The effect of sildenafil on pulmonary haemodynamics in a canine model of chronic embolic pulmonary hypertension

2020 ◽  
Vol 133 ◽  
pp. 106-110
Author(s):  
Ryota Akabane ◽  
Atsushi Sakatani ◽  
Mizuki Ogawa ◽  
Masayoshi Nagakawa ◽  
Hirosumi Miyakawa ◽  
...  
2012 ◽  
Vol 194 (2) ◽  
pp. 215-221 ◽  
Author(s):  
Yasutomo Hori ◽  
Tsuyoshi Uchide ◽  
Ryuta Saitoh ◽  
Daisuke Thoei ◽  
Makiko Uchida ◽  
...  

1988 ◽  
Vol 255 (5) ◽  
pp. H1232-H1239 ◽  
Author(s):  
H. J. Priebe

This study was performed to determine 1) the effects of acute pulmonary embolization (induced by injection of autologous muscle) on right ventricular (RV) performance, coronary hemodynamics, and gas exchange; and 2) the efficacy of subsequent administration of nitroglycerin, prostaglandin E1, and hydralazine with regard to improvement in RV function and gas exchange in eight open-chest dogs. After embolization, pulmonary artery (PA) pressure and vascular resistance (PVR) increased three- to fivefold without changes in RV end-diastolic dimensions (ultrasonic dimension technique) or pressure. However, systolic dimensions increased, and stroke volume (SV) fell. Gas exchange, lung compliance, and pH worsened. Subsequent administration of nitroglycerin (5 micrograms.kg-1.min-1) and prostaglandin E1 (0.2 micrograms.kg-1.min-1) caused further decreases in SV and pH. In contrast, hydralazine (mean 0.15 mg/kg) improved myocardial segment shortening, SV, PVR, pulmonary artery flow, and gas exchange. Coronary blood flow increased by 110%. Thus in this canine model of combined pulmonary hypertension and respiratory insufficiency, nitroglycerin and prostaglandin E1 exerted no beneficial cardiopulmonary effects. In contrast, hydralazine improved regional and global RV performance and gas exchange.


2016 ◽  
Vol 49 (2) ◽  
pp. 1601530 ◽  
Author(s):  
Tsogyal D. Latshang ◽  
Michael Furian ◽  
Sayaka S. Aeschbacher ◽  
Silvia Ulrich ◽  
Batyr Osmonov ◽  
...  

This case–control study evaluates a possible association between high altitude pulmonary hypertension (HAPH) and sleep apnoea in people living at high altitude.Ninety highlanders living at altitudes >2500 m without excessive erythrocytosis and with normal spirometry were studied at 3250 m (Aksay, Kyrgyzstan); 34 healthy lowlanders living below 800 m were studied at 760 m (Bishkek, Kyrgyzstan). Echocardiography, polysomnography and other outcomes were assessed. Thirty-six highlanders with elevated mean pulmonary artery pressure (mPAP) >30 mmHg (31–42 mmHg by echocardiography) were designated as HAPH+. Their data were compared to that of 54 healthy highlanders (HH, mPAP 13–28 mmHg) and 34 healthy lowlanders (LL, mPAP 8–24 mmHg).The HAPH+ group (median age 52 years (interquartile range 47–59) had a higher apnoea–hypopnoea index (AHI) of 33.8 events·h−1(26.9–54.6) and spent a greater percentage of the night-time with an oxygen saturation <90% (T<90; 78% (61–89)) than the HH group (median age 39 years (32–48), AHI 9.0 events·h−1(3.6–16), T<90 33% (10–69)) and the LL group (median age 40 years (30–47), AHI 4.3 events·h−1(1.4–12.6), T<90 0% (0–0)); p<0.007 for AHI and T<90, respectively, in HAPH+versusothers. In highlanders, multivariable regression analysis confirmed an independent association between mPAP and both AHI and T<90, when controlled for age, gender and body mass index.Pulmonary hypertension in highlanders is associated with sleep apnoea and hypoxaemia even when adjusted for age, gender and body mass index, suggesting pathophysiologic interactions between pulmonary haemodynamics and sleep apnoea.


2021 ◽  
Vol 30 (161) ◽  
pp. 210053
Author(s):  
Ashraful Haque ◽  
David G. Kiely ◽  
Gabor Kovacs ◽  
A.A. Roger Thompson ◽  
Robin Condliffe

Pulmonary hypertension (PH) commonly affects patients with systemic sclerosis (SSc) and is associated with significant morbidity and increased mortality. PH is a heterogenous condition and several different forms can be associated with SSc, including pulmonary arterial hypertension (PAH) resulting from a pulmonary arterial vasculopathy, PH due to left heart disease and PH due to interstitial lung disease. The incidence of pulmonary veno-occlusive disease is also increased. Accurate and early diagnosis to allow optimal treatment is, therefore, essential. Recent changes to diagnostic haemodynamic criteria at the 6th World Symposium on Pulmonary Hypertension have resulted in therapeutic uncertainty regarding patients with borderline pulmonary haemodynamics. Furthermore, the optimal pulmonary vascular resistance threshold for diagnosing PAH and the role of exercise in identifying early disease require further elucidation. In this article we review the epidemiology, diagnosis, outcomes and treatment of the spectrum of pulmonary vascular phenotypes associated with SSc.


CHEST Journal ◽  
1991 ◽  
Vol 100 (2) ◽  
pp. 474-479 ◽  
Author(s):  
G. William Henry ◽  
Hiroshi Katayama ◽  
Manuel E. Lores ◽  
Carol L. Lucas ◽  
Jose I. Ferreiro

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