PubMed Health⌕ Search

Biomedical subjects

M Ashraf

Publications and source records attributed to M Ashraf.

At least 163 records · Page 9Linked to original sources
PubMed1982

Prevention of calcium paradox-related myocardial cell injury with diltiazem, a calcium channel blocking agent.

The effect of diltiazem on creatine kinase release and tissue adenosine triphosphate content was investigated during calcium paradox in the isolated perfused rat heart. Creatine kinase loss was minimal during the calcium-free phase, but there was a 100-fold increase in creatine kinase release after reperfusion with normal calcium-containing medium. Diltiazem reduced creatine kinase loss by 35 percent when added to calcium-free medium and by approximately 80 percent when added to both calcium-free and reperfusion media. Adenosine triphosphate content was significantly increased from 2.98 mumol in untreated calcium paradox hearts to 5 mumol/g dry weight in diltiazem-treated hearts. With hypothermia the calcium paradox injury was completely inhibited if the temperature of calcium-free perfusion was maintained at 15 degrees C. Diltiazem appears to exert its protective effect through its ability to prevent the cellular separation and alterations in the gap junctions during calcium deprivation of cells and to limit calcium entry into the cells after reperfusion with calcium-containing medium.

Adenosine Triphosphate↗
PubMed1982

In vitro catabolism of human plasma very low density lipoproteins. Effects of VLDL concentration on the interconversion of high density lipoprotein subfractions.

The effect of lipolysis of human plasma very low density lipoproteins (VLDL) on the distribution of high density lipoprotein subfractions was studied in an in vitro system consisting of purified bovine milk lipoprotein lipase and albumin. The distribution of lipids and apoproteins (apoC-II and apoC-III) within the lipoprotein fractions corresponding to HDL2 (d = 1.063-1.120 g/ml) and HDL3 (d = 1.120-1.210 g/ml) was dependent upon the concentration of VLDL in the incubation mixture. After lipolysis of an incubation mixture containing VLDL-triglyceride (0.6 mg triglyceride/ml) and HDL3 (0.1 mg protein/ml), most of the lipid and apoproteins were recovered in HDL3. At higher concentrations of VLDL-triglyceride relative to HDL3-protein (1.8 or 2.4 mg of VLDL-triglyceride and 0.1 mg of HDL3-protein) the amount of lipid and apoprotein isolated in the HDL3 density fraction decreased after lipolysis and there was an increase in the amount isolated between d 1.063-1.120 g/ml. These results provide additional evidence for the conversion of HDL3 to HDL2 during lipolysis. Furthermore, they suggest that the relative distribution of plasma HDL2 and HDL3 is related to the rate of catabolism of triglyceride-rich lipoproteins.

Animals↗
PubMed1982

Transmural cellular damage and blood flow distribution in early ischemia in pig hearts.

Transmural histological changes were determined morphometrically in the left ventricular free wall of 20 pigs after ligation of distal left anterior descending coronary artery for 10, 20, 40, and 120 minutes. Hemodynamics were recorded and regional blood flow distribution was measured in the ischemic zone. Coronary occlusion produced regional transmural ischemia without producing significant systemic hemodynamic change. The microsphere blood flow technique revealed that blood flow was less than 0.05 ml/min per g in all layers of the ischemic zone, i.e., inner, middle, and outer thirds. Ischemic cellular damage was classified and quantified from grade 0 to grade 5 (0 being normal and 5 being the most severe damage) with light microscopy and confirmed by electron microscopy. Layers of 200 micrometers immediately beneath the endocardium and epicardium showed minimal ischemic damage of less than grade 1.4 regardless of duration of ischemia in all hearts. In the ischemic left ventricular wall, except for the above layers, a definite transmural gradient of the cellular damage existed from the inner third (grade 2.3 +/- 0.1) to the outer third (grade 1.3 +/- 0.2) at 20 minutes of ischemia and at 40 minutes of ischemia (grades 3.6 +/- 0.1 and 1.9 +/- 0.3, respectively). The transmural ischemic damage gradient disappeared at 120 minutes of ischemia, where the inner and outer third ischemic grades were both 5.0 +/- 0.1. The data suggest that the limited ischemic damage which occurs in the few cell layers beneath endocardium and epicardium may be explained by regional collateral blood flow. An early ischemic damage wavefront phenomenon does exist in the pig myocardium and is independent of myocardial blood flow and its distribution. The transmural cell damage gradient may be the result of transmural gradients of wall stress and intramyocardial pressure in vivo. Therefore, it appears that factors other than blood flow are the major determinants of ischemic cellular damage in the left ventricular wall of hearts lacking a collateral blood supply.

Animals↗
PubMed1982

Preparation of normal and ischemic myocardial tissue for scanning electron microscopy.

Normal and ischemic myocardium was prepared by slicing and cryofracture techniques for examination with the SEM. The tissues were dehydrated in ethanol and Freon 113 (slicing method) or were cryofractured in Freon 113 cooled with liquid nitrogen, followed by critical point drying and coating with gold and palladium. Some osmicated tissue pieces were treated with thiocarbohydrazide for examination without metal coating. Some hearts were infiltrated with silver particles and were examined with backscattered electron imaging technique (BSI). The cryofractured tissue provided the most useful and consistent surface features of the cell organelles with a minimum of mechanical disorder compared to other methods. Although the myocardium prepared by slicing method revealed the interior of the cells, it contained several frayed edges and loose myofibrils making interpretation of the ischemic myocardium difficult. The normal cells exhibited myofibrils covered by transverse tubules at the level of Z bands as confirmed by BSI using silver particles as an extracellular tracer and numerous oval to elongated mitochondria located between the myofibrils. An extensive network of tubules (sarcoplasmic reticulum) over the sarcomeres and nuclei were observed. The changes observed by SEM in the ischemic hearts were consistent with those seen in TEM. With prolonged coronary ligation the changes became obvious. The T-tubules were often broken and nuclei were distorted. The myofibrils were disorganized and formed homogeneous bands. These SEM studies suggest that myocardium prepared by cryofracture technique yields information on normal and ischemic cell structure consistent with data obtained by TEM.

Animals↗
PubMed1982

Surface ultrastructural changes in dog small intestinal mucosa following ischemia.

Scanning electron microscopy was used to study normal and ischemic dog ileum. Ileal ischemia was produced by complete ligation of a side branch mesenteric artery for two and four hours and by reduced blood supply by narrowing the artery (50%) for two and four hours. The tissue was fixed by immersion and processed for scanning electron microscopy. Tissue from the same sites was also prepared for light and transmission electron microscopy. Scanning electron microscopy showed the polygonal shaped epithelial cells covered by a regular array of microvilli. With transmission electron microscopy these microvilli appeared as closely packed, parallel, and cylindrical processes. During complete occlusion for two hours, the upper portions of the villi had severe damage where epithelial cells were missing. However, at the base of the villi, epithelial cells were recognizable with irregular shaped microvilli and the glycocalyx was fragmented. After four hours of ischemia, there was an absence of epithelial cells and blood vessels were greatly engorged, protruding against the basal lamina. By light microscopy villar architecture appeared unaltered with 50% reduced blood flow for two and four hours and the epithelial cells exhibited no unusual microvillar pattern. However, after 50% occlusion for four hours, the microvilli appeared wider by scanning electron microscopy. This was confirmed by transmission electron microscopy where the microvilli not only appeared wider but were also shortened. The glycocalyx was unaltered.

Animals↗
PubMed1981

Histologic, ultrastructural, and enzymatic measurements of infarct size following coronary artery stenosis and occlusion.

Coronary artery narrowing (CAN), which reduced resting coronary blood flow (BF) by 50%, was induced in 10 conscious dogs and was maintained for 4 hours. Five additional dogs (group 1) with complete coronary artery occlusion were compared to the dogs with CAN. Serum isoenzymes of creatine phosphokinase (CK) and lactate dehydrogenase (LD) were monitored hourly in all groups. After 36 hours, samples were obtained for regional myocardial BF, quantitative histology, and quantitative ultrastructural (EM) morphology. Six dogs with CAN had small infarcts (MI) of less than 1 gm and persistent myocardial cell injury (group 2). The other four dogs with CAN has only persistent myocardial cell injury by ultrastructural criteria (group 3). Peak serum CK activities in groups 2 and 3 were similar, as well MI sizes calculated from serum CK and myocardial depletion. MB CK was of diagnostic value in group 1 but not in groups 2 and 3. The ratio of LD 1/LD 2 had diagnostic value in all three groups. MI size by enzyme estimates was consistently higher than planimetered MI size at autopsy in both groups 1 and 2. All three groups had significant amounts of ultrastructural damage outside of histologically demonstrated. MI. These findings suggest that (1) gross and histologic MI size determination of 36 hours after ischemia underestimate extent of damage, and (2) ultrastructural cell changes cause significant release of CK and LD in coronary disease (CAD).

Animals↗
PubMed1981

Surface ultrastructural features of isolated perfused rat hearts during calcium paradox.

Cellular damage caused by calcium (Ca++) paradox is of significant importance under both experimental and clinical conditions. Electron microscopy was used to study the surface changes of the isolated rat hearts perfused with normal Krebs-Henseleit (KH) medium, Ca++-free KH medium, Ca++-free KH medium followed by normal KH medium. The hearts perfused with Ca++-free medium and normal KH medium showed elongated parallel myofibrils with transverse ridges spaced at regular intervals. The major change in Ca++- free hearts consisted of wide cellular separation. For the Ca++- paradox hearts, wht myofibrils were twisted and narrowed at several locations. The myocardial fiber surfaces were bulged out, frequently with sarcolemmal ruptures and holes. Supercontraction of cells caused breaks in the sarcolemma and aggregation of mitochondria at the cell periphery. These results suggest that Ca++-depletion primarily affects the myocardial cell junctions which, following reintroduction of Ca++, accelerate the entry of Ca++ into the cells, supercontraction of cells and stretching of sarcolemma.

Animals↗
PubMed1980

Cytochemical studies on peroxisomes in rat and guinea pig myocardium.

The enzymatic activity and distribution of peroxisomes (microbodies) in rat and guinea pig hearts were studied cytochemically, by means of oxidation of 3-3'-diaminobenzidine (DAB) and by using B-glycerophosphate and cytidine-5'-monophosphate as substrates. Peroxisomes were localized in proximity to mitochondria and sarcoplasmic reticulum and measured from 0.2 micrometers to 0.5 micrometers in diameter in both animal species. DAB positive bodies were seen both at pH 9.0 and pH 5.0 in rat myocardial cells. However, in guinea pig myocardial cells the reaction was observed only at pH 9.0, or very faintly at pH 5.0. Acid and alkaline phosphatases were not demonstrated in the peroxisomes. Lipid droplets were surrounded by a ring of dense granular reaction product for enzymes, such as acid and alkaline phosphatase, and lipofuscin granules were limited by acid phosphatase or DAB reaction products. The pathophysiological function of peroxisomes is discussed.

Acid Phosphatase↗
PubMed1980

The nucleolus in telophase, interphase and prophase.

The ultrastructure of telophase to interphase has been followed in a green alga, Spirogyra submargaritata. A series of changes transitional between the late anaphase chromatid, the decondensing chromatid of telophase, and the 'pale fibrillar material' occupying channels in the nucleolus at interphase have been demonstrated. Early stages in the regeneration of the nucleolus are described. It has been shown that the pale fibrillar material in the nucleolus is attached to, and continuous with, the fully condensed (chromocentric) part of the nucleolar-organizing chromosome at interphase. It is also shown that in early prophase, the channels in the nucleolonema of the nucleolus are no longer occupied by pale fibrillar material, but instead a long section of condensed chromosome is present, traversing the nucleolonema. It is contended that these observations taken together constitute evidence that the pale fibrillar material of the nucleolus is the chromatin of the nucleolar-organizing region of the chromosome, expanded for transcription. A model of the nucleolus as it is seen in most electron-microscope sections, and as it can be interpreted in the light of present-day knowledge about it, is presented. A brief review of the relevant literature considers the views supporting the mode, and the contrary views, implicating the use of the term 'nucleolar organizer', that are still current at the present time.

Cell Nucleolus↗
PubMed1980

An evolution of malignant mixed müllerian tumor.

In an unusual example of malignant mixed müllerian tumor, a tumor originated in the uterine corpus as an endometrial carcinoma consisting of ordinary endometrial adenocarcinoma, papillary adenocarcinoma, mucinous adenocarcinoma, and squamous cell carcinoma. Following hysterectomy, the tumor recurred at the vaginal vault as poorly differentiated papillary adenocarcinoma. During the second recurrence as a pelvic tumor about 3 years after hysterectomy, the tumor evolved into a malignant mixed müllerian tumor with predominance of sarcomatous element. The latter included undifferentiated sarcoma, endometrial stromal sarcoma, fibromyxosarcoma, leiomyosarcoma and rhabdomyosarcoma. These findings support the contention of Sternberg et al. that a malignant mixed müllerian tumor may exceptionally originate in an endometrial carcinoma.

Adenocarcinoma↗
PubMed1979

Correlative studies on sarcolemmal ultrastructure, permeability, and loss of intracellular enzymes in the isolated heart perfused with calcium-free medium.

Effects of calcium-free perfusion and calcium-free perfusion followed by reperfusion with calcium on sarcolemmal structure, sarcolemmal permeability, and creatine phosphokinase loss were investigated in isolated perfused rat hearts. Release of creatine phosphokinase was significant (P less than 0.0002) after 4-5 minutes of perfusion with Ca++-free medium, but later releases in comparison to their immediately preceding periods became significant only after more than 20-minute perfusion. Poor correlation between enzyme loss and lanthanum permeability prior to 20 minutes of Ca++-free perfusion was noted. After 20 minutes of Ca++-free perfusion, the basal lamina was separated from the plasma membrane, and lanthanum was seen in the cytoplasm. The intramembranous particles began to aggregate at that time. The morphologic and enzymatic changes were dramatic following reperfusion of calcium-free perfused hearts. Morphologic changes in these hearts included separation of basal lamina, cellular separation at the intercalated disk, dissolution of actin filaments at the region of I band, contraction bands, cell swelling, and staining or filling of mitochondrial membranes with La+++. Increased sarcolemmal permeability was associated with tears and aggregation of intramembranous particles in the sarcolemmal lipid bilayers. These results suggest that reperfusion of Ca++-free perfused cells causes irreversible damage to the sarcolemmal lipid bilayer, and the degree of alterations induced in the cells is dependent upon the initial duration of Ca++-free perfusion.

Animals↗
PubMed1978

Structural alterations of the porcine heterograft after various durations of implantation.

Morphologic changes in six glutaraldehyde-fixed porcine heterografts recovered from five patients were studied with light and scanning electron microscopy. Light microscopy showed minimal changes in the valves recovered after 2 months of implantation. Fibrin deposits, red blood cell trapping, disruption of the valve matrix and interstitial edema were noted in heterografts 2 months and 2 years after implantation. In valves examined with scanning electron microscopy, 6 hours after implantation the surface changes varied from normal to patchy disruptions. Two months after inplantation, subendothelial fibers were conspicuous and the geometry of endothelial cells was changed. In valves examined after 6 months in place, many nuclei were burst and fibrin strands were seen over the surfaces. Bacterial infection was observed in two cases. The endothelial cells in the valve implanted for 2 years were completely obscured and some areas were densely covered with fibrillar material where blood cells were trapped in the mesh.

Adult↗