Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The direct and indirect actions of two active components of slow-reacting substance of anaphylaxis, leukotrienes C4 (LTC4) and D4 (LTD4), were studied in chronically instrumented unanesthetized sheep. Intravenous injection of 3 micrograms of LTD4 caused immediate marked pulmonary arterial hypertension which returned to baseline in 6.5 +/- 1.0 min. Dynamic compliance of the lungs (Cdyn) and left atrial (PLA) and aortic (Paorta) blood pressure fell concomitantly with the increases in pulmonary artery pressure (PPA). PLA and Paorta then increased above baseline and heart rate deceased significantly. LTD4 caused only small increases in lung lymph flow but did increase lung lymph concentrations of thromboxane B2. Lung lymph concentrations of 6-keto-prostaglandin F1 alpha did not increase following LTD4 infusion. The increase in PPA after 3-micrograms injections of LTD4 was greater than that caused by 10-micrograms injections of prostaglandin H2-analog. Injections of 10-30 micrograms of LTC4 caused only minor increases in PPA but did cause bradycardia and delayed increases in PLA and Paorta. The cyclooxygenase inhibitors meclofenamate and ibuprofen inhibited the increases in PPA caused by LTD4 but not the later bradycardia or increases in PLA and Paorta. The thromboxane synthetase inhibitor UK-38485 attenuated the early increase in PPA and moderated the later increases in PLA and Paorta and bradycardia caused by LTD4 injection. The response of unanesthetized sheep to LTD4 is mediated, at least in part, indirectly by stimulation of the cyclooxygenase pathway of arachidonate metabolism.
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PMID:Direct and indirect effects of leukotriene D4 on the lungs of unanesthetized sheep. 311 26

Nicotine and cigarette smoke extract show acute physiological effects: increasing tracheal pressure (PTR), pulmonary artery pressure (PPA), systemic blood pressure (PSYST), and left atrium pressure (PLA); and decreasing cardiac output (QAORTA) and blood flow to the left lower lobe (QLLL). In addition, cigarette smoking induces bronchoconstriction, thus decreasing peak flow, FVC, and FEV1.0 in healthy subjects. It has also been demonstrated that cigarette smoking caused temporary slowing of mucociliary clearance in the lung and that cigarette smoke increases the activity of aryl hydrocarbon hydroxylase which metabolizes benzo[alpha]pyrene. We demonstrated that serum angiotensin I converting enzyme (ACE) activity showed a significant increase immediately after smoking and returned to the control level 20 min after smoking. We also demonstrated that plasma histamine levels showed a marked decrease after smoking. Furthermore, the effects of cigarette smoke and related substances on prostaglandin, thromboxane, testosterone, cyclic nucleotides metabolism, and protein synthesis were also investigated.
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PMID:Effects of cigarette smoking on metabolic events in the lung. 330

Pulmonary microemboli can create an ARDS-like state in dogs (high pulmonary vascular resistance, pulmonary oedema and arterial hypoxemia). CPPV can correct the hypoxemia of pulmonary microemboli but reduces cardiac output (Q) and tissue oxygenation. This paper compares the effect of improving Q by infusing volume, reducing afterload, or increasing myocardial contractility. Four groups of seven dogs were studied. All had 0.125 g . kg-1 of starch microemboli (63-74 microns) infused and then CPPV at 15 cm H2O applied. The control group had no further treatment applied. In three other groups volume (dextran) or dobutamine or nitroprusside (NTP) was infused to return Q to the level before CPPV was applied. All treatments (volume, dobutamine and NTP) improved Q and O2 transport. Only the volume group had a significant increase in pulmonary microvascular pressure, Pmv = PLA + 0.4 (PPA - PLA) from 2.53 +/- 0.27 to 3.35 +/- 0.13 kPa, p less than 0.05. Only the volume group demonstrated a significant increase in lung water above (double) the control group as measured by a double indicator dilution technique (ETVL) and post mortem lung weights. We conclude volume infusions to improve a CPPV depressed Q may increase lung water and that better treatment would be to infuse NTP or dobutamine, thus maintaining a lower Pmv and therefore lung water. As a corollary the least CPPV should be applied to maintain adequate oxygenation and create the least need for interventions to improve Q.
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PMID:The effects of dobutamine, nitroprusside, or volume expansion on cardiac output and lung water after CPPV. 351 43

The pressure within the water-filled cuff of an endotracheal tube (PTE) was used as a measure of tracheal smooth muscle tone in ten patients undergoing cardiopulmonary bypass (CPB). Pulmonary artery pressure (PPA) and left atrial pressure (PLA) were also monitored. Institution of CPB, with acute reduction of pulmonary blood flow and lung deflation, caused no significant change in PTE. Crystalloid cardioplegic administration without left ventricular decompression (VENT) resulted in statistically significant increases of PPA (from 1.33 +/- 0.15 to 1.88 +/- 0.2 kPa) (p less than 0.05) and of PLA (from 1.2 +/- 0.11 to 2.2 +/- 0.31 kPa) (p less than 0.05). Coincident with these changes a statistically significant increase in PTE (from 4.95 +/- 0.21 to 5.24 +/- 0.27 kPa) (p less than 0.05) was detected. This increase in PTE was significantly greater than the small random variations noted in PTE prior to cardioplegic infusion with constant PLA and PPA. Thus, minimal tracheomotor constriction in response to cardioplegia administration occurred. Larger increases in PTE were noted during cardiac compression suggesting that the water-filled cuff could have detected larger increases if they had occurred. These transient changes do not reflect clinically detectable increases in airway resistance at the termination of CPB when lung ventilation is started. Neither of these two physiological stimuli, lung deflation or cardioplegia administration, cause clinically significant increases of large airway tone during CPB.
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PMID:Tracheomotor response to cardiopulmonary bypass: influence of lung deflation and cardiac distension. 400 72

The effects of digoxin on pulmonary vascular resistance (PVR) were evaluated in normoxic (N) and hypoxic (H) newborn lambs with normal and elevated PVR, respectively. Lambs were anesthetized and instrumented to enable continuous measurement of mean pulmonary arterial pressure (PPA), mean left atrial pressure (PLA), mean pulmonary blood flow (Qp), and mean aortic pressure (PAO). Digoxin (10-20 micrograms/kg) was injected via central venous catheters in 11 N lambs and 4 H lambs. Under N conditions, baseline PVR was equal to 0.12 mm Hg/ml/min/kg, PPA was 33 mm Hg, PLA was 6 mm Hg, Qp was 235 ml/min/kg, and PAO was 69 mm Hg. Following digoxin, mean PVR increased by 24% (P less than 0.001) and PPA increased by 23% (P less than 0.001) for an average duration of 199 sec while QP increased by 5% (P less than 0.02) and PLA was constant suggesting a direct vasoconstrictive effect. Under H conditions, baseline PVR was equal to 0.26 mm Hg/ml/min/kg, PPA was 58 mm Hg, PLA was 4 mm Hg, Qp was 208 ml/min/kg, and PAo was 65 mm Hg. Following digoxin, mean PVR, Qp, PLA, and PAo did not change appreciably although PPA had a uniform increase of 5% (P less than 0.001). The blunted response may suggest that either the pulmonary vascular bed was maximally constricted or that digoxin and hypoxia share a common mechanism. In conclusion, digoxin has a direct pulmonary vasoconstrictor action in newborn lambs. Because of its short duration, this action probably should not alter the clinical use of this drug in newborn humans.
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PMID:Pulmonary vascular response to digoxin in newborn lambs. 652 30

Hemodynamic responses to prostacyclin (PGI2) were studied in sheep in the conscious state as well as under pentobarbital-halothane anesthesia. PGI2 in doses of 0.02-1.0 microgram/kg were administered as a bolus into the right or left atrium in the conscious sheep. PGI2 decreased systemic arterial pressure (PSA), systemic (SVR) and pulmonary vascular resistance (PVR) and increased cardiac output (CO) and heart rate (HR) in a dose-dependent manner. The changes of each parameter were almost similar regardless of the sites of administration. Pulmonary arterial pressure (PPA) was increased. There was no change in left (PLA) or right atrial pressure (PRA). A bolus administration of 0.5 microgram/kg of PGI2 in the anesthetized sheep produced a decrease in PSA, SVR and PVR, and increase in CO and HR. PPA remained unchanged when administered into the right atrium and increased slightly when administered into the left atrium. PLA and PRA did not change. Comparing hemodynamic responses to 0.5 microgram/kg of PGI2 of the conscious and anesthetized states, decrease in PSA was smaller and increases in CO and HR were greater in the former. Decreases in SVR and PVR were similar in both states. Increase in PPA was greater in the conscious sheep. This data confirms that PGI2 dilates the systemic as well as the pulmonary circulation of the sheep and an inactivation of this compound in the lungs is minimal. Furthermore, it may be suggested that general anesthesia significantly alters hemodynamic responses to PGI2 in the sheep.
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PMID:Hemodynamic responses to prostacyclin (PGI2) in the conscious sheep. 675 86

The distribution function of pulmonary transit times (fPTT) defines contact time between blood and vascular bed, which affects gas exchange and endothelial metabolic functions. This study was undertaken to assess effects of abnormal pulmonary inflow (PPA) and outflow pressures (PLA) on fPTT. Three groups were studied: five patients with elevated PLA and passive pulmonary hypertension (LVD-Ab), eight with normal PLA (LVD-Nl), and six with pulmonary disease and various levels of PPA (PD). Empirical complex exponential functions were convoluted on right and left ventricular indicator-dilution curves to derive fPTT; mean transit time (Mo1), standard deviation (Sm2), and cube root of the third moment about Mo1 (Sm3) were calculated by standard equations. A single linear regression of Sm3 and Sm2 on Mo1 was observed for all patients, regardless of disease process. Inverse relations between Mo1, Sm2, and Sm3 and blood flow were highly significant, but dispersion volumes (DV = Mo1 x flow) were higher in patients with elevated PPA. Significant linear regressions of fPTT parameters on PPA, derived in LVD-Nl and LVD-Ab patients, failed to predict Mo1, Sm2, and Sm3 for the PD group, whereas linear regressions on PLA accurately predicted Mo1, Sm2, and Sm3 in the PD group. Relations between fPTT parameters and PLA were equally well fit by exponential equations in all 19 patients, consistent with an asymptotic pressure-volume relation of distensible vessels. Microvascular pressure (PMV), combining PPA and PLA, was not a better predictor of fPTT parameters in LVD-NL and LVD-Ab patients but provided a slightly closer estimate of relative dispersion and skewness in PD patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Distribution function of transit times in the human pulmonary circulation. 800 83

Inhaled nitric oxide (NO) is effective as a selective pulmonary vasodilator, but its effects on uninjured lungs subjected to normoxia and hypoxia have not been fully studied. The authors sought the response of pulmonary vascular resistance (PVR) to inhaled NO in piglet lungs devoid of ischemic injury in a model of reversible pulmonary hypertension. If the changes were dose-responsive, the authors asked whether the PVR changes were related to normoxia or hypoxia, and hypothesized that the change would be more pronounced for hypoxia than normoxia. In situ isolated piglet lungs were prepared by occlusive tracheostomy and ligation of the ductus arteriosus and aorta. Cannulae positioned in the left atrium and pulmonary artery were connected to a standard extracorporeal membrane oxygenation (ECMO) circuit, and flow was increased to approximate cardiac output. After stabilization, piglets (aged 5 to 14 days, weighing 3.2 to 6.4 kg) were divided into two groups of four each: normoxic (FIO2 0.30, normal PVR) and hypoxic (FIO2 0.07, increased PVR). NO was administered at 10 to 80 parts per million (ppm) in increments of 10 ppm, for 5 minutes at each concentration, with a return to baseline before each new dose. Flow, pulmonary arterial (PA) and left atrial (LA) pressures were continuously monitored, from which PVR was calculated (PVR = [PPA - PLA]/flow) and expressed as log delta PVR. Data were analyzed statistically by repeated measures of analysis of variance, comparing log delta PVR to baseline at each dose of NO, and comparing log delta PVR for normoxic and hypoxic lungs at each dose of NO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of inhaled nitric oxide on normoxic and hypoxic isolated in situ neonatal pig lungs perfused by extracorporeal membrane oxygenation. 817 5

The production of 4-hydroxyphenyllactic acid (4-HO-PLA), a novel antifungal compound, was studied in Lactobacillus sp. SK007 growth. When grown in MRS broth, the strain could produce 75 microg/ml HO-4-PLA, which was the highest reported so far. Tyrosine and 4-hydroxyphenylpyruvic acid (HO-4-PPA) supplements during fermentation could both increase the HO-4-PLA production yield, and the effect of HO-4-PPA on HO-4-PLA production was remarkably better than that of tyrosine. Using HO-4-PPA as substrate could effectively produce HO-4-PLA, which reached 1.26 mg/ml.
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PMID:Production of 4-hydroxyphenyllactic acid by Lactobacillus sp. SK007 fermentation. 2022 79

We examine the transfer of graphene grown by chemical vapor deposition (CVD) with polymer scaffolds of poly(methyl methacrylate) (PMMA), poly(lactic acid) (PLA), poly(phthalaldehyde) (PPA), and poly(bisphenol A carbonate) (PC). We find that optimally reactive PC scaffolds provide the cleanest graphene transfers without any annealing, after extensive comparison with optical microscopy, x-ray photoelectron spectroscopy, atomic force microscopy, and scanning tunneling microscopy. Comparatively, films transferred with PLA, PPA, PMMA/PC, and PMMA have a two-fold higher roughness and a five-fold higher chemical doping. Using PC scaffolds, we demonstrate the clean transfer of CVD multilayer graphene, fluorinated graphene, and hexagonal boron nitride. Our annealing free, PC transfers enable the use of atomically-clean nanomaterials in biomolecule encapsulation and flexible electronic applications.
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PMID:Annealing free, clean graphene transfer using alternative polymer scaffolds. 2558 Sep 91


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