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At least 1,225 records · Page 68Linked to original sources
PubMed1989

Neural influences on the human pulmonary circulation as a defence reaction to volume depletion.

The role of the autonomic nervous system in the regulation of pulmonary vasomotility in man is unsettled and great emphasis is usually given to changes in flow as the main regulating mechanism. In order to simulate hypovolemia, which might reduce the mechanical influence of flow and disclose a neural mechanism, we decreased venous return through balloon distention in the inferior vena cava in 12 normal subjects, during right heart catheterization performed for diagnostic purposes. Caval obstruction was graduated to reduce cardiac output, right atrial and pulmonary arterial pressures, without altering systemic arterial pressure and heart rate. The sympathetic nervous system was activated by arithmetic and cold pressor tests. During the former, the increase in cardiac output was more than halved by venous return restraint, as compared to the unrestrained condition, and clear pulmonary vasoconstriction, instead of vasodilatation, was observed. During the cold test, cardiac output remained almost steady, in the absence as in the presence of balloon expansion. In both conditions pulmonary arteriolar resistance rose, but in the latter this increase was more than doubled. This study suggests that the autonomic nervous system is involved in the regulation of pulmonary vasomotility in man, its role being unveiled when the mechanical influence of flow is reduced by mimicking a hypovolemic state.

Adult↗
PubMed1992

L-arginine restores endothelium-dependent relaxation in pulmonary circulation of chronically hypoxic rats.

We investigated whether loss of endothelial-derived relaxing factor (EDRF) activity in the pulmonary vessels of chronically hypoxic rats could be restored by pretreatment with L-arginine. We measured vasodilation to acetylcholine (ACh), calcium ionophore A23187, or linsidomine (Sin-1) under conditions of increased vascular tone induced by U-46619 (50 pmol/min), as well as vasoconstriction to endothelin-1 (ET) in isolated lungs pretreated with meclofenamate (3 microM). In lungs from normoxic (N) rats, in vitro L- or D-arginine (10(-3) M) did not alter vasodilation to the endothelium-dependent agents ACh (10(-9)-10(-6) M) and A23187 (10(-9)-10(-7) M), but NG-monomethyl-L-arginine (10(-3) M) completely abolished it. In lungs from rats exposed to 3 wk of hypoxia (H), vasodilation to ACh or A23187 was fully restored after in vitro L-arginine (10(-3) M) or N alpha-benzoyl-L-arginine (5 x 10(-5) M) but remained abolished after D-arginine, L-citrulline, L-ornithine, or L-argininosuccinic acid. In vivo pretreatment of H rats with L-arginine (300 mg/kg iv) 30 min before isolating the lung also restored vasodilation to A23187. Vasodilation to the endothelium-independent agent Sin-1 was similar in both groups of lungs and was not altered by in vitro L-arginine. L-arginine attenuated the increased pressor response to ET (300 pmol) of H rat lungs but had no effect in N rats. Our results demonstrate that loss of EDRF activity associated with hypoxic pulmonary hypertension may be reversed by supplying L-arginine.

Acetylcholine↗
PubMed1982

[The effect of bronchial reactivity on the hemodynamics of the pulmonary circulation in the early diagnosis of chronic non-specific lung diseases].

For the early diagnostics of chronic nonspecific pulmonary disease reversible functional disorders in persons without any symptoms and those with manifest obstruction should be identified. Provocation tests with acetylcholine-ultrasonic-aerosol have proved themselves. In 25 persons without any respiratory symptoms and in 27 patients with manifest obstruction the reactions of increased airway resistance to the hemodynamic of the pulmonary circuit were studied. It is possible to separate clearly groups with different pulmonary artery stream resistance measured by means of microheart-catheterization after inhalation of 0.01% acetylcholine-ultrasonic-aerosol.

Acetylcholine↗
PubMed1979

Purification and properties of angiotensin I-converting enzyme in human lung and its role on the metabolism of vasoactive peptides in pulmonary circulation.

Purification of angiotensin I-converting enzyme from human lung and characteristics of the enzyme was studied. Experimental pneumonitis was produced in rabbits and the change of the activity of angiotensin I-converting enzyme was studied in purpose to clarify the role of this enzyme in the metabolism of vasoactive peptides in the lung. Purification was performed using trypsin treatment, acid treatment, DE52-cellulose column chromatography, hydroxyapatite chromatography and Sephadex G-200 gel filtration. The enzyme after final step showed a single band on disc gel electrophoresis. Experimental pneumonitis was produced by injection of Complete Freund's adjuvant (acute pneumonitis) and of N-nitroso-N-methylurethane (chronic pneumonitis). In acute experiment, angiotensin I-converting enzyme activity in pulmonary tissue and in plasma was significantly decreased. In perfusion experiment, conversion of angiotensin I to angiotensin II and inactivation of bradykinin were also significantly decreased. In case of decreased activity of angiotensin I-converting enzyme in the lung, less angiotensin II will be released into systemic circulation and bradykinin will pass through the pulmonary circulation into systemic circulation, thus this may result in the decrease of systemic blood pressure.

Acute Disease↗
PubMed1996

Interaction between cold and hypoxia on pulmonary circulation in COPD.

This study was designed to investigate the interaction of mild and localized cold exposure and hypoxia on pulmonary hemodynamics in chronic obstructive pulmonary disease (COPD). Nineteen patients with COPD were studied at sea level and seven at an altitude of 2,640 m. For all patients, pulmonary hemodynamic measurements were performed 10 min after insertion of a catheter in a femoral vein and following 10 min of cold exposure. Cold exposure was restricted to the forehead, and subjects breathed air at ambient temperature. Flow and temperature of air (1.5 L.s(-1), 5 degrees C) to the forehead were chosen to cool down the forehead skin to approximately 20 degrees C without discomfort for the subject. For the seven patients studied at high altitude, the same measurements were also performed after 5 min of oxygen supplementation with and without cold exposure. At sea level, an increase in pulmonary vascular resistance (PVR) during cold exposure was inversely related to the initial PaO2. In six severe hypoxic subjects (PaO2 < 50 mm Hg), PVR increased by 24%. At high altitude, PVR was significantly increased by 15%. After O2 supplementation, cold exposure did not induce an increase in PVR. We concluded that mild and localized cold exposure to the forehead only induced an increase in PVR in COPD patients with severe hypoxia. Moreover, in cold exposure responders, O2 supplementation negated the effect of cold exposure on pulmonary hemodynamics.

Cold Temperature↗
PubMed2000

Nitric oxide: modulation of the pulmonary circulation.

Nitric oxide (NO) is synthetized throughout the body by the enzyme NO synthase (NOS), cyclic GMP transduction pathway causes pulmonary vasodilatation anti-platelets aggregation and inhibition of leukocyte adhesion. Inducible NOS is expressed in leukocytes in response to a variety of inflammatory stimuli and can be inhibited by corticosteroids. Inhaled NO is a selective pulmonary vasodilator. In USA inhaled NO was approved by FDA for hypoxemic respiratory failure in infants and children. In adults it may be useful in various clinical therapy: pulmonary hypertension, lung transplantation, ARDS but new clinical investigations are necessary.

Administration, Inhalation↗