Faculty Opinions recommendation of Impact of arterial load and loading sequence on left ventricular tissue velocities in humans.

Author(s):  
Michael Frenneaux
2007 ◽  
Vol 50 (16) ◽  
pp. 1570-1577 ◽  
Author(s):  
Barry A. Borlaug ◽  
Vojtech Melenovsky ◽  
Margaret M. Redfield ◽  
Kristy Kessler ◽  
Hyuk-Jae Chang ◽  
...  

2010 ◽  
Vol 109 (3) ◽  
pp. 752-757 ◽  
Author(s):  
Svein Erik Gaustad ◽  
Alf O. Brubakk ◽  
Morten Høydal ◽  
Daniele Catalucci ◽  
Gianluigi Condorelli ◽  
...  

Diving and decompression performed under immersed conditions have been shown to reduce cardiac function. The mechanisms for these changes are not known. The effect of immersion before a simulated hyperbaric dive on cardiomyocyte function was studied. Twenty-three rats were assigned to four groups: control, 1 h thermoneutral immersion, dry dive, and 1 h thermoneutral immersion before a dive (preimmersion dive). Rats exposed to a dive were compressed to 700 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa/min. Postdive, the animals were anesthetized and the right ventricle insonated for bubble detection using ultrasound. Isolation of cardiomyocytes from the left ventricle was performed and studied using an inverted fluorescence microscope with video-based sarcomere spacing. Compared with a dry dive, preimmersion dive significantly increased bubble production and decreased the survival time (bubble grade 1 vs. 5, and survival time 60 vs. 17 min, respectively). Preimmersion dive lead to 18% decreased cardiomyocyte shortening, 20% slower diastolic relengthening, and 22% higher calcium amplitudes compared with controls. The protein levels of the sarco-endoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and phospholamban phosphorylation in the left ventricular tissue were significantly reduced after both dry and preimmersion dive compared with control and immersed animals. The data suggest that immersion before a dive results in impaired cardiomyocyte and Ca2+ handling and may be a cellular explanation to reduced cardiac function observed in humans after a dive.


2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 163
Author(s):  
Brock T. Jensen ◽  
David S. Hydock ◽  
Chia-Ying Lien ◽  
Carole M. Schneider ◽  
Reid Hayward

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Rayile Aisa ◽  
Zhaoxia Yu ◽  
Xiangyang Zhang ◽  
Dilinuer Maimaitiyiming ◽  
Lipeng Huang ◽  
...  

Aims. The aim of this study was to investigate the effects of the aqueous extract of Nardostachys chinensis Batalin (NCBAE) on blood pressure and cardiac hypertrophy using two-kidney one-clip (2K1C) hypertensive rats. Methods. 2K1C rat models were set up by clipping the left renal artery. Sham-operated rats underwent the same surgical procedure except for renal arterial clipping. 2K1C hypertensive rats were orally given NCBAE at doses of 210, 420, and 630 mg·kg−1·d−1 for 6 weeks. Twelve weeks after surgery, rat SBP and echocardiographic parameters were measured, cardiac histopathology was assessed, serum NO and LDH were detected, and the expression of Bcl-2 and caspase-3 of left ventricular tissue was assessed by western blot. Results. Treatment with NCBAE resulted in a decrease of SBP, LVPWd, LVPWs, IVSd, IVSs, LVW/BW ratio, and cardiomyocyte CSA, an increase of LVEF, and inhibition of 2K1C-induced reduction in serum NO and elevation of LDH compared with 2K1C group. NCBAE intervention also showed a significant increase of Bcl-2 expression and reduction of cleaved caspase-3 level dose-dependently in left ventricular tissue. Conclusion. Our data demonstrate that NCBAE has an antihypertensive property and protective effect on 2K1C-induced cardiac hypertrophy especially at the dose of 630 mg·kg−1·d−1.


2011 ◽  
Vol 47 (12) ◽  
pp. 648-655 ◽  
Author(s):  
Mitsuru HIGASHIMORI ◽  
Ryohei ISHII ◽  
Kenjiro TADAKUMA ◽  
Makoto KANEKO ◽  
Syunsuke TAMAKI ◽  
...  

Author(s):  
Tom E. Claessens ◽  
Ernst R. Rietzschel ◽  
Marc L. De Buyzere ◽  
Dirk De Bacquer ◽  
Guy De Backer ◽  
...  

The contractile state of the human left ventricle (LV) is often assessed by its end-systolic elastance (Ees) [1]. This index is calculated as the slope of the linear end-systolic pressure-volume relationship (ESPVR), which connects the upper left corners of pressure-volume loops obtained under various loading conditions (figure 1).


2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S15
Author(s):  
C. Cerutti ◽  
M. Kurdi ◽  
R. El Feghali ◽  
J. Randon ◽  
M. R. Gustin ◽  
...  

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