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At least 19 recordsLinked to original sources

PubMed1976

Effective pulmonary capillary blood flow in infants with birth asphyxia.

Effective pulmonary capillary blood flow was measured on the first day of life in twenty term infants with birth asphyxia and twenty-five normal term infants. The infants studied showed no clinical or laboratory evidence of respiratory distress. The mean effective pulmonary capillary blood flow of 121 ml/kg/min in the birth asphyxia group was significantly lower than the mean of 162 ml/kg/min in the normal group. The possible relationship of birth asphyxia and pulmonary hypoperfusion in the aetiology of the idiopathic respiratory distress syndrome is discussed.

Asphyxia Neonatorum↗

PubMed1979

Role of single-breath carbon monoxide-diffusing capacity in monitoring the pulmonary effects of bleomycin in germ cell tumor patients.

Serial pulmonary function tests including single-breath carbon monoxide-diffusing capacity (DLCO), forced vital capacity (FVC), and forced expiratory volume in 1 sec were performed in a relatively homogeneous group of male patients with germ cell tumors treated with vinblastine, bleomycin, and cis-diamminedichloroplatinum. Of the pulmonary function tests used, the DLCO was shown to be the most sensitive indicator of subclinical bleomycin pulmonary effects. Decreases in DLCO were both total dose and schedule dependent. Patients receiving their total dose of bleomycin at a rate of 25 +/- 2 (S.D.) units/week developed a linear decrease in DLCO with increasing total doses of bleomycin. Changes in FVC did not correlate with bleomycin total dose. Although both the mean DLCO and FVC decreased after completion of bleomycin therapy, the mean FVC returned to base-line levels rapidly, whereas the decrease in mean DLCO was persistent for several months. When routine volumetric tests (FVC and forced expiratory volume in 1 sec) and DLCO are used in a systematic manner, DLCO is the most sensitive indicator of the subclinical pulmonary effects of bleomycin in germ cell tumor patients treated with vinblastine, bleomycin, and cis-diamminedichloroplatinum.

Adult↗

PubMed1978

Cardiac and pulmonary effects of therapy with albuterol and isoproterenol.

This study evaluated the cardiac and pulmonary effects of administering multiple inhaled doses of albuterol, isoproterenol sulfate, and placebo in ten patients with reversible obstructive disease of the airways. The pulmonary effects of therapy with albuterol were similar in magnitude to those of isoproterenol but lasted longer. The inotropic and chronotropic effects of therapy with isoproterenol were greater than those of albuterol. It appears that albuterol has beta2-adrenergic selectivity over a wide range of dosages and is an effective bronchodilator drug.

Adolescent↗

PubMed1975

Pulmonary microembolism associated with massive transfusion: II. The basic pathophysiology of its pulmonary effects.

In animals pulmonary hypertension, a decrease in total body O2 consumption and metabolic acidosis occur after transfusion of blood with an elevated screen filtration pressure (SFP) through standard blood transfusion filters. The purpose of this study was to define in detail the pulmonary abnormalities that develop following transfusion of blood with an elevated SFP through standard blood transfusion filters. Exchange transfusions of approximately twice blood volume were administered through standard commercially available blood transfusion filters (measured pore size--200 microns) to 6 animals. SFP measurements verified the presence of large numbers of aggregates in the transfusions. Although filters reduced SFP of the stored blood somewhat, numerous microaggregates passed the filters, and post-filtration SFP remained high. After transfusion average O2 consumption decreased to 77% of normal and metabolic acidosis developed. Pulmonary arterial hypertension was associated with an increase in pulmonary shunting of blood and a decrease in pulmonary diffusing capacity. The presence of extensive numbers of microemboli in the pulmonary arteriolar and capillary bed was confirmed by microscopic examination of lung tissue.

Acidosis↗

PubMed1991

Cardiovascular and pulmonary effects of morphine in conscious pigs.

Cardiovascular and pulmonary effects of morphine (1 mg/kg bolus iv) were investigated in conscious chronically instrumented pigs, a species exhibiting an excitable response. Control animals received an equivalent volume (less than 2 ml) of normal saline. Morphine induced an immediate but small increase in cardiac output and substantial increases in heart rate, mean systemic and pulmonary arterial pressure, left and right ventricular work, hematocrit, and hemoglobin concentration, but did not change stroke volume or systemic vascular resistance. Morphine administration also led to a gradual increase in ventilatory rate and rapid increases in tidal volume, expired and alveolar ventilation, ventilation-perfusion ratio, and shunt fraction. In addition, morphine administration produced substantial decrements in arterial and mixed venous PO2, hemoglobin saturation and mixed venous O2 content; no change in arterial O2 content; and a widening of the arteriovenous O2 difference. Arterial O2 transport was increased slightly. Finally, it produced substantial increments in arterial and mixed venous PCO2 and substantial decrements in arterial and mixed venous pH. It was concluded that arterial O2 delivery did not adequately rise to meet tissue O2 demand, in part because an appropriate increase in cardiac output was attenuated by morphine, and in part because morphine impaired pulmonary gas exchange.

Animals↗

PubMed1989

Comparison of the cardiovascular and pulmonary effects of oral celiprolol, propranolol and placebo in normal volunteers.

1. The effects on heart rate, blood pressure and pulmonary function of single oral doses of celiprolol hydrochloride (400 mg), and propranolol (40 mg) were compared with placebo in 12 healthy volunteers, in a double-blind three-period crossover study. 2. Celiprolol had no effect on heart rate while propranolol caused a significant reduction compared with placebo. Systolic blood pressure was reduced by propranolol but not celiprolol, whereas standing diastolic blood pressure was lowered by both drugs. 3. The maximal expiratory flow at 50% vital capacity (MEF.50), was significantly lower after propranolol compared with placebo and celiprolol. Celiprolol had no effect on the flow-volume loop parameters. 4. Effective pulmonary blood flow was significantly increased by celiprolol, but reduced by propranolol. 5. A high incidence of subjective side-effects were experienced on celiprolol (10/12; particularly unpleasant in 5). Side-effects were experienced to a lesser extent on placebo (8/12). Only one volunteer experienced a side-effect on propranolol. 6. Oral celiprolol exerts its hypotensive effect by vasodilatation without reflex tachycardia. It does not cause airways obstruction in healthy subjects.

Adrenergic beta-Antagonists↗

PubMed1992

Pulmonary effects of inhaled zinc oxide in human subjects, guinea pigs, rats, and rabbits.

Occupational exposure to freshly formed zinc oxide (ZnO) particles (less than 1.0 micron aerodynamic diameter) produces a well-characterized response known as metal fume fever. An 8-hr threshold limit value (TLV) of 5 mg/m3 has been established to prevent adverse health effects because of exposure to ZnO fumes. Because animal toxicity studies have demonstrated pulmonary effects near the current TLV, the present study examined the time course and dose-response of the pulmonary injury produced by inhaled ZnO in guinea pigs, rats, rabbits, and human volunteers. The test animals were exposed to 0, 2.5, or 5.0 mg/m3 ZnO for up to 3 hr and their lungs lavaged. Both the lavage fluid and recovered cells were examined for evidence of inflammation or altered cell function. The lavage fluid from guinea pigs and rats exposed to 5 mg/m3 had significant increases in total cells, lactate dehydrogenase, beta-glucuronidase, and protein content. These changes were greatest 24 hr after exposure. Guinea pig alveolar macrophage function was depressed as evidenced by in vitro phagocytosis of opsonized latex beads. Significant changes in lavage fluid parameters were also observed in guinea pigs and rats exposed to 2.5 mg/m3 ZnO. In contrast, rabbits showed no increase in biochemical or cellular parameters following a 2-hr exposure to 5 mg/m3 ZnO. Differences in total lung burden of ZnO, as determined in additional animals by atomic absorption spectroscopy, appeared to account for the observed differences in species responses. Although the lungs of guinea pigs and rats retained approximately 20% and 12% of the inhaled dose, respectively, rabbits retained only 5%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1976

Effective pulmonary blood flow in preterm and light-for-date infants.

Using a method employing low concentrations (3%) of nitrous oxide, we measured effective pulmonary capillary blood flow (Qpc eff) in 23 preterm infants, 26 light-for-date infants, and 15 infants who were both preterm and light-for-date. All infants studied had no clinical or laboratory evidence of idiopathic respiratory distress syndrome (IRDS) and were studied before the age of 48 hours. The mean Qpc eff of 175 ml/kg/min in preterm infants (a group at high risk of developing IRDS), although significantly less than the mean of 214 ml/kg/min found in light-for-date infants (a group with a low risk of developing IRDS), was similar to that reported in normal term infants. The mean result for preterm, light-for-date infants was 189 ml/kg/min. No evidence was found that preterm infants were predisposed to IRDS as a consequence of preexisting pulmonary hypoperfusion.

Birth Weight↗

PubMed1986

Celiprolol, atenolol and propranolol: a comparison of pulmonary effects in asthmatic patients.

Celiprolol, a new beta-adrenoceptor antagonist, blocks serotonin- and methacholine-mediated bronchoconstriction in animals, even in the presence of propranolol. In two, randomized, placebo-controlled, 5-way crossover trials, the pulmonary effects of celiprolol 200 and 400 mg, propranolol 40 mg and atenolol 100 mg were compared in 34 asthmatic patients. Pulmonary function was measured after single doses of each agent, and again following subsequent, graded doses of albuterol or isoproterenol aerosol. Changes in one-second forced expiratory volume (FEV1) and maximal midexpiratory flow rate (FEF25-75) prior to albuterol or isoproterenol were positive after placebo and both doses of celiprolol. Propranolol, and to a lesser extent, atenolol, caused significant reductions in both measures of pulmonary function. Overall changes in FEV1 following each drug plus isoproterenol or albuterol were positive, in the rank order, celiprolol approximately placebo greater than atenolol greater than propranolol. Propranolol pretreatment caused a significant reduction in the effect of bronchodilator. Unlike atenolol and propranolol, celiprolol was highly bronchosparing and did not antagonize sympathomimetic bronchodilators.

Adrenergic beta-Antagonists↗

PubMed1987

Chronic pulmonary effects in guinea pigs from prolonged inhalation of cotton dust.

Inhalation of cotton dust has been associated with development of byssinosis. An animal model has been described recently in which guinea pigs exposed to cotton dust for a 6-week period demonstrated acute respiratory reactions consisting of increased breathing frequency, reduced tidal volume, and airflow fluctuations most prominent on the first day of exposure following a period without exposure, often referred to as a "Monday" response (Ellakkani et al., 1984). The current study examined the effects of cotton dust inhalation for 52 weeks in order to evaluate the animal model for ability to demonstrate more chronic effects of cotton dust exposure. Twenty guinea pigs were exposed to 21 mg/m3 cotton dust for 6 hr/day, 5 days/week, for 52 weeks. Twenty control animals received sham exposure. Parameters used to indicate chronic effects included respiratory measurements, weight gain, lung volume and weight, and histopathological evaluation. Respiratory measurements were taken while animals were breathing ambient air and also while breathing a mixture of 10% CO2, 20% O2, and 70% N2. Pulmonary effects were noted to change during the 12 months of exposure. For the first 3 months experimental animals displayed an increase in breathing frequency and a decrease in breathing volume measured as whole-body plethysmographic pressure. These effects were pronounced on the "Monday" of each week. During Months 3-6, reactions occurred on each day of exposure, although Monday responses were most severe. After 6 months, respiratory reactions were pronounced daily. Other indications of a chronic effect of exposure were increased lung volume, measured by water displacement, 15.0 +/- 3.3 ml (mean +/- SD) for the exposed group, compared with 9.8 +/- 2.0 ml for the controls; increased lung weight 9.4 +/- 1.5 g vs 7.0 +/- 0.8 g; and bronchiolar epithelial hyperplasia and hyperplasia of alveolar type II cells. Additionally, a histomorphometric study of the lungs performed by others (Coulombe et al., 1986) detected changes in the peripheral conducting airways, including increased thickness of bronchiolar epithelium and increased thickness of septa at the alveolar level, denoting chronic exposure. Taken together, these results indicated chronic respiratory effects in guinea pigs as a result of 52 weeks of continued exposure to cotton dust. The parallel in development of symptoms in guinea pigs and in humans exposed to cotton dust indicates that the guinea pig is a suitable model for byssinosis.

Animals↗

PubMed1992

Dose-dependent pulmonary effects of inhaled endotoxin in guinea pigs.

As a cell wall component of gram-negative bacteria, endotoxin is thought to play a significant role in the respiratory effects of inhaled organic dusts which are microbially contaminated. Assessment of occupational survey data and clinical studies suggests that few measureable, acute functional changes occur below 30-50 ng/m3 endotoxin (as sampled in airborne dust with a vertical elutriator). Little information is available on the inflammatory effects of inhaled endotoxin at these low concentrations. The present study examined the dose-response relationship between inhaled endotoxin and functional, biochemical, and histological endpoints in the lungs of guinea pigs. Animals were exposed to 0.03 to 50.5 micrograms/m3 aerosolized endotoxin or the vehicle water for 4 hr. At 2 hr into exposure, significant decreases in specific airway conductance were observed only in animals exposed to 9.6 and 50.5 micrograms/m3 endotoxin (17.3 +/- 1.2 and 35.5 +/- 0.5% decreases from baseline values, respectively (mean +/- SE)). Total cell count and lactate dehydrogenase levels in bronchoalveolar lavage fluid were significantly elevated at 24 hr after exposure in all endotoxin-exposed groups except the lowest dose, 0.03 micrograms/m3 (P < 0.05). Polymorphonuclear leukocyte influx into the alveolar region was also dependent on the concentration of inhaled endotoxin. Thus, LDH activity, a biochemical marker of cell injury, and total cell counts and polymorphonuclear leukocytes, markers of inflammation, were more sensitive indices of adverse pulmonary effects from inhaled endotoxin than a functional measurement. These results suggest that subtle inflammatory changes may occur at airborne endotoxin concentrations which may produce no acute respiratory symptoms.

Administration, Inhalation↗

PubMed1979

Cardiovascular and pulmonary effects of thromboxane B2 in the dog.

The hemodynamic properties of thromboxane B2 (TxB2), a product of prostaglandin endoperoxide metabolism, have not been thoroughly described. TxB2 is a bronchoconstrictor, but its effects on the systemic circulation and circulating platelets are unknown. Its precursor, thromboxane A2(TxA2), is a potent vasoconstrictor as well as a platelet-aggregating agent. Using intact anesthetized dogs, we investigated the effects of TxB2 on pulmonary artery pressure (PAP), airway pressure (AP), systemic arterial pressure (SAP), and myocardial contractility (MC). Vascular responses were evaluated in relation to changes in platelet population and aggregability. Intravenous TxB2 (25 and 50 micrograms/kg) increased AP (mean 62% and 69%) and PAP (50% and 86%), respectively, whereas SAP and MC responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP responses were inconsistent. Left ventricular injections (25 micrograms/kg) also increased AP (36%) and PAP (36%). Intraventricular administration of TxB2 produced a consistent elevation of SAP (10%) with a concomitant fall in MC (11%). These vascular responses were not consistent with alterations in platelet number or aggregability. A tachyphylactic response to TxB2 developed in AP and PAP at both dose levels and with both routes of administration. Intravenous and intraventricular TxB2 (25 micrograms/kg) produced a parallel decreasing response in PAP, suggesting the possible saturation of TxB2 binding sites or the depletion of a catabolic enzyme in the lung.

Animals↗

PubMed1990

Distribution, localization, and pulmonary effects of yttrium chloride following intratracheal instillation into the rat.

Metabolic behavior and pulmonary toxicity of yttrium chloride (YCl3) deposited in the lung was investigated. Yttrium chloride was instilled intratracheally into rats and the time-course and dose-related changes in distribution of Y between lung tissue and bronchoalveolar lavage fluid (BALF) and pulmonary inflammatory responses were investigated. Pulmonary clearance of Y was very slow and the half-life was estimated to be 168 days. Yttrium content in the supernatant of BALF did not exceed 5 micrograms Y/lung even when a dose of 200 micrograms Y/rat was administered, suggesting that the alveolar surface fluid could retain at most 5 micrograms Y. On the other hand, Y content in the pellet of BALF changed with the number of macrophages retrieved in BALF in both time-course and dose-response experiments. Transmission electron microscopy and X-ray microanalysis suggested that Y was localized in lysosomes of alveolar and interstitial macrophages, and basement membranes. These results clearly explain the long pulmonary half-life of Y. beta-Glucuronidase activity and calcium and phosphorous contents in the supernatant of BALF increased significantly even at the lowest dose (10 micrograms Y/rat). Comparative dose-effect profiles of lactate dehydrogenase activity in BALF supernatant revealed that 1 mol of YCl3 is equivalent to about one-third mole of cadmium compounds and about 3 mol of zinc oxide in the potency for acute pulmonary toxicity.

Animals↗

PubMed1991

Acute pulmonary effects of nitrogen dioxide exposure during exercise in competitive athletes.

The acute pulmonary responses of athletes after short-term exposure to ambient concentrations of NO2 during heavy exercise have been examined. Intercollegiate male athletes were screened for history of cardiac disease, respiratory disease, allergic conditions and extensive exposure to pollutants. After completion of serum IgE level determination, exercise tolerance test and methacholine challenge test with normal results, nine healthy subjects 18 to 23 years of age were exposed to filtered air and to 0.18 and 0.30 ppm NO2 for 30 min on different days while exercising on a treadmill. Pulmonary function parameters were measured before and after each exposure. In this study, no statistically significant changes were observed in FEV1, RT PEFR, and Vmax50% after exposure to 0.18 and 0.30 ppm NO2. For these selected healthy athletes, short-term exposure to ambient NO2 levels during heavy exercise does not affect adversely the pulmonary function.

Adult↗

PubMedDate not supplied

[Hemodynamic and pulmonary effects of nifedipine].

The authors reviewed the actions of nifedipine, a blocker of calcium channels, on the systemic and pulmonary circulation. The mechanism of action of the drug on the systemic and pulmonary circulation and on the gas exchange is discussed. The main effects of nifedipine on the coronary circulation and indications for therapeutic use of the drug are discussed on the topics of coronary insufficiency, systemic and pulmonary blood hypertension, acute respiratory failure, and Raynaud's phenomenon.

Animals↗

PubMed1992

Endothelin: systemic arterial and pulmonary effects of a new peptide with potent biologic properties.

Endothelial cells produce the 21-amino acid peptide endothelin, which is formed from its precursor, big endothelin, via the activity of converting enzyme. The basal production of the peptide is stimulated by epinephrine, angiotensin II, arginine vasopressin, transforming growth factor beta, thrombin, interleukin-1, and hypoxia. In vascular smooth muscle, endothelin binds to a specific receptor (ETA-subtype), which activates phospholipase C, leads to the formation of inositol trisphosphate, diacylglycerol (which activates protein kinase C), and increased intracellular Ca2+. In certain blood vessels, the endothelin receptor on vascular smooth muscle is linked to a voltage-operated Ca2+ channel via a G-protein. This explains why Ca2+ antagonists inhibit endothelin-induced contractions in certain, but not all, blood vessels. In the human forearm circulation, Ca2+ antagonists do prevent endothelin-induced contractions and unmask endothelin-induced vasodilation mediated by endothelial prostacyclin production (via the ETB-receptor). The pulmonary circulation plays an important role in the metabolism of endothelin, as the lungs take up large quantities of the peptide during passage. Endothelin has profound vasoconstrictor effects in the pulmonary circulation (and also in bronchial tissue), and its production is augmented in pulmonary hypertension. In systemic hypertension, the circulating endothelin levels appear to be normal. In atherosclerosis and other forms of vascular disease, circulating endothelin levels are increased. Thus, endothelin is a potent mediator in the systemic and pulmonary circulation and, in particular, in diseases of the vasculature.

Animals↗

PubMed1977

The possible roles of histamine, 5-hydroxytryptamine and prostaglandin F2alpha as mediators of the acute pulmonary effects of endotoxin.

1 In an attempt to investigate the possible role of released vasoactive substances in mediating the pulmonary pressor responses to E. coli endotoxin, cats were pretreated with histamine, 5-hydroxytryptamine (5-HT) or prostaglandin antagonists, with a histamine depleting agent (compound 48/80) or with an inhibitor of prostaglandin synthetase (sodium meclofenamate).2 The administration of endotoxin (2 mg/kg) resulted in a rapidly developing pulmonary hypertension (pressure twice normal after 2-3 min), increases in right atrial and intratracheal pressures, systemic hypotension and bradycardia. These effects were unaffected by methysergide in a dose sufficient to prevent the effects of intravenously administered 5-HT.3 Endotoxin responses were also unaffected by a combination of mepyramine and burimamide in doses sufficient to reduce markedly the effects of intravenously-administered histamine. In cats pretreated (chronically or acutely) with compound 48/80, endotoxin induced a transient pulmonary pressor response which was not maintained.4 The pulmonary and systemic responses to endotoxin were prevented by the prior administration of the prostaglandin antagonist, polyphloretin phosphate and by pretreatment with the prostaglandin synthetase inhibitor, sodium meclofenamate.5 It is concluded that a pulmonary vasoconstrictor prostaglandin is involved in the acute response to endotoxin in the cat.

Animals↗

PubMed1989

Renal and pulmonary effects of angiotensin converting enzyme inhibition in chronic hypoxic lung disease.

The effects of 28 days' treatment with captopril or with placebo on renal and pulmonary function were evaluated in nine patients with stable pulmonary heart disease. Captopril (25 mg twice daily) caused a 17% rise in effective renal plasma flow but no change in glomerular filtration rate, resulting in a fall in filtration fraction likely to favour natriuresis. Captopril did not alter FEV1, lung volumes, or arterial oxygen or carbon dioxide tension.

Aged↗