scholarly journals Systemic Blood Pressure Response to Changes in Right Ventricular Function

1964 ◽  
Vol 14 (5) ◽  
pp. 461-466 ◽  
Author(s):  
ALAN L. PINKERSON ◽  
PETER A. KOT
Keyword(s):  
Blood Pressure ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Blood Pressure Response ◽  
Systemic Blood Pressure ◽  
Pressure Response ◽  
Systemic Blood

scholarly journals Pulmonary Vasodilation by Sildenafil in Acute Pulmonary Embolism—A Randomized Explorative Trial

2020 ◽  
Author(s):  
Asger Andersen ◽  
Farhad Waziri ◽  
Jacob Gammelgaard Schultz ◽  
Sarah Holmboe ◽  
Søren Warberg Becker ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Pulmonary Embolism ◽  
High Risk ◽  
Cardiac Index ◽  
Oral Dose ◽  
Right Ventricular ◽  
Single Oral Dose ◽  
Ventricular Function ◽  
Right Ventricular Function ◽  
Pulmonary Vasodilation

Abstract Background: To investigate if acute pulmonary vasodilation by sildenafil improves right ventricular function in patients with acute intermediate-high risk pulmonary embolism (PE).Methods: Patients with PE were randomized to a single oral dose of sildenafil 50mg (n=10) or placebo (n=10) as add-on to conventional therapy. Right ventricular function was evaluated immediately before and shortly after (0.5-1.5h) randomization by right heart catheterization (RHC), trans-thoracic echocardiography (TTE), and cardiac magnetic resonance (CMR). The primary efficacy endpoint was cardiac index measured by CMR.Results: Patients had acute intermediate-high risk PE verified by computed tomography pulmonary angiography, systolic blood pressure of 135 ± 18 (mean ± SD) mmHg, increased right ventricular/left ventricular ratio 1.1 ± 0.09 and increased troponin T 167 ± 144 ng/L. Sildenafil treatment did not improve cardiac index compared to baseline (0.02 ± 0.36 l/min/m2, p=0.89) and neither did placebo (0.00 ± 0.34 l/min/m2, p=0.97).Conclusion: A single oral dose of 50 mg sildenafil did not improve cardiac index but lowered systemic blood pressure in patients with acute intermediate-high risk PE.Trial Registration: The trial was retrospectively registered at www.clinicaltrials.gov (NCT04283240) February 2nd 2020, https://clinicaltrials.gov/ct2/show/NCT04283240?term=NCT04283240&draw=2&rank=1

Impact of central haemodynamics on left ventricular function in individuals with an exaggerated blood pressure response to exercise

2015 ◽  
Vol 33 (3) ◽  
pp. 612-620 ◽  
Author(s):  
Chi Young Shim ◽  
Geu-Ru Hong ◽  
Sungha Park ◽  
Woo-In Yang ◽  
Donghoon Choi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Blood Pressure Response ◽  
Left Ventricular ◽  
Pressure Response ◽  
Response To Exercise

scholarly journals Effects of Chronic Nicotine Inhalation on Systemic and Pulmonary Blood Pressure and Right Ventricular Remodeling in Mice

Hypertension ◽  
2020 ◽  
Vol 75 (5) ◽  
pp. 1305-1314 ◽  
Author(s):  
Joshua M. Oakes ◽  
Jiaxi Xu ◽  
Tamara M. Morris ◽  
Nicholas D. Fried ◽  
Charlotte S. Pearson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Left Ventricle ◽  
Right Ventricular ◽  
Cardiac Remodeling ◽  
Systolic Pressure ◽  
Systemic Blood Pressure ◽  
Right Ventricular Systolic Pressure ◽  
Systemic Blood ◽  
Ventricular Systolic Pressure ◽  
Chronic Nicotine

Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases; however, the role of nicotine in the pathogenesis of these diseases is incompletely understood. The purpose of this study was to examine the effects of chronic nicotine inhalation on the development of cardiovascular and pulmonary disease with a focus on blood pressure and cardiac remodeling. Male C57BL6/J mice were exposed to air (control) or nicotine vapor (daily, 12 hour on/12 hour off) for 8 weeks. Systemic blood pressure was recorded weekly by radio-telemetry, and cardiac remodeling was monitored by echocardiography. At the end of the 8 weeks, mice were subjected to right heart catheterization to measure right ventricular systolic pressure. Nicotine-exposed mice exhibited elevated systemic blood pressure from weeks 1 to 3, which then returned to baseline from weeks 4 to 8, indicating development of tolerance to nicotine. At 8 weeks, significantly increased right ventricular systolic pressure was detected in nicotine-exposed mice compared with the air controls. Echocardiography showed that 8-week nicotine inhalation resulted in right ventricular (RV) hypertrophy with increased RV free wall thickness and a trend of increase in RV internal diameter. In contrast, there were no significant structural or functional changes in the left ventricle following nicotine exposure. Mechanistically, we observed increased expression of angiotensin-converting enzyme and enhanced activation of mitogen-activated protein kinase pathways in the RV but not in the left ventricle. We conclude that chronic nicotine inhalation alters both systemic and pulmonary blood pressure with the latter accompanied by RV remodeling, possibly leading to progressive and persistent pulmonary hypertension.

Effect of recurrent episodic hypocapnic, eucapnic, and hypercapnic hypoxia on systemic blood pressure

1995 ◽  
Vol 78 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
E. C. Fletcher ◽  
G. Bao ◽  
C. C. Miller
Keyword(s):  
Blood Pressure ◽  
Rat Model ◽  
Blood Pressure Response ◽  
Systemic Blood Pressure ◽  
Protective Mechanism ◽  
Systemic Blood ◽  
Blood Pressure Elevation ◽  
Arterial Blood ◽  
Episodic Hypoxia ◽  
Hypoxic Group

We have described a rat model that responds to chronic (8 h/day, 35 days) repetitive nonapneic episodic (cycled every 30 s) hypocapnic hypoxia with sustained increase in systemic blood pressure. Because the usual blood gas change of apnea is mildly increased CO2, we hypothesized that episodic hypoxia ranging from eucapnea to hypercapnia might cause a greater chronic increase in blood pressure than hypocapnic hypoxia in this model. Five groups of male Sprague-Dawley rats were studied: unhandled group received no treatment, sham group received compressed air in their chambers, hypocapnic hypoxic group received episodic hypoxia for 35 days, eucapnic hypoxic group received the same level of hypoxia but with 7–10% inspired fraction of CO2, and hybercarbic hypoxic group received hypoxia with 11–14% inspired fraction of CO2. Mean arterial blood pressure was measured in unrestrained conscious animals at baseline and after 35 days under their respective study conditions. Neither episodic eucapnic nor hypercarbic hypoxia had any additional effect on the changes in chronic diurnal blood pressure compared with hypocapnic hypoxia. These results suggest that the sympathetic nervous system or other neurohumoral systems contributing to chronic diurnal blood pressure elevation may be maximally stimulated by hypoxia or there may be some protective mechanism limiting the blood pressure response to asphyxia in this rat model.

Sign in / Sign up

Export Citation Format

Share Document