Effect of neuropeptide Y on hemodynamics of the rabbit lung.
Animals; Cisterna Magna; Hemodynamics/*physiology; In Vitro Techniques; Injections; Neuropeptide Y/blood/pharmacology/*physiology; Norepinephrine/pharmacology; Perfusion; Pulmonary Circulation/drug effects/*physiology; Rabbits; Sympathetic Nervous System/drug effects/physiology; Vascular Resistance/drug effects/physiology; Vasoconstriction/drug effects/physiology; Vasoconstrictor Agents/pharmacology; Veratrine/administration & dosage/pharmacology
We evaluated the effect of neuropeptide Y (NPY) on the hemodynamics of the isolated rabbit lung perfused at constant flow and outflow pressure. Doses of 10(-8) and 10(-7) M NPY increased pulmonary arterial pressure (Ppa) from 11.5 +/- 1.0 (SE) mmHg to, respectively, 16.4 +/- 1.5 and 26.0 +/- 3.8 mmHg (P \textless 0.05, n = 5 mmHg lungs), with 78 +/- 4% of the increase at 10(-7) M resulting from an increased arterial resistance. At the latter dose, pulmonary capillary pressure increased from 5.8 +/- 0.9 to 9.4 +/- 1.0 mmHg (P \textless 0.05). When administered in the presence of norepinephrine, 10(-8) and 10(-7) M NPY (n = 6) produced extreme increases in Ppa to 66.1 +/- 20.5 and 114.7 +/- 25.5 mmHg, respectively, that were due primarily to an increased arterial resistance. To determine the significance of circulating NPY as a pulmonary vasoactive agent, we measured plasma NPY-like immunoreactivity in anesthetized rabbits after massively activating the sympathetic nervous system with veratrine. NPY-like immunoreactivity increased from 74 +/- 10 to 111 +/- 10 (SE) pM (P \textless 0.05). Thus, although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconstriction in the intact rabbit.
Lang S A; Maron M B
Journal of applied physiology (Bethesda, Md. : 1985)
1998
1998-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1998.84.2.618" target="_blank" rel="noreferrer noopener">10.1152/jappl.1998.84.2.618</a>
Pulmonary vasoconstriction in a canine model of neurogenic pulmonary edema.
Animal; Animals; Catecholamines/physiology; Disease Models; Dogs; Female; Hypertension; In Vitro Techniques; Male; Perfusion; Pulmonary Circulation/drug effects/*physiology; Pulmonary Edema/chemically induced/*physiopathology; Pulmonary/chemically induced/physiopathology; Splenectomy; Sympathetic Nervous System/drug effects/physiopathology; Vasoconstriction/drug effects/*physiology; Veratrine
The intracisternal administration of veratrine to the chloralose-anesthetized dog produces pulmonary hypertension (PH) and neurogenic pulmonary edema (NPE). To determine whether pulmonary vasoconstriction, mediated by a circulating agent, contributes to the PH, the left lower lung lobe (LLL) perfusion of seven splenectomized (to keep hematocrit and blood viscosity constant) dogs was isolated so the LLL could be perfused at constant flow and outflow pressure with blood pumped from the pulmonary artery. The LLL was denervated by removing it from the dog. Veratrine (40-160 micrograms/kg) increased LLL arterial pressure by 39.2% and produced large increases in plasma catecholamine concentrations. The double-occlusion technique indicated that 74% of the increase in the LLL arteriovenous pressure gradient was due to an increase in venous tone. This pattern of vasoconstriction was similar to that previously observed during the infusion of exogenous catecholamines and suggested that catecholamines mediated the LLL response. The more severe degree of PH observed in the intact animal in NPE, however, suggests that passive rather than active changes in pulmonary hemodynamics are predominantly responsible for the development of PH in this disorder.
Maron M B
Journal of applied physiology (Bethesda, Md. : 1985)
1990
1990-03
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jappl.1990.68.3.912" target="_blank" rel="noreferrer noopener">10.1152/jappl.1990.68.3.912</a>