scholarly journals Modulation of Intersectin-1s Lung Expression Induces Obliterative Remodeling and Severe Plexiform Arteriopathy in the Murine Pulmonary Vascular Bed

2017 ◽  
Vol 187 (3) ◽  
pp. 528-542 ◽  
Author(s):  
Monal Patel ◽  
Dan Predescu ◽  
Cristina Bardita ◽  
Jiwang Chen ◽  
Niranjan Jeganathan ◽  
...  
Keyword(s):  
Vascular Bed ◽  
Pulmonary Vascular Bed

Effect of Ligation of Left Pulmonary Artery at Birth on Maturation of Pulmonary Vascular Bed

Respiration ◽  
1962 ◽  
Vol 19 (5) ◽  
pp. 362-369
Author(s):  
Peter E. Pool ◽  
Keith H. Averill ◽  
John H.K. Vogel
Keyword(s):  
Pulmonary Artery ◽  
Left Pulmonary Artery ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

Responses to L-163,491, a nonpeptide angiotensin II mimic, in the pulmonary vascular bed of the cat

1995 ◽  
Vol 287 (2) ◽  
pp. 163-168 ◽  
Author(s):  
Alan D. Kaye ◽  
Bobby D. Nossaman ◽  
Salah Kivlighn ◽  
Ikhlass N. Ibrahim ◽  
Bracken J. De Witt ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

Postural variations in dead space and CO2 gradients breathing air and O2

1962 ◽  
Vol 17 (3) ◽  
pp. 417-420 ◽  
Author(s):  
C. P. Larson ◽  
J. W. Severinghaus
Keyword(s):  
Dead Space ◽  
Normal Limit ◽  
Healthy Adult ◽  
Sitting Position ◽  
Alveolar Dead Space ◽  
Vascular Bed ◽  
Postural Changes ◽  
Physiologic Dead Space ◽  
Pulmonary Vascular Bed

Effects of postural changes on anatomic and physiologic dead space and arterial-alveolar CO2gradients were studied in 11 healthy, adult subjects breathing air and O2. Results indicate that, on moving from the supine to the sitting position, Vads and Vpds increased by corresponding amounts (42 and 37 ml) with no increase in alveolar dead space or volume of lung which is nonperfused. Arterial-alveolar CO2 gradients were unaffected by posture, but more than doubled with O2 breathing, suggesting that O2 may relax the pulmonary vascular bed and diminish perfusion of highest lung segments. Isoproterenol aerosol (0.5%) produced significant bronchodilatation (27 ml increase in Vads), but only small and inconsistent increases in alveolar dead space and CO2 gradients. The PDS/Vt ratio in these subjects while sitting, breathing air, averaged 31 ± 6%, which is higher than the normally accepted value of 30%. As a result, the upper normal limit for PDS/Vt has been increased to 40% in our laboratories. Submitted on January 22, 1962

Comparative effects of L-NNA and alkyl esters of L-NNA on pulmonary vasodilator responses to ACh, BK, and SP

1994 ◽  
Vol 266 (6) ◽  
pp. H2416-H2422 ◽  
Author(s):  
D. Y. Cheng ◽  
B. J. DeWitt ◽  
T. J. McMahon ◽  
P. J. Kadowitz
Keyword(s):  
Substance P ◽  
Vagal Stimulation ◽  
Benzyl Ester ◽  
No Synthase ◽  
Flow Conditions ◽  
Inhibitory Effects ◽  
Vascular Bed ◽  
Pulmonary Vasodilator ◽  
Benzyl Esters ◽  
Pulmonary Vascular Bed

The comparative effects of the nitric oxide (NO) synthase inhibitors N omega-nitro-L-arginine (L-NNA), N omega-nitro-L-arginine methyl ester (L-NAME), and N omega-nitro-L-arginine benzyl ester (L-NABE) on baseline tone and on vasodilator responses to acetylcholine (ACh), bradykinin (BK), and substance P (SP) were compared in the pulmonary vascular bed of the cat under constant flow conditions. After administration of the NO synthase inhibitors in intravenous doses of 100 mg/kg, the increase in lobar arterial pressure and the attenuation of vasodilator responses to ACh, BK, and SP were similar, whereas responses to adenosine and felodipine, endothelium-independent vasodilator agents, were not altered. In addition to inhibiting responses to ACh, BK, and substance P, the NO synthase inhibitors enhanced vasodilator responses to S-nitroso-N-acetylpenicillamine and NO. Moreover, atropine inhibited pulmonary vasodilator responses to ACh but not to SP or BK, and L-NAME or L-NABE had no effect on the decrease in heart rate in response to efferent vagal stimulation, a muscarinic receptor-mediated response that is independent of NO release. The similar inhibitory effects of L-NNA, L-NAME, and L-NABE on vasodilator responses to ACh, BK, and SP suggest that the L-arginine analogue, L-NNA, as well as the methyl and benzyl esters of L-NNA are useful probes for studying NO-mediated endothelium-dependent responses in the pulmonary vascular bed of the intact-chest cat.(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for Distinct Endothelin Receptors in the Pulmonary Vascular Bed in vivo

1991 ◽  
Vol 17 ◽  
pp. S370-373 ◽  
Author(s):  
Howard L. Lippton ◽  
Gordon A. Cohen ◽  
Martha Knight ◽  
Ivan F. McMurtry ◽  
Doug Gillot ◽  
...  
Keyword(s):  
Endothelin Receptors ◽  
Vascular Bed ◽  
Pulmonary Vascular Bed

Responses to propofol in the pulmonary vascular bed of the rat

1999 ◽  
Vol 43 (4) ◽  
pp. 431-437 ◽  
Author(s):  
A. Kaye ◽  
M. Anwar ◽  
R. Banister ◽  
C. Feng ◽  
K. Turner ◽  
...  
Keyword(s):  
Vascular Bed ◽  
Pulmonary Vascular Bed
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