Ventricular asynchronism in the dog

1962 ◽  
Vol 17 (3) ◽  
pp. 479-481 ◽  
Author(s):  
Philip Samet ◽  
William H. Bernstein ◽  
Robert S. Litwak

Dissociation of electrical and mechanical asynchronism in the canine right and left ventricles has been studied by simultaneous registration of right and left ventricular pressure and strain gauge arch curves and the electrocardiogram. Observations were made during sinus rhythm and during acetylstrophanthidin-induced ventricular premature beats with widened aberrant QRS complexes. The data demonstrate only limited mechanical asynchronism during the asynchronous electrical depolarization of ventricular premature systoles. Submitted on October 19, 1961

Author(s):  
Stefan F. J. Langer

<pre class="western">Background Observations of short term uniformity or microrhythmical undulation in ventricular pressure courses at sinus rhythm are lacking but necessary to describe cardiac status. The present investigation aims for (a) detecting repetitive similarity patterns in ventricular pressure at isolated sinus rhythm, (b) tagging hemodynamic parameters which contribute most to dissimilarity, and (c) for a stochastical characterisation of the random component in mutual similarity. Methods Left-ventricular pressure curves from isolated working small animal hearts, at sinus rhythm and electrical stimulation, are analysed by autocorrelation. Results Ventricular pressure courses consistently reach their peak coefficient of autocorrelation either at one-beat lag (monorhythm) or at two-beat lag (duorhythm). Replacing sinus rhythm with strictly even electrical right-atrial stimulation provokes more duorhythms to occur (Langer paradox). Duorhythms become scarcer at hypothermia and high cardiac output. Repetition of very similarly shaped beats accords with an exponential law. Variability of twelve hemodynamic parameters, regarding microrhythm, is given as a Table. Conclusions (a) Incidence of alternating patterns (duorhythms) suggests the presence of effective heterometric autoregulation (Frank-Starling law). Consequently, a pacing test may assess contractile reserve in certain conditions. Higher multi-beat patterns occur by chance at isolated sinus rhythm. (b) Interbeat variability of relevant hemodynamic parameters complies with the initial conclusion. Statistical pooling of data from consecutive beats seems permissible; pooling alterant beats separately will do better. (c) Random fluctuation is a constituent part of medium-term ventricular pressure course. Mutually very similar beats occur stochastically by a Poisson process with fade-out. Deviations accord with the presence of mono- or duorhythms.</pre>


1959 ◽  
Vol 14 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Philip Samet ◽  
William H. Bernstein ◽  
Robert S. Litwak ◽  
William H. Meyer ◽  
Louis Lemberg

Dissociation of electrical and mechanical asynchronism in the right and left ventricle of the dog has been studied by simultaneous registration of the precordial electrocardiogram and right and left ventricular pressure curves. Observations were made during sinus rhythm and during digitalis-induced ventricular premature beats with widened aberrant QRS complexes. Measurements were made of the time of onset of isometric contraction in the ventricles, relative to each other, and to the onset of the QRS complex. The results indicate that mechanical asynchronism in onset of isometric contraction is not a necessary consequence of the asynchronous electrical depolarization of ventricular premature systoles. Submitted on November 10, 1958


1977 ◽  
Vol 233 (5) ◽  
pp. H555-H561 ◽  
Author(s):  
A. V. Goodyer ◽  
B. Y. Wong

Strength-interval curves, relating an index of the contractile vigor of premature beats to their coupling intervals, were elicited in anesthetized, open-chest dogs prepared for atrial or ventricular pacing and the high-fidelity measurement of left ventricular pressure. During inotropic interventions, changes of the curves were evaluated in terms of the parameters (slopes and intercepts) of their straight lines of best fit. These parameters were altered by isoproterenol, propranolol, and heart rate, and were correlated closely with paired values of isovolumic Vmax (of driven beats). The strength-interval curves were reproducible and were not affected by large changes of venous return or arterial blood pressure. These results provide a basis for the use of strength-interval curves for the evaluation of ventricular contractile state, using fluid-filled catheters for the measurement of left ventricular pressure.


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 ◽  
...  

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond

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.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jingtao Na ◽  
Haifeng Jin ◽  
Xin Wang ◽  
Kan Huang ◽  
Shuang Sun ◽  
...  

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.


2010 ◽  
Vol 196 ◽  
pp. S253
Author(s):  
A. Simonnard ◽  
A.M. Bétat ◽  
S. Loriot ◽  
R. Forster

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