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Biomedical subjects

C F Nassar

Publications and source records attributed to C F Nassar.

53 records · Page 3Linked to original sources
PubMed1986

Gastric pH changes following intramedullary electrical stimulation in anesthetized and decerebrate cats.

In anesthetized and decerebrate cats, a pH-sensitive glass electrode inserted into the gastric antral region through a fistula recorded immediate pH changes. In the anesthetized cats (pentobarbital sodium, 35-40 mg/kg, i.p.), electrical stimulation within the medulla oblongata with a coaxial electrode (train of pulses at 300-500 Hz for 10-30 sec; individual pulse width 0.1-0.5 msec and amplitude not exceeding 0.5 mA) induced an increase in gastric acid secretion equivalent to a delta pH of 1.26 +/- 0.1 units. In the decerebrate (following induction with ether), the same type of stimulation elicited a more intense gastric acid secretion equivalent to a delta pH of 5.18 +/- 0.09 units which is significantly different (P less than 0.001) from that recorded in the anesthetized cats. Reversible blockage of the vagus nerves eliminated these responses during the block. Our results indicate that electrical stimulation in the posterior region of the medulla oblongata evokes an immediate and significant increase in gastric acid secretion, which is mediated through the vagus nerve, and is most evident in decerebrate unanesthetized cats.

Animals↗
PubMed1986

Dopamine receptors in normal and diabetic liver plasma membrane.

Dopamine binding to liver plasma membrane isolated from diabetic livers was significantly reduced (P less than 0.01) as compared to dopamine binding to the normal membrane. Diabetic membranes exhibited a significant decrease (P less than 0.01) in specific dopamine binding as compared to the normal membranes; whereas no significant change (P less than 0.5) was noticed in the nonspecific binding patterns. The dopamine binding capacity of both membranes is temperature dependent. Procaine at different concentrations inhibited significantly (P less than 0.01) dopamine binding to normal and diabetic membranes. Treatment of the normal and diabetic membranes with insulin showed a 33% decrease in the binding capacity of the normal and 42% decrease in the binding capacity of the diabetic membrane.

Animals↗
PubMed1985

Effect of aminophylline on calcium transport across the rat diaphragm.

Calcium accumulation in muscle strips isolated from rat diaphragm reached steady state after 90 min with intracellular to extracellular ratio (IN/OUT) of 3.0. Calcium uptake by rat diaphragm is a saturable and carrier mediated process that is significantly enhanced in the presence of aminophylline in a dose-dependent pattern that produced maximal effect at 18.75 micrograms/ml. A Lineweaver-Burk plot shows Jmax = 25 microM/hr per g dry wt and Kt = 3.19 mM for the control, and Jmax = 26 microM/hr per g dry wt and Kt = 2.27 mM in the presence of 18.75 micrograms/ml aminophylline. Aminophylline had no effect on cell volume and water of the diaphragmatic cells.

Aminophylline↗
PubMed1985

Receptors of prostaglandin E1 in the plasma membrane of normal liver. Effect of membrane fluidity on PGE1 binding.

Prostaglandin E1 binding to isolated liver plasma membrane as a function of PGE1 concentration showed saturability of the binding sites at PGE1 concentration of 2.5 X 10(-4) M. Scatchard analysis revealed heterogeneous population of binding sites with a binding capacity of 470 and 990 nmol/mg protein for the higher and lower affinity binding sites respectively. PGE1 binding to liver plasma membrane was progressively and significantly decreased (P less than 0.01) as the incubation temperature was reduced to 22 degrees and 4 degrees C. Procaine at 1 X 10(-3) M concentration showed a significant decrease (P less than 0.01) in the binding capacity of the liver plasma membrane. Colchicine plus cytochalasin-B inhibited PGE1 binding significantly (P less than 0.01) but their inhibition is not equivalent to that of procaine.

Alprostadil↗
PubMed1984

The effect of local anesthetics on calcium transport across the rat and turtle small intestine.

Procaine at different concentrations enhanced significantly (P less than 0.01) calcium accumulation in rat intestinal cells, whereas the same concentrations of procaine inhibited significantly (P less than 0.01) calcium uptake by the turtle small intestine. Unidirectional calcium influx across the rat small intestine was significantly enhanced (P less than 0.001) by the presence of procaine in the preincubation medium. However, procaine had no effect on calcium influx across the turtle intestinal cells. The cell water content and the cell volume were not altered by preincubating the intestinal tissues with procaine in both animals.

Anesthetics, Local↗
PubMed1984

Calcium binding to normal, regenerating and diabetic liver plasma membrane.

Calcium binding to liver plasma membrane isolated from diabetic and regenerating livers was significantly reduced (P less than 0.01) when compared to Ca binding to the normal membrane. Procaine at different concentrations inhibited significantly (P less than 0.01) calcium binding to the normal, diabetic and regenerating liver plasma membrane, with the most pronounced inhibition noticed in the normal. Colchicine at a concentration exceeding 5 X 10(-4)M showed a significant decrease (P less than 0.01) in calcium binding to the normal, diabetic and regenerating liver plasma membrane with the maximum inhibition noticed in the regenerating liver membrane.

Animals↗
PubMed1984

Cytoskeletal control of alanine transport across the rat and turtle small intestine.

Procaine inhibited significantly (P less than 0.01) alanine accumulation in the rat intestinal strips in a concentration-dependent pattern, whereas it showed no effect on alanine uptake by the turtle intestinal cells. Colchicine and Vinca alkaloids at 5 X 10(-4) and 1.5 X 10(-6) M respectively caused a significant inhibition (P less than 0.01) of intracellular alanine concentration in the rat with no effect noticed in the turtle. Unidirectional influx of alanine across the brush border membrane of the rat was significantly (P less than 0.01) reduced in the presence of procaine, colchicine and vincristine in the preincubation medium. The same drugs did not show any effect on alanine influx into the turtle small intestine. Electron microscopy showed major structural alterations in the cytoskeletal organization of the turtle intestine in response to procaine, colchicine or vincristine treatment. It is proposed that microtubular system may participate in the overall transport mechanism of alanine across the small intestine.

Alanine↗
PubMed1984

Pyridoxine binding to normal and diabetic liver plasma membrane.

Pyridoxine binding to liver plasma membrane isolated from livers of normal and streptozotocin-induced diabetic rats was investigated. The effect of increasing concentration of pyridoxine on its binding to the membranes revealed a concentration-dependent and saturable process with a significant decrease in the high affinity receptor sites of the diabetic membrane. Moreover, the incubation of the membranes with procaine, colchicine and vincristine increased significantly pyridoxine binding to normal and diabetic membrane. Treatment of the normal and diabetic membranes with insulin did not affect pyridoxine binding. It could be suggested that streptozotocin-induced diabetes caused an alteration in the pyridoxine binding capacity of the liver plasma membrane which might be due to certain structural changes in the membrane.

Animals↗
PubMed1984

Effect of prostaglandin E1 on bile flow in the rat.

The effect of intravenous administration of prostaglandin E1 on bile flow in the rat was investigated. PGE1 infused at concentrations of 4.5, 7.5 and 15 micrograms/kg body weight/min caused an initial increase in bile acid-independent bile flow rate which peaked within 30 min and was followed by a significant decrease (p less than 0.01) below the control value. However, PGE1 administered intravenously at an infusion rate of 15 micrograms X kg-1 X min-1 showed a significant decrease (p less than 0.01) in bile acid-dependent bile flow rate.

Alprostadil↗
PubMed1983

Enzymatic inhibition of lysine transport across rat and turtle small intestine.

Trypsin, Phospholipase-D and Neuraminidase at different concentrations inhibited significantly (P less than 0.001) lysine accumulation in rat intestinal cells, whereas Chymotrypsin did not show any significant effect. Trypsin, Chymotrypsin and Phospholipase-D did not show any significant change in lysine accumulation when incubated with mucosal strips isolated from turtle intestine; however, Neuraminidase caused a significant decrease in lysine uptake by these strips. Unidirectional lysine influx across the rat small intestine was significantly reduced (P less than 0.01) by the presence of Trypsin, Phospholipase-D and Neuraminidase in the preincubation solution, and its influx across the turtle small intestine was significantly inhibited (P less than 0.01) by Neuraminidase only. The cell water content and the cell volume were not altered by preincubating the intestinal tissues with any of the enzymes in both animals.

Animals↗
PubMed1982

Factors regulating prostaglandin uptake by rat small intestine.

The uptake of prostaglandin E1 by rat intestine mucosal strips was investigated. The results indicate that: (1) PGE1 did not accumulate in the epithelial cells of rat intestine. The intracellular to extracellular distribution ratio did not reach unity in spite of the extended periods of incubation. (2) A decrease in the sodium gradient across the brush-border membrane of intestinal cells significantly inhibited PGE1 uptake by the mucosal strips. (3) PGE1 uptake increases with increasing concentration of potassium in the incubation medium with a tendency for saturation at high K+ levels. (4) Calcium and magnesium ions had no effect on the steady-state uptake of PGE1 by the epithelial cells of rat intestine. (5) Addition of sodium carbonate or phosphate to the incubation medium significantly decreased PGE1 uptake by the intestinal cells. (6) Further studies of PGE1 uptake reveal a temperature-dependent process with a Q10 of 2.8.

Animals↗
PubMed1981

Prostaglandin E1 influx across mucosal membrane of mammalian intestine.

The influx of prostaglandin E1 (PGE1) across the mucosal membrane of mammalian intestinal cells was examined. Our results suggest that: (1) the mechanism of PGE1 influx across the mucosal membrane of mammalian intestinal cells is a carrier-mediated transfer process; (2) PGE1 influx into the intestinal cells is inhibited in the presence of 1 X 10(-4) M ouabain in the preincubation medium, and (3) PGE1 influx is dependent on the presence of sodium in the extracellular medium, and is altered by reversal of the sodium gradient that normally exists across the mucosal membrane.

Alprostadil↗
PubMed1980

Agglutination kinetics of normal and diabetic adult rat hepatocytes.

This paper describes Concanavalin A-induced agglutination of viable rat hepatocytes obtained by collagenase perfusion from normal and streptozocin-treated diabetic rats. An irreversible cell-to-cell agglutination model is proposed to explain hepatocyte flocculation. The rate of agglutination is concentration dependent with respect to Concanavalin A, and is twice as fast in normal as compared to diabetic hepatocytes. Sticking probability constants ranging from 18.48 x 10(7) to 4.6 x 10(7) cm-1 . hepatocyte-1 and 8.32 x 10(7) to 2.31 x 10(7) cm-1 . hepatocyte-1 are calculated as a measure of agglutination for normal and diabetic cells respectively. These findings suggest that the cytoplasmic membranes of normal cells possess agglutinin receptors which are more numerous and/or differently arranged than those existing in diabetic cells.

Agglutination↗
PubMed1980

Alanine influx across serosal border of Testudo graeca intestine.

The influx of alanine across the serosal membrane of Testudo graeca intestinal cells with preserved epithelial orientation was examined. Our results suggest that: 1. The mechanism of alanine influx across the serosal membrane of turtle intesintal cells is a carrier-mediated process that has the characteristics of facilitated diffusion. 2. Alanine influx mechanism is independent of intra- and extra-cellular changes in Na+ and K+ concentrations, and is not altered by reversal of Na+ and K+ gradients across the serosal membrane. 3. In Na+-free media the mechanism of transport of alanine at the mucosal membrane has the same pattern of competitive inhibition by amino acids as the serosal.

Alanine↗