Influence of acute alcohol intoxication on the left ventricular pressure-volume relations of the rat heart

1980 ◽  
Vol 75 (1) ◽  
pp. 279-280
Author(s):  
A. Hepp ◽  
H. Schier ◽  
K. Kochsiek
Keyword(s):  
Rat Heart ◽  
Alcohol Intoxication ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Acute Alcohol Intoxication

Calcium Influx Inhibition: Possible Mechanism of the Negative Effect of Tetrahydropalmatine on Left Ventricular Pressure in Isolated Rat Heart

Planta Medica ◽  
1999 ◽  
Vol 65 (4) ◽  
pp. 340-342 ◽  
Author(s):  
Paul Chan ◽  
Wen-Ta Chiu ◽  
Yi-Jen Chen ◽  
Pao-Jean Wu ◽  
Juei-Tang Cheng
Keyword(s):  
Rat Heart ◽  
Calcium Influx ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Ventricular Pressure ◽  
Negative Effect ◽  
Isolated Rat

Mathematical modelling of the calcium–left ventricular pressure relationship in the intact diabetic rat heart

2008 ◽  
Vol 193 (3) ◽  
pp. 205-217 ◽  
Author(s):  
J. Op Den Buijs ◽  
L. Ligeti ◽  
T. Ivanics ◽  
Z. Miklós ◽  
G. J. Van Der Vusse ◽  
...  
Keyword(s):  
Mathematical Modelling ◽  
Rat Heart ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Diabetic Rat

Functional evaluation of the rat heart in situ

1975 ◽  
Vol 39 (6) ◽  
pp. 1043-1047 ◽  
Author(s):  
R. T. Dowell ◽  
A. F. Cutilletta ◽  
P. C. Sodt
Keyword(s):  
Rat Heart ◽  
Function Analysis ◽  
Heart Function ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Aortic Flow ◽  
Ventricular Pressure ◽  
Functional Evaluation ◽  
Flow Measurements

We have developed methods for evaluating muscle function in the intact rat heart in situ using a contractility index (dP/dt)P-1, calculated from left ventricular pressure derivative-left ventricular pressure loop plots. Aortic flow measurements were also taken to further characterize in situ rat heart function. The preparation remained functionally stable and was within physiological blood gas and pH limits for at least 30 min following surgical procedures. The contractility index was not influenced by increased afterload, decreased preload or increased heart rate; however, appropriate changes were observed following isoproterenol and propranolol administration. Appropriate changes in aortic flow measurements were observed also with the above interventions. These studies demonstrate that the in situ rat heart is a stable physiological experimental preparation. It should be useful for evaluating heart function since a contractility index derived from pressure-velocity relationships and measurements necessary for pump function analysis can be obtained simultaneously.

Beat-to-Beat Analysis of Left Ventricular Pressure-Volume Relation and Stroke Volume by Conductance Catheter and Aortic Modelflow in Cardiomyoplasty Patients

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 2010-2017 ◽  
Author(s):  
J.J. Schreuder ◽  
F.H. van der Veen ◽  
E.T. van der Velde ◽  
F. Delahaye ◽  
O. Alfieri ◽  
...  
Keyword(s):  
Stroke Volume ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Conductance Catheter ◽  
Volume Relation

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

scholarly journals The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jingtao Na ◽  
Haifeng Jin ◽  
Xin Wang ◽  
Kan Huang ◽  
Shuang Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Expression Patterns ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Luciferase Reporter ◽  
Left Ventricular Ejection ◽  
Tunel Staining ◽  
Ventricular Ejection Fraction

Abstract Background Heart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating  targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3. Methods Firstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry. Results HDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined. Conclusion Collectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

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