Porcine pulmonary artery distension during static pressure inflation

2013 ◽  
Author(s):  
Yik Ching Lee ◽  
Alys Clark ◽  
Mathew Fuld ◽  
Susan Haynes ◽  
Abhay Divekar ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Static Pressure ◽  
Porcine Pulmonary Artery

Hypoxia induces the synthesis of tropomyosin in cultured porcine pulmonary artery endothelial cells

1994 ◽  
Vol 267 (3) ◽  
pp. L271-L281 ◽  
Author(s):  
U. J. Rao ◽  
N. D. Denslow ◽  
E. R. Block
Keyword(s):  
Endothelial Cells ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Pulmonary Artery ◽  
Monolayer Culture ◽  
Cross Reactivity ◽  
Two Dimensional Gel Electrophoresis ◽  
Molecular Masses ◽  
35 Kda Protein ◽  
Porcine Pulmonary Artery

The present study examined the effect of hypoxia on protein synthesis by porcine pulmonary artery endothelial cells (PAEC). Hypoxia decreased protein synthesis in PAEC, but two-dimensional gel electrophoresis of [35S]methionine-labeled PAEC proteins demonstrated the increased synthesis of a set of proteins having molecular masses (M(r)) of 35, 36.5, 45, 116, and 205 kDa. The synthesis of the 35-, 36.5-, and 45-kDa proteins was increased in preconfluent and postconfluent cells. The 35- and 45-kDa proteins were not induced by hyperthermia, whereas the 36.5-kDa protein was induced slightly by hyperthermia. Induction of the 36.5- and 45-kDa proteins required a minimum of 8 h of hypoxia, whereas induction of the 35-kDa protein required only 4 h of exposure to hypoxia. The upregulated synthesis of the 35-, 36.5-, and 45-kDa proteins was reversible with return to normoxia. Actinomycin D, an inhibitor of transcription, did not block the hypoxic induction of the 35- and 36.5-kDa proteins but did block induction of the 45-kDa protein. The partial amino acid sequence of the 35-kDa protein obtained from cyanogen bromide cleavage of the molecule was Asp-Ala-Ile-Lys-Lys-Lys-Met-Gln-Met-Leu-Lys-Leu-Asp-Lys-Glu. This partial sequence of the 35-kDa protein identically matches the sequence of tropomyosin. Amino acid composition data and the isoelectric point (4.8) were also typical of tropomyosin. Finally, specific cross-reactivity was detected between the 35-kDa protein and a monoclonal antibody to chicken gizzard tropomyosin on immunoblot. Thus hypoxia induces the synthesis of tropomyosin, a major microfilament-associated protein, in porcine PAEC in monolayer culture.

Effect of hypoxia on phospholipid metabolism in porcine pulmonary artery endothelial cells

1992 ◽  
Vol 262 (5) ◽  
pp. L606-L613 ◽  
Author(s):  
G. B. Bhat ◽  
E. R. Block
Keyword(s):  
Endothelial Cells ◽  
Fatty Acid ◽  
Pulmonary Artery ◽  
Fatty Acid Fraction ◽  
Phospholipid Metabolism ◽  
Fatty Acid Esters ◽  
Hypoxic Exposure ◽  
Synthetase Activity ◽  
Diacylglycerol Lipase ◽  
Porcine Pulmonary Artery

The effect of exposure of porcine pulmonary artery endothelial cells to hypoxic (0% O2) and normoxic (20% O2) conditions for 24 and 48 h on phospholipid metabolism was studied. Sonicates prepared from endothelial cells that were exposed to 24 h of hypoxia showed significant increases in phospholipase A1 (91%), phospholipase C (75%), and diacylglycerol lipase (57%) activities. Hypoxic exposure of cells for 48 h caused an increase in diacylglycerol lipase activity (54%) only. Hypoxia also caused significant decreases in ATP levels and ATP-dependent arachidonyl coenzyme A (CoA) synthetase activity. Phospholipase A2, lysophosphatidylcholine acyltransferase, and diacylglycerol acyltransferase activities were not influenced by 24 or 48 h of hypoxia. When endothelial cells were prelabeled with [3H]arachidonic acid and then exposed to hypoxia, increased counts were recovered from the free fatty acid fraction of medium and from the cell fatty acid esters, lysophospholipids, diacylglycerols, and triacylglycerols. There was a concomitant decreased recovery of counts from cell phospholipids. These results indicate that hypoxic exposure of endothelial cells altered phospholipid metabolism by activating deacylation pathways and inhibiting reacylation via ATP-dependent arachidonyl CoA synthetase.

Acute and Chronic Effects of Dexfenfluramine on the Porcine Pulmonary Artery

1998 ◽  
Vol 30 (3) ◽  
pp. 403-410 ◽  
Author(s):  
Bernabas Desta ◽  
Scott Steed ◽  
Denis Ravel ◽  
Nicole Laudignon ◽  
Paul M Vanhoutte ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Chronic Effects ◽  
Acute And Chronic Effects ◽  
Porcine Pulmonary Artery

scholarly journals Effects of dexmedetomidine on porcine pulmonary artery vascular smooth muscle

2019 ◽  
Author(s):  
Mami Chikuda ◽  
Kenichi Sato
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Vascular Smooth Muscle ◽  
Local Anesthetics ◽  
Pulmonary Arteries ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Duration Of Action ◽  
Porcine Pulmonary Artery ◽  
Ca2 Channels

Abstract Background Dexmedetomidine is added to local anesthetics to increase their potency and extend their duration of action, thus providing postoperative analgesia with a single administration. However, the effects and mechanism of action of dexmedetomidine on pulmonary arteries have not been determined. The aim of this study was to investigate the effect of dexmedetomidine on pulmonary artery vascular smooth muscle, evaluating changes in contraction tension. Methods Endothelium-denuded porcine pulmonary arteries were sliced into 2- to 3-mm rings. Changes in isometric contraction tension were measured with the addition of various substances at various concentrations, under different conditions of baseline stimulation (with KCl, Adrenaline, caffeine, or histamine) and different conditions of Ca2+ depletion with intracellular reservoirs or extracellular stores depleted. Results Dexmedetomidine increased the contraction tension induced by high-KCl depolarization in a concentration-dependent manner. Dexmedetomidine inhibited receptor-activated Ca2+ channels (RACCs) and phosphatidylinositol-1,4,5-triphosphate-induced Ca2+ release (IICR), but not Ca2+-induced Ca2+ release (CICR). Conclusions Dex increased the contraction tension resulting from depolarization stimulation by high KCl in a concentration-dependent manner in porcine pulmonary artery vascular smooth muscle. The enhancement of high KCl-induced contraction with Dex addition was mediated by α2 receptors. Dex suppressed increases in contraction tension induced by receptor stimulation with adrenaline, also in a concentration-dependent manner. Dex inhibited RACC and IICR, but not CICR. Elucidating the effects and mechanisms of action of Dex in the central arteries is likely to be useful as basic data for creating Dex-containing local anesthetics.

ROLE OF DIETARY FATTY ACIDS AND PLATELETS IN MODULATING PORCINE PULMONARY ARTERY CONTRACTILITY

1998 ◽  
Vol 89 (Supplement) ◽  
pp. 389A
Author(s):  
Michael J. Murray ◽  
Lynn Harstad ◽  
&NA; Evans
Keyword(s):  
Fatty Acids ◽  
Pulmonary Artery ◽  
Dietary Fatty Acids ◽  
Porcine Pulmonary Artery
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