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Biomedical subjects

R J Bing

Publications and source records attributed to R J Bing.

At least 55 records · Page 3Linked to original sources
PubMed1993

Lysophosphatidylcholine-induced vascular relaxation and production of cGMP are mediated by endothelium-derived relaxing factor.

Endothelial cells produce powerful vasorelaxant substances, among them an endothelium-derived relaxing factor that is believed to be nitric oxide. It relaxes vascular smooth muscle via activation of guanylate cyclase and a subsequent rise in cyclic GMP level. Lysophosphatidylcholine is a potent endothelium-dependent vascular smooth muscle relaxant. Its action, similar to that of endothelium-derived relaxing factor, mediates an increase of cGMP in smooth muscle cells. The experiments reported here demonstrate that inhibitors of nitric oxide formation, such as N-omega-nitro-L-arginine and its methyl ester, inhibit relaxation and cyclic GMP formation by lysophosphatidylcholine in bovine pulmonary artery strips with intact endothelium in a dose-dependent manner. N-omega-Nitro-D-arginine methyl ester does not inhibit relaxation; L-arginine, but not D-arginine, reverses the effect of N-omega-nitro-L-arginine and its methyl ester. It is concluded that lysophosphatidylcholine-induced endothelium-dependent vasorelaxation is endothelium-derived relaxing factor-mediated.

Animals↗
PubMed1992

The effect of immune mediators (cytokines) on the release of endothelium-derived relaxing factor (EDRF) and of prostacyclin by freshly harvested endothelial cells.

The effect of recombinant tumor necrosis factor and other cytokines stimulated by LPS (lipopolysaccharide), on the release of endothelial-derived relaxing factor and of prostacyclin was investigated using freshly harvested endothelial cells attached to plastic microcarrier beads. The results show that the cytokines failed to interfere with the release of EDRF and prostacyclin under the conditions of these experiments.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

A simplified method for the determination of nitric oxide in biological solutions.

A new simplified procedure for determination of nitric oxide (NO) in biological solutions is described utilizing a new reducing system of nitric oxide prior to chemiluminescence. Advantages of the new method makes heating of the reducing solution unnecessary and avoids cooling and condensation of generated vapors. Only traces of acid with a high boiling point are used. The method permits analysis of small sample volumes (200 microL). The basal production of nitric oxide by freshly harvested endothelial cells ranged from 100 to 880 picomoles.

Animals↗
PubMed1992

Cytokine production from freshly harvested human mononuclear cells attached to plastic beads.

The release of tumor necrosis factor (TNF), interleukin-1 beta (IL-1) and granulocyte-macrophage colony-stimulating factor (GM-CSF) from freshly harvested monocytes and lymphocytes attached to plastic beads was investigated. Previous studies had shown that freshly harvested endothelial cells attached to microcarrier beads release an endothelium-derived relaxing factor. Attachment of freshly harvested lymphocytes and monocytes to plastic beads created a dense network, consisting of 25% monocytes and 75% lymphocytes as shown by flow cytometry. Viability of cells was 90%. Monocytes were characterized by phagocytosis and non-specific esterase stain. Freshly harvested cells stimulated with lipoprotein lipase (LPS) released TNF and IL-1. Non-stimulated cells also produced GM-CSF five hours after collection of blood.

Cell Aggregation↗
PubMed1992

Dopa: then and now.

Explore the source record for details and available documents.

Dihydroxyphenylalanine↗
PubMed1991

Release of prostacyclin, endothelium-derived relaxing factor and endothelin by freshly harvested cells attached to microcarrier beads.

Cultured endothelial cells have been used in the past as a source of endothelium-derived relaxing factor (EDRF) and of prostacyclin (PGI2). Although cell cultures are essential for observation of prolonged exposure to media or when there is delayed response, they are time consuming and sterile conditions are essential. In the present study, we report that endothelial cells, freshly harvested from bovine aortas, readily attached themselves to cytodex-3 microcarrier beads and released an endothelium-derived relaxing factor (EDRF), prostacyclin (PGI2) and increased the amount of cyclic GMP in vascular smooth muscle. Attachment to microcarrier beads was essential since it increased the surface area and the number of attached cells and permitted collection of cell free filtrates because of the formation of dense networks of cells and beads. As a result superfusion of cells and beads on the filter did not dislodge bound cells which remain on the filter. Conditioned filtrates from freshly harvested endothelial cells attached to microcarrier beads caused marked relaxation of endothelium-deprived bovine pulmonary artery strips. The degree of relaxation depended on the number of cells; maximal relaxation occurred with 50 million cells at ED50 of 14 million. High values of cyclic GMP were found in vascular smooth muscle exposed to conditioned filtrate. The calcium ionophore A23187 further increased the amount of cyclic GMP. Large amounts of PGI2 were released by freshly harvested endothelial cells particularly after stimulation with the calcium ionophore. In contrast, endothelin production by freshly harvested cells attached to microcarrier beads was barely detectable after 30 min incubation and was beyond the limit of detection by bioassay procedures. Freshly harvested endothelial cells attached to microcarrier beads appear to be a useful adjunct to tissue cultures under specific experimental conditions.

Animals↗
PubMed1991

The effect of lysophosphatidylcholine on coronary and renal circulation in the rabbit.

It has been shown that different lysophosphatidylcholines (LPC) possess relaxing properties in vascular strips. We report on the effect of intraatrial injection of LPC micelles into white New Zealand rabbits. Changes in renal and coronary flow were determined by radioactive microspheres. Coronary blood flow increased significantly following administration of LPC, while no significant changes were observed in renal blood flow, cardiac output and myocardial contractility. Coronary, renal and total vascular resistance, as well as mean arterial pressure, dropped significantly. Cardiac arrhythmia and hemolysis were not noted. The results demonstrate the vasorelaxant effect of LPC in vivo.

Animals↗
PubMed1991

Reduction of biological effluents in purge and trap micro reaction vessels and detection of endothelium-derived nitric oxide (edno) by chemiluminescence.

Various analytical approaches have been used to measure endothelium-derived nitric oxide (NO). We have detected NO in perfusates with a sample size as low as 2 ml after acidification with 4 N HC1 to pH less than 2 at 25 degrees C by using a Nitric Oxide Analyser (Sievers, Colorado). This procedure had the advantage that the detectable level of NO was enhanced by the self-decomposition of HNO2 when the PH less than pKa of NHO2 (pKa = 3.15) and also the reaction temperature of 25 degrees C substantially increased the half-line of NO. Palmer, et al., measured NO released by cultured porcine endothelial cells by chemiluminescence after passing cell effluents continuously at a rate of 5 ml/min into 75 ml of 1% sodium iodide in glacial acetic acid. The larger volumes involved in this method for continuous refluxing, made it less desirable for the detection of endothelium-derived nitric oxide. Feelisch et al. utilized the activation of soluble guanylate cyclase, as well as, the quantitative oxidation of oxyhemoglobin to methemoglobin in aqueous solutions by NO as a means of measuring nitric oxide. We describe here a modification of our earlier micromethod which now enables us to detect NO after complete reduction with glacial acetic acid and sodium iodide. A comparison of the two procedures indicate that while freshly prepared NO standard solutions gave identical chemiluminescence response with and without reduction, effluents from bovine intrapulmonary artery under basal conditions gave substantially higher values upon reduction.

Animals↗
PubMed1991

The use of microcarrier beads in the production of endothelium-derived relaxing factor by freshly harvested endothelial cells.

This study is concerned with the use of freshly harvested bovine endothelial cells attached to microcarrier beads in the production of the endothelium-derived relaxing factor (EDRF). The results are compared to production of EDRF by endothelial cells grown in tissue cultures. We found that freshly harvested cells attach themselves to microcarrier beads within minutes. This results in large surface/area volume ratio and permits superfusion of cells suspension on a filter (pore size of 25-30 microns), resulting in cell free filtrate. When superfusing an endothelium-deprived pulmonary artery strip, the effluent causes relaxation; the response depends on the number of superfused endothelial cells. The number of viable freshly harvested cells attached to microcarrier beads in 5 ml Krebs-Henseleit solution is small (30%), as compared to almost 100% for cultured cells. Despite this difference, percent relaxation induced for the same number of viable cells is identical for both groups. Scanning electromicrographs confirm anchorage of endothelial cells to microcarrier beads. While cultured cells cover the entire surface and are individually attached, freshly harvested cells are anchored as cell aggregates leaving some of the surface free. Attachment of freshly harvested endothelial cells to microcarrier beads offers an alternative for the study of the role of endothelial cells in the production of vasoactive substances.

Animals↗
PubMed1991

Nitroarginine does not inhibit lysophosphatidylcholine (LPC)-induced vascular relaxation and accumulation of cyclic GMP.

Lysophosphatidylcholine (LPC) is a potent endothelium-dependent vascular smooth muscle relaxant. The possibility that its action is mediated through endothelium-derived nitric oxide (EDNO), although suggestive, has not been proven. Both lysophosphatidylcholine and endothelium-derived nitric oxide relax by activating guanylate cyclase to form cyclic GMP. Based on the finding that EDNO formation is inhibited by NNA (N-omega-nitro-L-arginine), we followed cyclic GMP changes in bovine intrapulmonary arteries with LPC after incubation with NNA. Inhibition of cyclic GMP by LPC following NNA exposure would be suggestive of the production of EDNO by LPC. However, while NNA significantly inhibited accumulation of cyclic GMP after exposure to the calcium ionophore A23187 which releases EDNO, NNA failed to inhibit LPC-induced accumulation of cyclic GMP. The results indicate that LPC relaxes vascular smooth muscle through a non NO-mediated pathway.

Animals↗
PubMed1990

A model to study physiological activation of phospholipase A2 and vasorelaxation by lysophosphatidylcholine.

Earlier we demonstrated that micellar solutions of LPC caused endothelium-dependent relaxation of rabbit thoracic aorta and bovine intrapulmonary artery and vein through a cyclic GMP-dependent mechanism. The availability of LPC for vasorelaxation depends on its production by deacylation of PC by PLA2. We assessed the possible activation of PLA2 by commonly used vasorelaxants such as acetylcholine, bradykinin, calcium ionophore A23187 and thrombin and vasoconstrictors like histamine and phenylephrine in the presence of indomethacin in a model system where 14C PC was incorporated into bovine intrapulmonary arterial segments. Taking the ratio of 14C PC:LPC formed by exogenous PLA2 as an index of deacylation, we found that while all the agents relaxed the strips in an endothelium-dependent manner, only thrombin caused relaxation followed by an increase in 14C LPC and a concomittant decrease in 14C PC indicating activation of PLA2. Our data show that PC/PLA2 system can be activated to generate LPC for vascular relaxation under specific physiological conditions. This model system can be used to monitor PLA2 activity and LPC production to compensate flow and pressure induced changes in arteries.

Acetylcholine↗
PubMed1990

Pressure-induced contractions in bovine pulmonary artery preparations.

Experiments were conducted in a superfusion bioassay system in which the effluent of a bovine main pulmonary artery (generator) was allowed to superfuse a spirally cut precontracted bovine arterial strip (detector), which had been deprived of endothelium. Effluents of endothelium-intact generator relaxed the precontracted detector by an average of 22 +/- 4.1%. Following removal of endothelium of the generator, the relaxing effect of the effluent was only 1%. A rapid increase of transmural pressure in the generator to about 40 mm Hg for 3 min induced contraction of the detector (8.4 +/- 2%) above the histamine-induced tension. In the absence of endothelium, smaller contractions were obtained from the pressurized generator (4.9 +/- 1.8%). This effect was reversible after pressure release. Effluents of endothelium-deprived generator showed no significant vasoactivity. NG-Mono-methyl-L-arginine (L-NMMA, 3.3 x 10(-5) mol/l), a specific inhibitor of nitric oxide (NO), also depressed endothelium-dependent relaxation and caused a 10.5% increase in contraction of the endothelial effluent. When the endothelium-intact generator was exposed to both pressure and L-NMMA, an additive effect was noted. Based on these observations, it was concluded that transient increase of transmural pressure in bovine main pulmonary arteries depresses the endothelium-dependent relaxation and unmasks a small but significant contractile activity of the endothelial effluent.

Animals↗
PubMed1989

Effect of lysophosphatidylcholine on atherosclerotic rabbit arteries.

We report here on the effect of an endothelium-dependent vascular smooth muscle relaxant, lysophosphatidylcholine (LPC) on rabbit aortic strips and on hemodynamic changes by LPC in atherosclerotic animals. Cyclic GMP changes induced by LPC in atherosclerotic vessels were also determined. Atherosclerosis was produced by feeding a high cholesterol and saturated fatty acid diet. LPC was injected into the left atrium and coronary flow was measured by radioactive microspheres; in vitro, relaxation of precontracted aortic strips by lysophosphatidylcholine was also recorded. LPC failed to increase coronary flow in the presence of atherosclerosis. In isolated aortic strips, dose-response curves with acetylcholine and LPC showed diminished relaxation in atherosclerotic preparations, and cyclic GMP production following LPC was reduced. The results demonstrate that vascular relaxation by LPC, together with its ability to activate guanylate cyclase is dependent on the functional and morphological integrity of the vascular wall.

Animals↗
PubMed1989

Correlation of lysophosphatidylcholine-induced vs spontaneous relaxation to cyclic GMP levels in rabbit thoracic aorta.

We demonstrated previously that 10(-5)M micellar solution of lysophosphatidylcholine (LPC) produced relaxation of rabbit thoracic aorta in a dose-dependent manner. It was also noticed that histamine (HA)-precontracted strips relaxed spontaneously in the absence of LPC. We now measured the cyclic GMP changes during these two types of relaxation. Results indicate that while LPC-induced relaxation was mediated through cyclic GMP, spontaneous relaxation was not. The vasodilating effect of LPC was not due to its interference with cellular viability by solubilizing the membrane, because repeated additions of LPC produced identical degrees of relaxation and after three consecutive additions of LPC, the strips continued to relax to the same degree with acetylcholine (Ach) demonstrating the functional integrity of the endothelium. LPC/Cholesterol dispersions (1:0.5 mole percent) relaxed the strips to the same extent as the micellar solution of LPC, while 1:1 mole percent did not. The results stress the role of cyclic GMP in LPC-induced relaxation. They further suggest that LPC/Cholesterol ratio may determine the availability of LPC and regulate LPC-mediated processes.

Animals↗