scholarly journals Pulmonary Hypertension in COVID-19 Pneumoniae: It Is Not Always as It Seems

2020 ◽  
Author(s):  
Maria Cristina Pasqualetto ◽  
Maria Domenica Sorbo ◽  
Maria Vitiello ◽  
Chiara Ferrara ◽  
Moreno Scevola ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Pulmonary Hypertension ◽  
Viral Infection ◽  
Right Ventricular ◽  
Pulmonary Circulation ◽  
Venous Drainage ◽  
Endothelial Injury ◽  
Positive End Expiratory Pressure ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Haemodynamics

A patient affected by COVID-19 pneumonia may develop pulmonary hypertension (PH) and secondary right ventricular (RV) involvement, due to lung parenchymal and interstitial damage and altered pulmonary haemodynamics, even in non-advanced phases of the disease. This is a consequence of hypoxic vasoconstriction of the pulmonary circulation, the use of positive end-expiratory pressure (PEEP) in mechanical ventilation, pulmonary endothelial injury, and local inflammatory thrombotic and/or thromboembolic processes. We report the case of a young man admitted with a diagnosis of COVID-19 pneumoniae with PH unrelated to viral infection and in whom partial anomalous pulmonary venous drainage (PAPVD) was eventually diagnosed.

Proximal pulmonary arterial obstruction decreases the time constant of the pulmonary circulation and increases right ventricular afterload

2013 ◽  
Vol 114 (11) ◽  
pp. 1586-1592 ◽  
Author(s):  
Alberto Pagnamenta ◽  
Rebecca Vanderpool ◽  
Serge Brimioulle ◽  
Robert Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Time Constant ◽  
Pulse Pressure ◽  
Pulmonary Circulation ◽  
Characteristic Impedance ◽  
Ventricular Afterload ◽  
Hydraulic Load ◽  
Distal Obstruction ◽  
Pulmonary Arterial

The time constant of the pulmonary circulation, or product of pulmonary vascular resistance (PVR) and compliance (Ca), called the RC-time, has been reported to remain constant over a wide range of pressures, etiologies of pulmonary hypertension, and treatments. We wondered if increased wave reflection on proximal pulmonary vascular obstruction, like in operable chronic thromboembolic pulmonary hypertension, might also decrease the RC-time and thereby increase pulse pressure and right ventricular afterload. Pulmonary hypertension of variable severity was induced either by proximal obstruction (pulmonary arterial ensnarement) or distal obstruction (microembolism) eight anesthetized dogs. Pulmonary arterial pressures (Ppa) were measured with high-fidelity micromanometer-tipped catheters, and pulmonary flow with transonic technology. Pulmonary ensnarement increased mean Ppa, PVR, and characteristic impedance, decreased Ca and the RC-time (from 0.46 ± 0.07 to 0.30 ± 0.03 s), and increased the oscillatory component of hydraulic load (Wosc/Wtot) from 25 ± 2 to 29 ± 2%. Pulmonary microembolism increased mean Ppa and PVR, with no significant change in Ca and characteristic impedance, increased RC-time from 0.53 ± 0.09 to 0.74 ± 0.05 s, and decreased Wosc/Wtot from 26 ± 2 to 13 ± 2%. Pulse pressure increased more after pulmonary ensnarement than after microembolism. Concomitant measurements with fluid-filled catheters showed the same functional differences between the two types of pulmonary hypertension, with, however, an underestimation of Wosc. We conclude that pulmonary hypertension caused by proximal vs. distal obstruction is associated with a decreased RC-time and increased pulsatile component of right ventricular hydraulic load.

scholarly journals Cannabinoids—A New Perspective in Adjuvant Therapy for Pulmonary Hypertension

2021 ◽  
Vol 22 (18) ◽  
pp. 10048
Author(s):  
Anna Krzyżewska ◽  
Marta Baranowska-Kuczko ◽  
Krzysztof Mińczuk ◽  
Hanna Kozłowska
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Pulmonary Circulation ◽  
Cannabinoid Receptors ◽  
Experimental Studies ◽  
Pulmonary Arteries ◽  
Systolic Pressure ◽  
Ventricular Systolic Pressure ◽  
Beneficial Effects ◽  
Vasodilatory Effect

Currently, no treatment can completely cure pulmonary hypertension (PH), which can lead to right ventricular failure and, consequently, death. Therefore, searching for new therapies remains important. Increased resistance in pulmonary circulation is mainly caused by the excessive contraction and proliferation of small pulmonary arteries. Cannabinoids, a group of lipophilic compounds that all interact with cannabinoid receptors, exert a pulmonary vasodilatory effect through several different mechanisms, including mechanisms that depend on vascular endothelium and/or receptor-based mechanisms, and may also have anti-proliferative and anti-inflammatory properties. The vasodilatory effect is important in regulating pulmonary resistance, which can improve patients' quality of life. Moreover, experimental studies on the effects of cannabidiol (plant-derived, non-psychoactive cannabinoid) in animal PH models have shown that cannabidiol reduces right ventricular systolic pressure and excessive remodelling and decreases pulmonary vascular hypertrophy and pulmonary vascular resistance. Due to the potentially beneficial effects of cannabinoids on pulmonary circulation and PH, in this work, we review whether cannabinoids can be used as an adjunctive therapy for PH. However, clinical trials are still needed to recommend the use of cannabinoids in the treatment of PH.

Deletion of the eNOS gene has a greater impact on the pulmonary circulation of male than female mice

2005 ◽  
Vol 289 (2) ◽  
pp. L299-L366 ◽  
Author(s):  
Alyson A. Miller ◽  
Alison A. Hislop ◽  
Patrick J. Vallance ◽  
Sheila G. Haworth
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Adult Male ◽  
Pulmonary Circulation ◽  
Adult Life ◽  
Enos Gene ◽  
Fetal Life ◽  
Male And Female ◽  
Female Mice

Nitric oxide is involved in development and postnatal adaptation of the pulmonary circulation. This study aimed to determine whether genetic deletion of nitric oxide synthase (NOS) would lead to maldevelopment of the pulmonary arteries in fetal life, compromise adaptation to extrauterine life, and be associated with a pulmonary hypertensive phenotype in adult life and if any abnormalities were detected, were they sex dependent. Morphometric analyses were made on lung tissue from male and female fetal, newborn, 14-day-old, and adult endothelial NOS-deficient (eNOS−/−) or inducible NOS-deficient (iNOS−/−) and wild-type mice. Hemodynamic studies were carried out on adult mice with deletion of either eNOS or iNOS genes. We found that in eNOS−/− mice, lung development was normal in fetal, newborn, and adult lungs. Pulmonary arterial muscularity was greater than normal in both male and female eNOS−/− during fetal life and at birth, but the abnormality persisted only in male mice. Right ventricular hypertrophy was present in 14-day-old and adult male eNOS−/− but not in female mice. Adult male eNOS−/− mice had higher mean right ventricular and systemic pressures than female eNOS−/− mice ( P < 0.05). Thus deletion of the eNOS gene was associated with structural evidence of pulmonary hypertension in both sexes during fetal life, but pulmonary hypertension persisted only in the male. In neither sex did iNOS or neuronal NOS appear to compensate for the eNOS deletion. Adult iNOS−/− mice did not have structural or hemodynamic evidence of pulmonary hypertension. Possible compensatory mechanisms are discussed.

Attenuation of acute hypoxic pulmonary vasoconstriction and hypoxic pulmonary hypertension in mice by inhibition of Rho-kinase

2004 ◽  
Vol 287 (4) ◽  
pp. L656-L664 ◽  
Author(s):  
Karen A. Fagan ◽  
Masahiko Oka ◽  
Natalie R. Bauer ◽  
Sarah A. Gebb ◽  
D. Dunbar Ivy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Pulmonary Circulation ◽  
Vascular Remodeling ◽  
Chronic Hypoxia ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Rho Kinase ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Vasoconstriction

RhoA GTPase mediates a variety of cellular responses, including activation of the contractile apparatus, growth, and gene expression. Acute hypoxia activates RhoA and, in turn, its downstream effector, Rho-kinase, and previous studies in rats have suggested a role for Rho/Rho-kinase signaling in both acute and chronically hypoxic pulmonary vasoconstriction. We therefore hypothesized that activation of Rho/Rho-kinase in the pulmonary circulation of mice contributes to acute hypoxic pulmonary vasoconstriction and chronic hypoxia-induced pulmonary hypertension and vascular remodeling. In isolated, salt solution-perfused mouse lungs, acute administration of the Rho-kinase inhibitor Y-27632 (1 × 10−5 M) attenuated hypoxic vasoconstriction as well as that due to angiotensin II and KCl. Chronic treatment with Y-27632 (30 mg·kg−1·day−1) via subcutaneous osmotic pump decreased right ventricular systolic pressure, right ventricular hypertrophy, and neomuscularization of the distal pulmonary vasculature in mice exposed to hypobaric hypoxia for 14 days. Analysis of a small number of proximal pulmonary arteries suggested that Y-27632 treatment reduced the level of phospho-CPI-17, a Rho-kinase target, in hypoxic lungs. We also found that endothelial nitric oxide synthase protein in hypoxic lungs was augmented by Y-27632, suggesting that enhanced nitric oxide production might have played a role in the Y-27632-induced attenuation of chronically hypoxic pulmonary hypertension. In conclusion, Rho/Rho-kinase activation is important in the effects of both acute and chronic hypoxia on the pulmonary circulation of mice, possibly by contributing to both vasoconstriction and vascular remodeling.

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