Angiotensin II prevents hypoxic pulmonary hypertension and vascular changes in rat

1988 ◽  
Vol 254 (3) ◽  
pp. H500-H508 ◽  
Author(s):  
M. Rabinovitch ◽  
M. Mullen ◽  
H. C. Rosenberg ◽  
K. Maruyama ◽  
H. O'Brodovich ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Angiotensin Ii ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Vascular Changes ◽  
Hypoxic Pulmonary Hypertension ◽  
Artery Pressure

Angiotensin II, a vasoconstrictor, has been previously demonstrated to produce a secondary vasodilatation due to release of prostaglandins. Because of this effect, we investigated whether infusion of exogenous angiotensin II via miniosmopumps in rats during a 1-wk exposure to chronic hypobaric hypoxia might prevent pulmonary hypertension, right ventricular hypertrophy, and vascular changes. We instrumented the rats with indwelling cardiovascular catheters and compared the hemo-dynamic and structural response in animals given angiotensin II, indomethacin in addition to angiotensin II (to block prostaglandin production), or saline with or without indomethacin. We then determined whether angiotensin II infusion also prevents acute hypoxic pulmonary vasoconstriction. We observed that exogenous angiotensin II infusion abolished the rise in pulmonary artery pressure, the right ventricular hypertrophy, and the vascular changes induced during chronic hypoxia in control saline-infused rats with or without indomethacin. The protective effect of angiotensin II was lost when indomethacin was given to block prostaglandin synthesis. During acute hypoxia, both angiotensin II and prostacyclin infusions similarly prevented the rise in pulmonary artery pressure observed in saline-infused rats and in rats given indomethacin or saralasin in addition to angiotensin II. Thus exogenous angiotensin II infusion prevents chronic hypoxic pulmonary hypertension, associated right ventricular hypertrophy, and vascular changes and blocks acute hypoxic pulmonary hypertension, and this is likely related to its ability to release vasodilator prostaglandins.

scholarly journals Parathyroid hormone affects right heart hemodynamics and exacerbates pulmonary hypertension

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
Y J Joki ◽  
H K Konishi ◽  
K T Takasu ◽  
T M Minamino
Keyword(s):  
Pulmonary Hypertension ◽  
Parathyroid Hormone ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Right Heart ◽  
Pulmonary Hemodynamics ◽  
Artery Pressure

Abstract Background Pulmonary hypertension (PH) is characterized by increased pulmonary artery pressure and develops right heart failure. Parathyroid hormone (PTH) is secreted from parathyroid gland and regulates a calcium homeostasis. Recent studies have suggested that PTH also acts on the cardiovascular system and affects cardiovascular prognosis. We hypothesized that PTH would play a role in the pathogenesis of PH. Purpose This study aimed to investigate the effect of PTH on pulmonary hemodynamics. Method We measured serum PTH levels in patients who were suspected of PH and underwent right heart catheter examination. We used two types of PH animal models, hypoxia (Hx)-induced PH mouse model and Sugen/hypoxia (SuHx)-induced PH rat model. Hx mice were administered PTH daily for 3 weeks. SuHx rats underwent parathyroidectomy, after which they received SuHx treatment for 10weeks. We measured physical data and right ventricular systolic pressure (RVSP) in these models. We cultured pulmonary artery smooth muscle cell (PASMC) treated with PTH to analyze cell signaling, proliferation and migration. Result We enrolled 20 participants. PTH concentration was significantly correlated with mean pulmonary artery pressure (r=0.58, p=0.006) as well as with pulmonary vascular resistance (r=0.61, p=0.04). Receiver operating characteristic curve displayed a cut-off PTH level of 48.0pg/ml that offered optimal differentiation between patients with and without PH (100% sensitivity, 73% specificity). PTH treatment exacerbated right ventricular hypertrophy and increased RVSP (33.6mmHg vs. 48.2mmHg) in Hx mice compared with non-treated Hx mice (Figure 1). Conversely, parathyroidectomy significantly attenuated right ventricular hypertrophy and reduced RVSP (54.2mmHg vs. 29.3mmHg) in SuHx rats compared with sham-operated SuHx rats. PTH promoted migration and proliferation through ERK signaling in PASMC. Conclusion Our clinical and experimental data demonstrated a critical role of PTH in the development of PH and suggested that PTH would be a novel therapeutic target for PH treatment. FUNDunding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): Grant-in-Aid for Young Scientists Figure 1. PTH treatment exacerbated RVSP

Possible role of pulmonary blood volume in chronic hypoxic pulmonary hypertension

1993 ◽  
Vol 74 (6) ◽  
pp. 3020-3026 ◽  
Author(s):  
L. C. Ou ◽  
G. L. Sardella ◽  
N. S. Hill ◽  
C. D. Thron
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Blood Volume ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Blood Volume

Chronic hypoxia increases the total blood volume (TBV) and pulmonary arterial blood pressure (Ppa) and induces pulmonary vascular remodeling. The present study was undertaken to assess how the pulmonary blood volume (PBV) changes during hypoxia and the possible role of PBV in chronic hypoxic pulmonary hypertension. A novel method has been developed to measure the TBV, PBV, and Ppa in conscious rats. The method consists of chronic implantation of a loose ligature around the ascending aorta and pulmonary artery, so that when the ligature is drawn tightly, it traps the blood in the pulmonary vessels and left heart and simultaneously kills the rat. The pulmonary veins are then ligated to separate the left ventricular blood volume from the PBV. This surgical approach, together with chronic catheterization of the pulmonary artery and the use of 51Cr-labeled red blood cells, allows measurement of TBV, PBV, and Ppa. This method has been used to analyze the relationships between TBV and PBV and between Ppa or right ventricular hypertrophy and PBV in two rat strains with markedly different TBV and Ppa responses to chronic hypoxia. PBV per given lung weight did not increase and even decreased during hypoxia despite marked increases in TBV. There was a close correlation between Ppa or right ventricular hypertrophy and PBV in the two strains of chronically hypoxic animals, suggesting that a greater PBV plays a significant role in the development of severe chronic hypoxic pulmonary hypertension in the altitude-susceptible Hilltop rats.

scholarly journals Severe Pulmonary Hypertension in Acute Pulmonary Thromboembolism: More Common than Expected?

2020 ◽  
Author(s):  
Mahsa Behnemoon ◽  
Elham Laleh ◽  
Amin Sedokani ◽  
Ayatay Bahrami
Keyword(s):  
Pulmonary Embolism ◽  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Hospital Mortality ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Severe Pulmonary Hypertension ◽  
Artery Pressure ◽  
Acute Pe ◽  
Echocardiographic Findings

Abstract Background: Pulmonary embolism (PE) is a relatively common health problem and the third most common cause of cardiovascular death with a 15-20 percent mortality rate. Severe pulmonary arterial hypertension is not common in acute forms of the disease, and we usually expect only mild to moderate degrees of PAH in these patients. However, we have encountered numerous cases of severe pulmonary hypertension after acute PE in our practice. In this study, we aimed to evaluate the echocardiographic findings of patients admitted with documented PE in a 5 years study of two heart centers of Urmia.Methods: In this retrospective study, the data of 183 patients with a definitive diagnosis of acute pulmonary embolism based on pulmonary CT angiography have entered the study.Results: Of the 183 cases diagnosed with pulmonary embolism with an average age of 61.15 years, 45.4% were male and 54.6% were female. Shortness of breath, chest pain, and hemoptysis were seen in 88%, 49.2%, and 13.1% of patients, respectively. Tachypnea and tachycardia were the most common clinical findings with a frequency of 54.1%. Echocardiographic findings of right ventricular enlargement and right ventricular dysfunction were observed in 66.7% and 67.8% of patients, respectively and 42.1% of patients had severe pulmonary hypertension. We found a significant relationship between pulmonary artery pressure severity and shock state as well as in-hospital mortality. While only 3 patients out of 64 cases (4%) with normal or mildly elevated pulmonary artery pressure died in their hospital stay period, the mortality rate was 28.5% in patients with moderate or severe pulmonary artery hypertension (p-value=0.002).Conclusion: we found a relatively high frequency of severe pulmonary artery hypertension in patients admitted with the definite diagnosis of acute pulmonary embolism and there was a significant correlation between pulmonary artery pressure severity and shock state, as well as in-hospital mortality. So, echocardiographic findings including right ventricular systolic pressure and TR velocity may have additional prognostic value in the decision making of acute PE patients and could be helpful in reducing in-hospital mortality of this complex illness provided being included in prognostic models of acute PE, based on future studies.

A575 Hypoxic Pulmonary Hypertension And Right Ventricular Hypertrophy Is Increased By Congenital NOS3-Deficiency

1997 ◽  
Vol 87 (Supplement) ◽  
pp. 575A ◽  
Author(s):  
W. Steudel ◽  
M. Scherrer-Crosbie ◽  
J. Weimann ◽  
M.H. Picard ◽  
P.L. Huang ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Pulmonary Hypertension

Pulmonary artery pressure and cardiac function in children and adolescents after rapid ascent to 3,450 m

2012 ◽  
Vol 302 (12) ◽  
pp. H2646-H2653 ◽  
Author(s):  
Yves Allemann ◽  
Thomas Stuber ◽  
Stefano F. de Marchi ◽  
Emrush Rexhaj ◽  
Claudio Sartori ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
High Altitude ◽  
Children And Adolescents ◽  
Pulmonary Artery Pressure ◽  
Young Population ◽  
Artery Pressure ◽  
Rapid Ascent ◽  
Low Altitude

High-altitude destinations are visited by increasing numbers of children and adolescents. High-altitude hypoxia triggers pulmonary hypertension that in turn may have adverse effects on cardiac function and may induce life-threatening high-altitude pulmonary edema (HAPE), but there are limited data in this young population. We, therefore, assessed in 118 nonacclimatized healthy children and adolescents (mean ± SD; age: 11 ± 2 yr) the effects of rapid ascent to high altitude on pulmonary artery pressure and right and left ventricular function by echocardiography. Pulmonary artery pressure was estimated by measuring the systolic right ventricular to right atrial pressure gradient. The echocardiography was performed at low altitude and 40 h after rapid ascent to 3,450 m. Pulmonary artery pressure was more than twofold higher at high than at low altitude (35 ± 11 vs. 16 ± 3 mmHg; P < 0.0001), and there existed a wide variability of pulmonary artery pressure at high altitude with an estimated upper 95% limit of 52 mmHg. Moreover, pulmonary artery pressure and its altitude-induced increase were inversely related to age, resulting in an almost twofold larger increase in the 6- to 9- than in the 14- to 16-yr-old participants (24 ± 12 vs. 13 ± 8 mmHg; P = 0.004). Even in children with the most severe altitude-induced pulmonary hypertension, right ventricular systolic function did not decrease, but increased, and none of the children developed HAPE. HAPE appears to be a rare event in this young population after rapid ascent to this altitude at which major tourist destinations are located.

Quantification of right ventricular afterload in patients with and without pulmonary hypertension

2006 ◽  
Vol 291 (4) ◽  
pp. H1731-H1737 ◽  
Author(s):  
Jan-Willem Lankhaar ◽  
Nico Westerhof ◽  
Theo J. C. Faes ◽  
Koen M. J. Marques ◽  
J. Tim Marcus ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Arterial Compliance ◽  
Characteristic Impedance ◽  
Peripheral Resistance ◽  
Windkessel Model ◽  
Artery Pressure ◽  
Pulmonary Arterial

Right ventricular (RV) afterload is commonly defined as pulmonary vascular resistance, but this does not reflect the afterload to pulsatile flow. The purpose of this study was to quantify RV afterload more completely in patients with and without pulmonary hypertension (PH) using a three-element windkessel model. The model consists of peripheral resistance ( R), pulmonary arterial compliance ( C), and characteristic impedance ( Z). Using pulmonary artery pressure from right-heart catheterization and pulmonary artery flow from MRI velocity quantification, we estimated the windkessel parameters in patients with chronic thromboembolic PH (CTEPH; n = 10) and idiopathic pulmonary arterial hypertension (IPAH; n = 9). Patients suspected of PH but in whom PH was not found served as controls (NONPH; n = 10). R and Z were significantly lower and C significantly higher in the NONPH group than in both the CTEPH and IPAH groups ( P < 0.001). R and Z were significantly lower in the CTEPH group than in the IPAH group ( P < 0.05). The parameters R and C of all patients obeyed the relationship C = 0.75/ R ( R2 = 0.77), equivalent to a similar RC time in all patients. Mean pulmonary artery pressure P and C fitted well to C = 69.7/P (i.e., similar pressure dependence in all patients). Our results show that differences in RV afterload among groups with different forms of PH can be quantified with a windkessel model. Furthermore, the data suggest that the RC time and the elastic properties of the large pulmonary arteries remain unchanged in PH.

Changes in pulmonary structure and function induced by monocrotaline intoxication

1981 ◽  
Vol 240 (2) ◽  
pp. H149-H155 ◽  
Author(s):  
F. Ghodsi ◽  
J. A. Will
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Ventricular Hypertrophy ◽  
Pyrrolizidine Alkaloid ◽  
Histological Study ◽  
Right Ventricular Hypertrophy ◽  
Laboratory Animals ◽  
Functional Relationships ◽  
And Function

Monocrotaline, a pyrrolizidine alkaloid derived from Crotalaria spectabilis, is known to be toxic to a variety of domestic and laboratory animals and to humans. Major pathological effects induced by monocrotaline poisoning include hepatic cirrhosis and megalocytosis, venocclusive disease, pulmonary hypertension, and right ventricular hypertrophy. The present investigation explored the structural and functional relationships that exist between pulmonary artery pressure, small pulmonary artery medial thickness, and right ventricular hypertrophy. The results of this physiological and histological study on monocrotaline-intoxicated rats has demonstrated that there is a positive correlation between progressive pulmonary hypertension, thickening of the medical wall of small pulmonary vessels, and right ventricular hypertrophy as a function of time.

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