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Biomedical subjects

M Ansay

Publications and source records attributed to M Ansay.

At least 19 recordsLinked to original sources
PubMed1999

Effects of inhalation of dust and endotoxin on respiratory tracts of pigs.

OBJECTIVE: To assess the effects of inhalation of feed flour dust and dustborne endotoxin on respiratory tracts of pigs. ANIMALS: 29 healthy Belgian Landrace pigs. PROCEDURE: Pigs housed in an environmental chamber were exposed for 6 days to feed flour dust (1 to 15 mg/m3) and dustborne endotoxins (50 to 2,500 ng/m3). Effects were evaluated by measuring albumin concentration, lactate dehydrogenase (LDH) activity, cell composition of nasal lavage (NL) and bronchoalveolar lavage (BAL) fluids and blood, and percentages of CD4+ and CD8+ T lymphocytes in blood and lavage fluids. Dustborne endotoxin was obtained by mixing endotoxins from Escherichia coli (serotype O127:B8) with feed flour before spraying the flour in the environmental chamber. RESULTS: Exposure did not affect cell composition of NL fluid or blood. Total cell counts of BAL fluids were increased in all groups exposed to dust. Macrophage counts were increased in pigs exposed to inhalable dust concentrations as low as 4.4 mg/m3, and lymphocyte counts were increased in groups exposed to high dust concentrations. Percentages of CD4+ and CD8+ T lymphocytes in blood and lavage fluids were unchanged. In all dust-exposed groups, albumin content of BAL fluid was increased, whereas LDH activity was unaffected. Macrophage and lymphocyte infiltration and edema in the bronchi were identified by light microscopy. Effects attributable to E. coli endotoxin exposure were not identified. CONCLUSIONS: Inhalation of feed flour dust did not affect nasal mucosa but did induce bronchial airway inflammation. Dustborne endotoxins did not have effects attributable to endotoxin alone.

Albumins↗
PubMed1998

Comparison of ozone-induced effects on lung mechanics and hemodynamics in the rabbit.

The effects of rabbit exposure to ozone (O3)(0.4 ppm for 4 h) on pulmonary mechanical properties and hemodynamics have been investigated on the isolated perfused lung model. Tracheal pressure, airflow, and tidal volume were measured in order to calculate lung resistance (RL) and dynamic compliance (Cdyn). Using the arterial/venous/double occlusion method, the total pressure gradient (deltaPT) was partitioned into four components (arterial, pre-, postcapillary and venous). Dose-response curves to acetylcholine (ACh), substance P (SP), and histamine were constructed in lungs isolated from rabbits immediately or 48 h after air or O3 exposure O3 induced a significant increase in the baseline value of deltaPt, more markedly 48 h after the exposure. Immediately after the exposure, O3 partly inhibited the ACh-, SP-, and histamine-induced decreases in Cdyn and increases in RL. This inhibitory effect was still in part present 48 h after O3 treatment. In the groups studied immediately after exposure, O3 did not significantly modify the ACh-, SP-, and histamine-induced vasoconstriction. Forty-eight hours after exposure, O3 induced a contractile response to ACh and SP in the arterial segment but decreased the response to histamine. We conclude that O3 can induce direct vascular constriction. Directly, but also 48 h after exposure, O3 can inhibit the ACh-, SP-, and histamine-induced changes in lung mechanical properties. Ozone can also induce some changes in the intensity and in the location of the vascular responses to ACh, SP, and histamine.

Acetylcholine↗
PubMed1998

Effects of hyperchloremia on blood oxygen binding in healthy calves.

Three different levels of hyperchloremia were induced in healthy Friesian calves to study the effects of chloride on blood oxygen transport. By infusion, the calves received either 5 ml/kg of 0.9% NaCl (low-level hyperchloremia; group A), 5 ml/kg of 7.5% NaCl (moderate hyperchloremia; group B), or 7.5 ml/kg of 7.5% NaCl (high-level hyperchloremia; group C). Blood was sampled from the jugular vein and the brachial artery. Chloride concentration, hemoglobin content, arterial and venous pH, PCO2, and PO2 were determined. At each time point (0, 15, 30, 60, and 120 min), the whole blood oxygen equilibrium curve (OEC) was measured under standard conditions. In groups B and C, hyperchloremia was accompanied by a sustained rightward shift of the OEC, as indicated by the significant increase in the standard PO2 at 50% hemoglobin saturation. Infusion of hypertonic saline also induced relative acidosis. The arterial and venous OEC were calculated, with body temperature, pH, and PCO2 values in arterial and venous blood taken into account. The degree of blood desaturation between the arterial and the venous compartments [O2 exchange fraction (OEF%)] and the amount of oxygen released at tissue level by 100 ml of bovine blood (OEF vol%) were calculated from the arterial and venous OEC combined with the PO2 and hemoglobin concentration. The chloride-induced rightward shift of the OEC was reinforced by the relative acidosis, but the altered PO2 values combined with the lower hemoglobin concentration explained the absence of any significant difference in OEF (% and vol%). We conclude that infusion of hypertonic saline induces hyperchloremia and acidemia, which can explain the OEC rightward shift observed in arterial and peripheral venous blood.

Animals↗
PubMed1997

Ozone-induced stimulation of pulmonary sympathetic fibers: a protective mechanism against edema.

Tropospheric ozone exerts well-described toxic effects on the respiratory tract. Less documented, by contrast, is the ability of ozone to induce protective mechanisms against agents that are toxic to the lungs. In particular, interactions between ozone and the sympathetic nervous system have never been considered. Using a model of permeability edema in isolated perfused rabbit lungs, we report here that, immediately after exposure of rabbits to 0.4 ppm ozone for 4 hr, the pulmonary microvascular responses to acetylcholine and substance P are completely blocked. Several lines of evidence, including partial inhibition of the ozone-induced protective effect by several drugs (alpha2- and beta-adrenergic antagonists, neuropeptide Y antagonist, guanethidine), measured levels of released catecholamines in blood and urine and the in vitro response of isolated lungs exposed to 0.4 ppm ozone all seem to suggest that ozone can stimulate pulmonary adrenergic fibers and induce the local release of catecholamines and neuropeptide Y, this resulting in transient protection against pulmonary edema. We also showed that, 48 hr after the exposure, ozone increased the baseline microvascular permeability and the response to low concentrations of acetylcholine.

Acetylcholine↗
PubMed1997

Influence of age and breed on the binding of oxygen to red blood cells of bovine calves.

The influence of somatic growth and genetic selection on the whole blood oxygen equilibrium curve (OEC) was measured under standard conditions in double-muscled and dairy calves during their first 3 mo of life. Crossbreed animals were also investigated. Hemoglobin, 2,3-diphosphoglycerate (DPG), Cl, and Pi concentrations were also measured. The percentage of fetal hemoglobin (HbF) was determined. The influence of exogenous Cl, Pi, and pH on the OEC was also assessed. The PO2 at 50% hemoglobin saturation (P50) increased during somatic growth, probably because of the increase in DPG recorded in double-muscled neonates and to the progressive disappearance of HbF in both breeds. The oxygen exchange fraction (OEF%) was used to assess the combined influence of the OEC shift and OEC shape changes on blood oxygen desaturation under standard conditions, when the PO2 decreases within a physiological range. The OEF% showed an increase during the first month, then a stabilization. The effects of Cl, Pi, and pH in Friesian calves were similar as in adult cattle. Double-muscled neonates had a lower P50, OEF% values, and DPG concentrations and higher hemoglobin and Cl concentrations than Friesian neonates. The Pi concentration and the percentage of HbF were similar in both breeds. The pH and the Cl concentration had significantly less effect on the OEC in double-muscled than in Friesian calves. Crossbreed animals exhibited intermediate parameter values, between those recorded for double-muscled and Friesian calves. All differences between breeds progressively disappeared during the first month. These data show that blood function changes markedly in calves during the first month of life and that genetic selection can alter blood function.

Age Factors↗
PubMed1996

Relationship between parathion and paraoxon toxicokinetics, lung metabolic activity, and cholinesterase inhibition in guinea pig and rabbit lungs.

Kinetic parameters of parathion and paraoxon uptake were determined in isolated and perfused rabbit and guinea pig lungs. They were related to organophosphate-induced lung cholinesterase inhibition. A single pass procedure was used to perfuse the lungs with an artificial medium perfusate containing paraoxon or parathion. The paraoxon and parathion concentrations were determined in the effluents collected at chosen intervals over an 18-min period beginning at the start of perfusion. Three inflowing concentrations (1 nmol/ml, 10 nmol/ml, and 20 nmol/ml) were tested in guinea pig lungs and one (10 nmol/ml) in rabbit lungs. Cholinesterase activity was determined at time 0 and at the end of the experiment. The lungs abundantly extracted paraoxon and parathion over the perfusion period. The extraction ratio was consistently greater in guinea pig than in rabbit lungs. The uptake velocity varied biexponentially in time, suggesting the existence of two compartments. Initial uptake velocities (A, B) and slopes (alpha and beta) were calculated for both compartments. In guinea pigs, A, B and A + B increased proportionally to the supply rate of paraoxon and parathion while a and b remained constant. No significant difference was observed between parathion and paraoxon uptake kinetics. Parameter B was the only one to differ significantly between the two species (rabbits: 8.19 +/- 1.53 for parathion and 6.85 +/- 1.26 for paraoxon; guinea pigs: 12.75 +/- 0.88 for parathion and 15.02 +/- 3.84 for paraoxon). In the lungs of both species, there was a linear relation between y, the percentage of cholinesterase inhibition induced by either organophosphate, and X, the total amount of drug taken up by the lung tissue (in nmol/g/18 min). The following equations were obtained: y = 0.128 x + 0.979 (R2 = 0.89, p < 0.001 for paraoxon); y = 0.120 x - 6.57 (R2 = 0.82, p < 0.005 for parathion). No difference was observed between the two organophosphates. After treatment with the cytochrome P450 inhibitor piperonyl butoxide, the above relations ceased to apply, but this treatment did not influence the kinetics of paraoxon and parathion uptake. The IC50 value calculated for paraoxon, i.e., the paraoxon concentration required to produce 50% inhibition of lung cholinesterase activity, was similar for guinea pigs (2.22 10(-7) +/- 0.22 M) and rabbits (2.36 10(-7) +/- 0.24 M). In conclusion, the biexponential evolution of the velocity of paraoxon and parathion uptake by the lungs thus demonstrates the presence of two pools. The lower extraction ratios calculated for rabbit lungs reflect the lower initial uptake velocity of the second compartment. In the range of concentrations investigated in guinea pigs, no saturable mechanism could be demonstrated for paraoxon and parathion. Cytochrome P450-related lung metabolic activity, through which parathion is converted to paraoxon, appears as a major step in parathion-induced lung cholinesterase inhibition, although it does not appear to affect parathion toxicokinetics.

Animals↗
PubMed1996

A morphometric and functional study of the toxicity of atmospheric ammonia in the extrathoracic airways in pigs.

The effects of atmospheric ammonia (NH3) on the nasal and tracheal mucosa of pigs were investigated by morphometric and functional methods. Pigs were exposed to four concentrations of NH3 [5 (control), 25, 50 and 100 ppm] for 6 days in a specially designed air-pollutant exposure chamber. Samples were taken from the turbinates and the trachea, and the respiratory mucosa was examined by light and scanning electron microscopy. Dose-response curves to carbachol and isoproterenol were constructed using isolated strips of tracheal smooth muscle, with or without epithelium. In pigs exposed to ammonia, considerable mucosal injuries were observed in the turbinates but not in the trachea. The number of neutrophils in the epithelial layer and in the lamina propria, and epithelial hyperplasia were closely and significantly correlated with the concentrations of ammonia (r = 0.894, p < 0.001; r = 0.727, P < 0.001; and r = 0.818, p < 0.001, respectively). Except for the lamina propria, all these changes were significant (p < 0.05) at ammonia concentrations as low as 25 ppm. The percentage of the surface of the turbinate mucosa that was ciliated tended to decrease with increasing ammonia concentration (r = 0.439, p < 0.082). Ammonia induced smooth-muscle hyperresponsiveness to carbachol with a close linear correlation between individual values of the carbachol-induced maximal effect and the NH3 concentrations (r = 0.526, p < 0.003). While mechanical destruction of the epithelium induced an increase in Emax in the control group, no difference was observed between the intact and denuded strips from animals exposed to ammonia. The response to isoproterenol was not influenced by ammonia. It was concluded that quantitative histological analysis of the inflammatory infiltration and epithelial hyperplasia in the turbinates is a useful tool for quantifying the effects of atmospheric pollutants in pigs; a 6-day exposure to ammonia induces nasal irritation and functional disturbances of the tracheal smooth-muscle contractions at concentrations as low as 25 ppm.

Adrenergic beta-Agonists↗
PubMed1996

Interactions between acetylcholine and substance P effects on lung mechanics in the rabbit.

The pharmacological mechanisms involved in the acetylcholine (ACh)- and substance P (SP)-induced changes in pulmonary mechanics were studied in isolated perfused rabbit lungs. Tracheal pressure (Ptr) and airflow were measured by a Fleisch pneumotachograph and pressure transducers. Air volume, lung resistance (RL) and dynamic compliance (Cdyn) were calculated. ACh induced a dose-dependent increase in Ptr and RL, and a decrease in Cdyn. These effects were strongly prevented by atropine, and partly by SR140333, a neurokinin NK1 receptor antagonist; SR48968, a neurokinin NK2 receptor antagonist; indomethacin and antihistaminics. Ketanserin had no significant protective effect against ACh. SP also induced concentration-dependent increases in RL and decreases in Cdyn. SR140333 and atropine strongly inhibited the effects of SP, while ketanserin, SR48968, antihistaminics and indomethacin did not protect the lungs against this drug. 5-hydroxytryptamine induced no significant change in lung mechanic parameters. Cumulative concentrations of histamine increased RL and decreased Cdyn. We conclude that ACh-induced changes in lung resistance and compliance are in part mediated by a direct effect on airway smooth muscle and in part by the stimulation of C fibers, by the release of histamine from mast cells and by the synthesis of arachidonic acid metabolites. In turn, the effects of SP on lung mechanics are partly due to cholinergic activation.

Acetylcholine↗
PubMed1996

Chronic exposure of pigs to airborne dust and endotoxins in an environmental chamber: technical note.

A new experimental setup was developed to expose pigs to dust and airborne endotoxins in an environmental chamber, at levels liable to be encountered in pig farm buildings. The following parameters were evaluated in a chamber containing two pigs of 10 kg body-weight: inhalable and respirable dust gravimetric concentrations were measured using area samplers and expressed as mg/m3. The respirable dust concentration was also measured using a "TM digital microP respirable dust-measuring instrument', which has been shown to give similar results to the gravimetric method. The endotoxin concentration was evaluated using the Limulus-assay and expressed as ng/m3 of air containing the inhalable or respirable dust or as ng/mg of inhalable and respirable dust. Feed flour dust was introduced into the chamber to obtain different concentrations of inhalable and respirable dust ranging from 3.62 to 76.66 mg/m3 and from 0.24 to 1.40 mg/m3, respectively. The endotoxin concentration was modulated by mixing the feed flour with Escherichia coli endotoxins before blowing it into the chamber. The endotoxin concentrations in the air containing inhalable or respirable dust ranged from 28.9 to 270.0 ng/m3 and from 2.22 to 36.38 ng/m3, respectively, depending on the amount of endotoxins added to the dust. Data were also obtained in a piggery. The experimental setup detailed in this paper could be used to study the significance of air contaminants in the development of pig respiratory diseases.

Air Pollution, Indoor↗
PubMed1995

Modulation of acetylcholine, capsaicin and substance P effects by histamine H3 receptors in isolated perfused rabbit lungs.

The modulatory role of histamine H3 receptors in pulmonary oedema induced by acetylcholine, capsaicin and by exogenous substance P was investigated in isolated, ventilated rabbit lungs. Endothelial permeability was evaluated by measuring the capillary filtration coefficient (Kf,c). Acetylcholine (10(-8) to 10(-4) M), substance P (10(-10) to 10(-6) M), capsaicin (10(-4) M) and 5-hydroxytryptamine (5-HT) (10(-4) M) induced an increase in the Kf,c. Carboperamide, a novel histamine H3 receptor antagonist, induced a significant leftward shift of the concentration-response curve to acetylcholine and also enhanced the effect of capsaicin on the Kf,c, while it had no significant effect on the response to substance P and 5-HT. Imetit, a new histamine H3 receptor agonist, strongly inhibited the effects of acetylcholine and capsaicin. Imetit also strongly protected the lung against substance P effects but did not prevent the 5-HT-induced increase in the Kf,c. Carboperamide completely blocked the inhibitory effect of Imetit on the acetylcholine response. (R)-alpha-Methylhistamine, an other histamine H3 receptor agonist, had the same protective effect against acetylcholine response as Imetit. We conclude that histamine H3 receptors could protect the lung against acetylcholine- and capsaicin-induced oedema via a prejunctional modulatory effect on the C-fibres. However, since the response to exogenous substance P was also inhibited by histamine H3 receptor stimulation, the presence of such receptors at a postsynaptic level, probably on mast cells, was also suggested.

Acetylcholine↗
PubMed1995

Protective effect of various antagonists of inflammatory mediators against paraoxon-induced pulmonary edema in the rabbit.

The protective effect of some antagonists of various inflammatory mediators against paraoxon-induced increases in endothelial permeability has been investigated in isolated perfused rabbit lungs. The edema induced by paraoxon has been previously related to a chain reaction mediated by acetylcholine. Lungs were ventilated and blood-free perfused with a constant flow. Arterial and venous pressures and lung weight were continuously recorded. Endothelial permeability was evaluated by measuring the capillary filtration coefficient (Kf,c). Paraoxon (4 x 10(-4) M) was injected in the perfusion circuit, in lungs with or without pretreatment with atropine, ketanserin, clonidine, morphine, indomethacin, and terfenadine plus cimetidine. Paraoxon induced a time-dependent increase in the Kf,c, a maximal effect being recorded 60 min after the injection. All the antagonists used as pretreatment significantly reduced the maximal effect recorded after paraoxon. These results show that muscarinic receptor antagonists, inhibitors of neuropeptides release, cyclooxygenase inhibitors, and 5-hydroxytryptamine and histamine receptor antagonists can protect the lung against the edema induced by paraoxon. This protective effect is due to inhibition of the chain reaction triggered by acetylcholine.

Animals↗
PubMed1995

Mechanisms of substance P-induced pulmonary oedema in the rabbit: interactions between parasympathetic and excitatory NANC nerves.

The pharmacological mechanisms involved in the substance P (SP)-induced pulmonary oedema were studied in isolated perfused rabbit lungs. Substance P induced a dose-dependent increase in the capillary filtration coefficient (Kf,c), responsible for oedema. Atropine, hemicholinium-3 and ruthenium red pretreatment partly protected the lungs against SP effects, while tetrodotoxin and hexamethonium did not significantly modify them. (+/-)CP96,345, a NK1 receptor antagonist, completely inhibited the SP-induced increase in the Kf,c. Like SP, acetylcholine (ACh) and capsaicin also increased the Kf,c. Atropine and (+/-)CP96,345 completely blocked the oedema induced by both drugs. Tetrodotoxin and ruthenium red strongly inhibited the response to capsaicin and acetylcholine. It was concluded that SP-induced pulmonary oedema is in part mediated by a stimulating action on cholinergic efferent nerves, with subsequent release of endogenous acetylcholine. Acetylcholine can, in turn, stimulate the release of SP from excitatory non adrenergic, non cholinergic nerves. The effects induced by capsaicin and exogenous acetylcholine, thus endogenous SP, involve tetrodotoxin-sensitive mechanisms, while those produced by exogenous SP are tetrodotoxin-resistant.

Acetylcholine↗
PubMed1995

Endogenous nitric oxide modulates acetylcholine-induced edema and vasoconstriction in isolated perfused rabbit lungs.

The modulatory role of endogenous nitric oxide (NO) on pulmonary edema induced by acetylcholine (ACh), capsaicin, substance P (SP) and 5-hydroxytryptamine (5-HT) was investigated by using an inhibitor of NO synthase, N-omega-nitro-L-arginine (L-NNA). The effects of endogenous NO on the hemodynamic response to ACh, 5-HT and SP were also investigated. The capillary filtration coefficient (Kf,c), the total pressure gradient (delta Pt) and its four components [arterial (delta Pa), pre- (delta Pa') and post-capillary (delta Pv'), and venous gradient (delta Pv)] were evaluated on isolated, ventilated, perfused rabbit lungs. ACh (10(-8) to 10(-4) M) and SP (10(-10) to 10(-6) M) induced a concentration-dependent increase in the Kf,c. Capsaicin (10(-4) M) and 5-HT (10(-4) M) also increased this parameter. L-NNA (10(-4) M) completely inhibited the effects of ACh and capsaicin on the Kf,c, without preventing the effects of SP and 5-HT. ACh induced a concentration-dependent vasoconstriction in the precapillary segment. Pretreatment with L-NNA enhanced this increase in delta Pa' but also increased delta Pv' and delta Pv. 5-HT increased delta Pt and delta Pa proportionally to the concentration. This effect was enhanced by L-NNA, which also increased delta Pa'. SP had no significant hemodynamic effect. Pretreatment with L-NNA did not modify the response to SP. Sodium nitroprusside (10(-5) M) induced a left shift of the concentration-response curve to ACh on the Kf,c, although it did not change the response to SP. Sodium nitroprusside also inhibited the hemodynamic effect of ACh. It was concluded that endogenous NO is involved in ACh-and capsaicin-induced edema via a prejunctional stimulatory effect on the C-fibers. Endogenous NO can also modulate ACh- and 5-HT-induced vasoconstriction by exerting a vasodilator action on the whole pulmonary vascular bed.

Acetylcholine↗
PubMed1994

Multiple muscarinic receptor subtypes mediating pulmonary oedema in the rabbit.

The effects of various muscarinic antagonists on acetylcholine (ACh)-induced pulmonary oedema were studied in isolated perfused rabbit lungs. ACh induced a dose-dependent increase in the capillary filtration coefficient (Kf,c). This effect has been previously related to the activation of the capsaicin-sensitive nerve fibres and the release of substance P. Atropine, pirenzepine (M1-selective antagonist) and 4-DAMP (M3-selective antagonist) altered this response, producing a dose-dependent shift to the right of the ACh concentration-Kf,c response curve. By contrast, the M2-selective antagonist AFDX-116 shifted the ACh concentration-response curve to the left. Atropine, pirenzepine and 4-DAMP also significantly reduced the capsaicin-induced increase in the Kf,c, while AFDX-116 enhanced it. We conclude that multiple muscarinic receptor subtypes are present in the rabbit lung, located on the C-fibres, and are involved in the ACh-induced pulmonary oedema. M1 and M3 receptors seem to stimulate the release of neuropeptides from C-fibres, whereas M2 receptors have an inhibitory effect on these fibers.

Acetylcholine↗
PubMed1994

Effects of atmospheric ammonia on pulmonary hemodynamics and vascular permeability in pigs: interaction with endotoxins.

The influence of atmospheric ammonia on the somatic growth, the plasma cortisol and ammonia concentrations, and cell blood counts was investigated in pigs exposed to four concentrations (0, 25, 50, and 100 ppm) for 6 days in a specifically designed air-pollutants exposure chamber. The effects of this gas on pulmonary vascular hemodynamics and permeability and on the endotoxin-induced vascular response were also assessed using an isolated perfused lung preparation. The total pulmonary blood flow resistance (Rt) was partitioned into four components: arterial (Ra), pre-(Ra') and post-(Rv') capillary and venous (Rv). The capillary filtration coefficient (Kf,c) was evaluated by using a gravimetric technique. None of the concentrations of ammonia significantly modified the plasma cortisol and ammonia concentrations or the differential leukocyte percentages and total white blood cell count, suggesting an absence of stress related to ammonia. In exposed animals, lethargy and a concentration-related depression of the somatic growth were observed. The equation of the regression line plotted relating the mean values of the changes in body weight gain recorded over the exposure period expressed as percentages of the initial body weight (y) and ammonia concentrations (x) was: y = 3.204 - 0.177x + 0.001x2 (r = 0.99; p < or = 0.013). Endotoxin infused in the perfusion liquid of lungs from unexposed animals for 180 min induced a significant 208% increase in Rt (p < 0.001) which can be ascribed to a 338 and 180% increase in Ra' and Rv', respectively. Endotoxin infusion also induced a 62% (p < or = 0.001) increase in the Kf,c. Exposure of pigs to ammonia at any concentration did not modify the baseline values of any hemodynamic or permeability parameters. However, the hemodynamic response to endotoxins in lungs from pigs exposed to 100 ppm was significantly altered. The increase in Rt, Ra', and Rv' observed in unexposed pigs was completely abolished as shown by the limited changes in Rt (+34.9%). An intermediate reaction (+131.7%) was obtained in pigs exposed to 50 ppm. This inhibiting effect of ammonia was closely correlated with gas concentration by a linear regression (r = 0.99; p < or = 0.037). The changes in the Kf,c recorded in the control group were not modified by exposure to ammonia. It was concluded that exposure of pigs to aerial ammonia concentrations from 0 to 100 ppm for 6 days has no direct effect on the pulmonary microvascular hemodynamics and permeability and induces no stress response.(ABSTRACT TRUNCATED AT 400 WORDS)

Air Pollutants↗
PubMed1994

Modulatory effect of neuropeptide Y on acetylcholine-induced oedema and vasoconstriction in isolated perfused lungs of rabbit.

1. The modulatory role of neuropeptide Y (NPY) on pulmonary oedema induced by acetylcholine and capsaicin was investigated. The effects of NPY on the haemodynamic response to acetylcholine, phenylephrine and substance P were also investigated. 2. Isolated, ventilated, exsanguinated lungs of the rabbit were perfused with a constant flow of recirculating blood-free perfusate. The double/arterial/venous occlusion method was used to partition the total pressure gradient (delta Pt) into four components: the arterial gradient (delta Pa), the pre- and post-capillary gradients (respectively delta Pa' and delta Pv') and the venous pressure gradient (delta Pv). Endothelial permeability was evaluated by measuring the capillary filtration coefficient (Kf,c). 3. Acetylcholine (10(-8) M to 10(-4) M) and substance P (SP, 10(-10) M to 10(-6) M) induced a concentration-dependent increase in the Kf,c. Capsaicin (10(-4) M) and 5-hydroxytryptamine (5-HT) (10(-4) M) also increased this parameter. NPY (10(-8) M) completely inhibited the effects of acetylcholine and capsaicin on the Kf,c, without preventing the effects of substance P and 5-HT. 4. Acetylcholine induced concentration-dependent vasoconstriction in the precapillary segment. The effect was inhibited by NPY and aspirin, an inhibitor of cyclo-oxygenase, while ketanserin, a 5-HT2 receptor antagonist, and SR140333, a new NK1 antagonist, had no protective effect. Phenylephrine increased delta Pa at high concentration, an effect also inhibited by NPY and aspirin. Substance P had no significant haemodynamic effect. When injected together with NPY, substance P (10(-6) M) induced a significant increase in the total pressure gradient. 5. It was concluded that NPY can protect the lung against acetylcholine- and capsaicin-induced oedemavia a prejunctional modulatory effect on the C-fibres. NPY also inhibits acetylcholine-evoked precapillary and phenylephrine-induced arterial vasoconstriction, probably by interfering with cyclo-oxygenase products synthesis.

Acetylcholine↗
PubMed1994

Chloride and inorganic phosphate modulate binding of oxygen to bovine red blood cells.

The influence of Pi and Cl on the equilibrium of oxygen binding to bovine red blood cells was assessed by plotting the whole blood oxygen dissociation curve measured under standard conditions with and without added KCl and K2HPO4. Both salts shifted the oxygen dissociation curve to the right. This effect was more marked at the highest saturation levels. At a given saturation level, the anion-induced shift was linearly related to the concentration of salt added to the blood. Cl had a greater effect than Pi. The relationship between changes in Po2 at 50% hemoglobin saturation (in Torr) and concentrations of ions added (in mmol/l) was equal to 0.0515[Cl] + 0.0302[Pi] (r2 = 0.94; P < 0.001). These changes were not due to the hyperosmolality induced by salt addition, since sucrose added in place of salts was without effect on the measured parameters. The oxygen exchange fraction expressed as percentage of saturation, i.e., the difference in hemoglobin saturation when Po2 decreases from 130 to 40 Torr, was linearly correlated to added anion concentration (in mmol/l) (= 0.102[Cl] + 0.059[Pi] (r2 = 0.95; P < 0.001)). No significant interaction between the anions was observed; their effects were purely additive. This original mechanism of controlling the oxygen affinity of bovine blood may have clinical relevance: Cl and Pi could be used to increase oxygen transport efficiency in hypoxic animals.

Animals↗