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Hypoxic pulmonary vasoconstriction (HPV) is encountered during ascent to high altitude. Atrial natriuretic peptide (ANP) could be an option to treat HPV because of its natriuretic, diuretic, and vasodilatory properties. Data on effects of ANP on pulmonary and systemic circulation during HVP are conflicting, partly owing to anesthesia, surgical stress or uncontrolled dietary conditions. Therefore, ten conscious, chronically tracheotomized dogs were studied under standardized dietary conditions. The dogs were trained to breathe spontaneously at a ventilator circuit. Protocol: 30min of normoxia [inspiratory oxygen fraction (FiO2)=0.21] were followed by 30min of hypoxia without ANP infusion (Hypoxia I, FiO2=0.1). While maintaining hypoxia an intravenous infusion of atrial natriuretic peptide was started with 50ng·kg body wt-1·min-1 for 30min (Hypoxia+ANP1=low dose), followed by 1000ng·kg body wt-1·min-1 for 30min (Hypoxia+ANP2=high dose). Thereafter, ANP infusion was stopped and hypoxia maintained for a final 30min (Hypoxia II). Compared to normoxia, mean pulmonary arterial pressure (MPAP) (16±0.7 vs. 26±1.3mmHg) and pulmonary vascular resistance (PVR) (448±28 vs. 764±89dyn·s-1·cm-5) increased during Hypoxia I and decreased during Hypoxia+ANP 1 (MPAP 20±1mmHg, PVR 542±55dyn·s-1·cm-5) (P<0.05). The higher dose of ANP did not further decrease MPAP or PVR, but started to have a tendency to decrease mean arterial pressure and cardiac output. We conclude that low dose ANP is able to reduce HPV without affecting systemic circulation during acute hypoxia.
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Acute hypoxia induces a decrease in plasma renin activity (PRA), mediated, e.g., by an increase in adenosine concentration, calcium channel activity, or inhibition of ATP-sensitive potassium channels. The decrease in PRA results in a decrease in angiotensin II (AngII) and plasma aldosterone concentration (PAC). This study investigates whether these hypoxia-induced mechanisms can be inhibited by the L-type voltage-dependent calcium channel antagonist nifedipine. Eight conscious, chronically tracheotomized dogs received a low sodium diet (0.5 mmol Na·kg body wt-1·day-1). The dogs were studied twice in randomized order, either with nifedipine infusion (1.5 µg·kg body wt-1·min-1, Nifedipine) or without (Control). The dogs were breathing spontaneously: first hour, normoxia [inspiratory oxygen fraction (FiO2)=0.21]; second and third hour hypoxia (FiO2=0.1). In Controls, PRA (6.8±0.8 vs. 3.0±0.5 ngAngI·ml-1·min-1), AngII (13.3±1.9 vs. 7.3±1.9 pg/ml), and PAC (316±50 vs. 69±12 pg/ml) decreased during hypoxia (P<0.05). In Nifedipine experiments, PRA (6.5±0.9 vs. 10.5±2.4 ngAngI·ml-1·min-1) and AngII (14±1.1 vs. 18±3.9 pg/ml) increased during hypoxia, whereas the decrease in PAC (292±81 vs. 153±41 pg/ml) was blunted (P<0.05). These results foster the idea that the hypoxia-induced decrease in PRA involves L-type calcium channel activity.
Our study was designed to establish whether air pollution in urbanized industrial centers of southern Poland affects the process of glycosylation in a full-term human placenta. This process of glycosylation was analyzed by the quantitative determination of the binding of WGA and LCA lectins to placental villi. The study was performed on human placentas collected in 1990-91 and 2000-01 in regions of southern Poland differing in their degree of environmental pollution: the highly polluted areas of Upper Silesia and Cracow agglomeration. The Bieszczady area with low pollution was considered the control. The concentrations of nitrogen and sulfur oxides and the concentration of aerosols were used as markers of the degree of air pollution. The direct immunofluorescence reaction of the placenta tissues with fluorescein-labeled (FITC) lectins was used. The staining of the placenta tissues was examined under a fluorescence microscope linked to an analysis system. A microdensytometric method was used to assay the amount of tissue-bound lectins. The results showed no significant effect of the three main air pollutants in the study areas in southern Poland, i.e. nitrogen and sulfur oxides and high level of aerosols, on the structure of WGAand LCA-specific glycoconjugates in human placenta. However, the marked quantitative changes in the degree of lectin binding to placental cellular structures were noted within the last 10-year period in all studied regions.
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