for the presence of any soluble components by Sephadex G-25 chromatography. Scintigraphy in rabbits showed a high concentration of the colloid in the bone marrow. Tissue distribution studies in rabbits showed 26.7% of the injected dose at 1 h post-injection in the bone marrow collected from femoral shaft and head. Although liver and spleen showed considerable levels of activity, kidneys and compact bone did not show any uptake. The colloid cleared from the blood exponentionally with a first phase showing a relatively fast clearance while in the second phase it disappeared more slowly. Uptake of the colloid in human bone marrow was close to that in the rabbit and thus clinical evaluation is warranted.

Animals↗
PubMed1986

Distribution of 3H-nitrendipine in the isolated perfused rat heart as revealed by electron microscopic autoradiography.

Subcellular distribution of 3H-nitrendipine was investigated in the isolated perfused rat heart by means of electron microscopic autoradiography. Mechanical measurements of cardiac contractile activity (dP/dt) were performed on the hearts used for autoradiography. There was a non-random pattern of silver grain distribution over the myocardial cells. The grain density, i.e. percentage of total grains/percentage of cell area, was determined for each cell component. A grain density higher than one was noted on the cell membrane, T-tubules and capillaries, indicating a significant incorporation of 3H-nitrendipine into the structures. Concentrations of unlabeled nitrendipine containing radiolabeled nitrendipine caused increased grain density and a decreased contractile activity (dP/dt) by 6% to 30%. It is therefore possible that the pharmacological action of nitrendipine is associated with the localization of 3H-nitrendipine on or in the cell membrane, T-tubules and capillaries.

Animals↗
PubMed1985

Prevention of lactate production and myocyte injury in isolated rat hearts perfused with perfluorochemical emulsion.

The ability of an oxygenated perfluorocarbon (PFC) emulsion to prevent early signs of myocardial cell stress associated with Krebs-Henseleit (KH) perfusion was evaluated in isolated rat hearts supported in a Langendorff apparatus. Throughout the two-hour perfusion, hearts in both perfusion groups had similar left ventricular pressure and rates of left ventricular pressure development (dP/dt). After 2 h, coronary perfusate flow was 6.6 +/- 1.0 ml/min in the KH group and 2.2 +/- 0.1 ml/min in the PFC group. Oxygen content was 1.5 +/- 0.1 ml/100 ml and 3.4 +/- 0.1 ml/100 ml, in KH and PFC groups, respectively. Perfusate lactate levels rose from zero to 24.0 +/- 8.0 microgram/ml in the KH group and to 10.0 +/- 3.0 micrograms/ml in the PFC group. Reduction in myocardial cell injury and in total calcium content was also observed in hearts perfused with PFC emulsion. At the electron microscopic level, mitochondrial structure was preserved in both normal and injured myocytes of hearts perfused with PFC. We conclude that early signs of anaerobic metabolism are retarded by perfusion with PFC emulsions and that ventricular contractile performance is maintained at approximately one-half coronary perfusate flow in the PFC hearts. The mechanism whereby coronary flow is regulated downward in the PFC perfused hearts remains unanswered.

Animals↗
PubMed1985

Effect of glucocorticoid administration early in life on aortic prostaglandin synthesis and morphology in atherosclerosis-susceptible pigeons.

Effect of dexamethasone administration on aortic morphology, cholesterol content and synthesis of prostaglandins from (14C)-arachidonic acid in aorta of spontaneously atherosclerosis susceptible pigeons was examined. Dexamethasone markedly inhibited the synthesis of prostaglandin E2 and stimulated the synthesis of prostaglandin I2 in aorta. In aorta of glucocortocoid treated animals, endothelial abnormalities noted in control birds were decreased and numerous surface protrusions or 'microvilli' were noted. The possibility that glucocorticoid induced inhibition of PGE2 synthesis in pigeon aorta may contribute to improved aortic morphology is discussed.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Morphological changes in the coronary circulation following experimental myocardial ischemia in swine.

The diagonal branches of the left anterior descending coronary artery in ten pigs were ligated for 5, 15, 30, 60 and 120 minutes. Pieces of occluded vessels were fixed with 2.5% buffered glutaraldehyde and processed for scanning and transmission electron microscopy. After 5 to 30 minutes of occlusion, endoplasmic reticulum and mitochondria begin to swell, vacuoles appear, and the number of pinocytic vesicles in endothelial cells decrease. After 60 minutes, endothelial cells contained numerous vacuoles, endoplasmic reticulum and mitochondria were markedly swollen, leukocytes and fragments detached from smooth muscle cells had infiltrated the subendothelial space, and endothelial cells were partially disrupted. Following 120 minutes of occlusion, internal elastic lamina had split, leukocytes had migrated into tunica media and smooth muscle cells had obviously penetrated into the subendothelial space, but no endothelial denudation or associated platelet accumulation was seen. These observations indicate that leukocyte infiltration and intrusion of partially disrupted endothelial cells precede, and may promote proliferation of medial smooth muscle cells into the tunica intima during myocardial ischemia. The events are reported for large conduit arterial branches of a main coronary artery.

Animals↗