scholarly journals Effect of acutely increased left ventricular afterload on work output from the right ventricle in conscious dogs

2001 ◽  
Vol 121 (1) ◽  
pp. 116-124 ◽  
Author(s):  
Mohanraj K. Karunanithi ◽  
Jerzy Michniewicz ◽  
Jason A. Young ◽  
Michael P. Feneley
1986 ◽  
Vol 250 (6) ◽  
pp. H1022-H1029 ◽  
Author(s):  
C. W. White ◽  
M. J. Mirro ◽  
D. D. Lund ◽  
D. J. Skorton ◽  
N. G. Pandian ◽  
...  

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.


1990 ◽  
Vol 259 (6) ◽  
pp. H1736-H1742
Author(s):  
J. M. Stewart ◽  
J. Wang ◽  
A. Singer ◽  
G. A. Zeballos ◽  
M. Ochoa ◽  
...  

Although atrial stretch is the primary stimulus for atrial natriuretic factor (ANF) secretion, hormones may directly affect ANF secretion or may indirectly influence ANF by changing left ventricular afterload, thereby altering atrial stretch. To determine whether direct effects are important for the release of ANF in vivo, we measured changes in plasma ANF and in atrial wall function in the conscious dog after the administration of vasopressin, angiotensin II, and phenylephrine and by mechanically increasing left ventricular afterload by partial aortic occlusion. Injections of phenylephrine, angiotensin II, and arginine vasopressin (AVP) that were chosen to cause similar changes in systemic arterial pressure resulted in similar changes in atrial pressure and diameter. Maximum V wave atrial wall stress increased to 283 +/- 12, 311 +/- 41, 327 +/- 24, and 277 +/- 22 g/cm2 for AVP, angiotensin, phenylephrine, and occlusion, respectively, and plasma ANF increased to 242 +/- 81, 248 +/- 62, 299 +/- 95, and 190 +/- 53 pg/ml. There were significant linear correlations between left ventricular afterload and left atrial pressure, and each method for increasing left ventricular afterload shifted the position to the left on an atrial pressure-diameter, compliance curve, by a similar degree. Thus changes in left ventricular afterload result in changes in atrial wall function and similar changes in plasma ANF. No hormonal-specific increase in plasma ANF was found in conscious dogs after increases in afterload.


2021 ◽  
Vol 14 (2) ◽  
pp. e238076
Author(s):  
Bryan O'Sullivan ◽  
Richard Tanner ◽  
Peter Kelly ◽  
Gerard Fahy

A 75-year-old was treated for prostate adenocarcinoma with brachytherapy in September 2018. A routine follow-up chest radiograph 3 months later revealed a metallic object of the same dimensions as a brachytherapy pellet located in the right ventricle. Further imaging showed the brachtherapy pellet was located in the anterobasal right ventricular endocardium close to the tricuspid valve. Frequent asymptomatic premature ventricular contractions were observed with likely origin from the left ventricular outflow tract, an area remote from the site of the pellet. The patient remains asymptomatic and subsequent imaging shows that the position of the pellet has not changed.


1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  

To examine the status of ATP-sensitive K+ (K+ATP) channels and 1,4-dihydropyridine-sensitive Ca2+ (Ca2+DHP) channels during experimental cardiac failure, we have measured the radioligand binding properties of [3H]glyburide and [3H]PN 200 110, respectively, in tissue homogenates from the rat cardiac left ventricle, right ventricle, and brain 4 wk after myocardial infarction induced by left coronary artery ligation. The maximal values (Bmax) for [3H]glyburide and [3H]PN 200 110 binding were reduced by 39 and 40%, respectively, in the left ventricle, and these reductions showed a good correlation with the right ventricle-to-body weight ratio in heart-failure rats. The ligand binding affinities were not altered. In the hypertrophied right ventricle, Bmax values for both the ligands were not significantly different when data were normalized to DNA content or right ventricle weights but showed an apparent reduction when normalized to unit protein or tissue weight. Moderate reductions in channel densities were observed also in whole brain homogenates from heart failure rats. Assessment of muscarinic receptors, beta-adrenoceptors and alpha 1-adrenoceptors by [3H]quinuclidinyl benzilate, [3H]dihydroalprenolol, and [3H]prazosin showed reductions in left ventricular muscarinic and beta-adrenoceptor densities but not in alpha 1-adrenoceptor densities, consistent with earlier observations. It is suggested that these changes may in part contribute to the pathology of cardiac failure.


1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.


2005 ◽  
Vol 15 (4) ◽  
pp. 396-401 ◽  
Author(s):  
Thomas S. Mir ◽  
Jan Falkenberg ◽  
Bernd Friedrich ◽  
Urda Gottschalk ◽  
Throng Phi Lê ◽  
...  

Objective:To evaluate the role of the concentration of brain natriuretic peptide in the plasma, and its correlation with haemodynamic right ventricular parameters, in children with overload of the right ventricle due to congenital cardiac disease.Methods:We studied 31 children, with a mean age of 4.8 years, with volume or pressure overload of the right ventricle caused by congenital cardiac disease. Of the patients, 19 had undergone surgical biventricular correction of tetralogy of Fallot, 11 with pulmonary stenosis and 8 with pulmonary atresia, and 12 patients were studied prior to operations, 7 with atrial septal defects and 5 with anomalous pulmonary venous connections. We measured brain natriuretic peptide using Triage®, from Biosite, United States of America. We determined end-diastolic pressures of the right ventricle, and the peak ratio of right to left ventricular pressures, by cardiac catheterization and correlated them with concentrations of brain natriuretic peptide in the plasma.Results:The mean concentrations of brain natriuretic peptide were 87.7, with a range from 5 to 316, picograms per millilitre. Mean end-diastolic pressure in the right ventricle was 5.6, with a range from 2 to 10, millimetres of mercury, and the mean ratio of right to left ventricular pressure was 0.56, with a range from 0.24 to 1.03. There was a positive correlation between the concentrations of brain natriuretic peptide and the ratio of right to left ventricular pressure (r equal to 0.7844, p less than 0.0001) in all patients. These positive correlations remained when the children with tetralogy of Fallot, and those with atrial septal defects or anomalous pulmonary venous connection, were analysed as separate groups. We also found a weak correlation was shown between end-diastolic right ventricular pressure and concentrations of brain natriuretic peptide in the plasma (r equal to 0.5947, p equal to 0.0004).Conclusion:There is a significant correlation between right ventricular haemodynamic parameters and concentrations of brain natriuretic peptide in the plasma of children with right ventricular overload due to different types of congenital cardiac disease. The monitoring of brain natriuretic peptide may provide a non-invasive and safe quantitative follow up of the right ventricular pressure and volume overload in these patients.


1989 ◽  
Vol 256 (2) ◽  
pp. H352-H360 ◽  
Author(s):  
M. Nagata ◽  
M. Lavallee

The contractile function of heterogeneously perfused segments (HET) after circumflex coronary artery occlusion (CAO) was examined in conscious dogs. At 1 h after CAO, regional shortening (SH) in nonischemic segments did not change from pre-CAO base line, and regional endocardial blood flow (REBF) increased (P less than 0.05) to 1.52 +/- 0.20 from 1.06 +/- 0.08 ml.min-1.g of tissue-1. In ischemic segments, SH was replaced by paradoxical bulging, and REBF averaged 0.07 +/- 0.02 ml.min-1.g of tissue-1. In HET with one crystal of each pair in nonischemic myocardium and the other in severely ischemic myocardium, SH at 1 h after CAO was reduced (P less than 0.01) by 53.2 +/- 3.4%. REBF maps constructed with serial sections of ventricular rings containing the crystals revealed that in HET 50 +/- 5% of the myocardium was ischemic. Therefore, in the acute phase of ischemia, the reductions in SH in HET were proportional to the amount of ischemic myocardium between recording sites. In HET, SH significantly recovered (P less than 0.01) over 4 wk after CAO but remained depressed by 26.8 +/- 5.1%. In contrast, SH in ischemic segments did not improve after CAO. In HET, the effects of inotropic stimulation and changes in left ventricular afterload on SH (as percent of base line) were similar before and at 1-4 wk after CAO. Thus, in HET, the level of dysfunction is acutely determined by the amount of ischemic myocardium between recording sites. Over 4 wk after CAO, SH improved substantially in these segments, and contractile function was not adversely influenced by an inotropic stimulation or an increase in ventricular afterload.


1987 ◽  
Vol 252 (6) ◽  
pp. H1164-H1174
Author(s):  
O. A. Vengen ◽  
K. Lande ◽  
O. Ellingsen ◽  
A. Ilebekk

Cardiac adjustments to inotropic stimulation of the left side of the heart by continuous infusions of isoproterenol (0.6-0.8 microgram/min) and calcium chloride (240 mumol/min) into the left coronary artery were examined in open-chest pigs (17-36 kg) anesthetized with pentobarbital sodium. Both agents caused a reduction in the left ventricular (LV) preload and preejection segment length (PESL). Stroke volume (SV) rose by only 1.2 ml from 15.9 ml (P less than 0.01) during isoproterenol infusion, but when the reduction in LV PESL of 3.2% (P less than 0.01) was restored by saline infusion, SV increased by 27%. The LV PESL reduction was less at hypervolemia than at normovolemia. A computer-based model of the circulation predicted most of these changes and suggested redistribution of blood from the pulmonary to the systemic circulation. During isoproterenol infusion, the pulmonary arterial pressure fell, and the right ventricular end-ejection segment length declined. Reduced right ventricular afterload thus appears to be an important mechanism by which right ventricular output is increased during a selective increase in LV inotropy.


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