Differential changes in left and right ventricular SR calcium transport in congestive heart failure

1992 ◽  
Vol 262 (3) ◽  
pp. H868-H874 ◽  
Author(s):  
N. Afzal ◽  
N. S. Dhalla
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Maximal Velocity ◽  
Experimental Animals ◽  
Uptake Activity ◽  
Left And Right ◽  
The Right

To examine the status of sarcoplasmic reticulum (SR) with respect to Ca2+ transport in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated for 4, 8, and 16 wk. The left heart function was assessed with an intraventricular pressure transducer, and SR membrane fractions from the right ventricle and the viable left ventricle were isolated for measuring the ATP-dependent Ca2+ uptake activities. In comparison to sham-operated controls, SR Ca2+ uptake activity was decreased in viable left ventricle of the experimental animals at 4, 8, and 16 wk. On the other hand, SR Ca2+ uptake activity in the right ventricle was increased at 4 and 8 wk, but no change was apparent at 16 wk of coronary occlusion. The decrease in SR Ca2+ uptake in left ventricle and increase in right ventricle were associated with corresponding changes in maximal velocity values without any alterations in the affinity for Ca2+. These opposite changes in the right and left ventricles were dependent on the scar size as well as time after inducing the myocardial infarction. The SR Ca(2+)-stimulated adenosinetriphosphatase activity was decreased in left ventricle and increased in the right ventricle from 4 wk experimental animals. The results suggest differential remodeling of the SR membranes with respect to Ca(2+)-pump mechanisms in left and right ventricles during the development of congestive heart failure.

Differential changes in left and right ventricular adenylyl cyclase activities in congestive heart failure

1997 ◽  
Vol 272 (2) ◽  
pp. H884-H893 ◽  
Author(s):  
R. Sethi ◽  
K. S. Dhalla ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Adenylyl Cyclase ◽  
Adrenergic Receptors ◽  
The Status ◽  
Left And Right ◽  
The Right

The status of beta-adrenergic receptors and adenylyl cyclase in crude membranes from both left and right ventricles was examined when the left coronary artery in rats was occluded for 4, 8, and 16 wk. The adenylyl cyclase activity in the presence of isoproterenol was decreased in the uninfarcted (viable) left ventricle and increased in the right ventricle subsequent to myocardial infarction. The density of beta1-adrenergic receptors, unlike beta2-receptors, was reduced in the left ventricle, whereas no change in the characteristics of beta1- and beta2-adrenergic receptors was seen in the right ventricle. The catalytic activity of adenylyl cyclase was depressed in the viable left ventricle but was unchanged in the right ventricle. In comparison to sham controls, the basal, as well as NaF-, forskolin-, and 5'-guanylyl imidodiphosphate [Gpp(NH)p]-stimulated adenylyl cyclase activities were decreased in the left ventricle and increased in the right ventricle of the experimental animals. Opposite alterations in the adenylyl cyclase activities in left and right ventricles from infarcted animals were also seen when two types of purified sarcolemmal preparations were employed. These changes in adenylyl cyclase activities in the left and right ventricles were dependent on the degree of heart failure. Furthermore, adenosine 3',5'-cyclic monophosphate contents were higher in the right ventricle and lower in the left ventricle from infarcted animals injected with saline, isoproterenol, or forskolin in comparison to the controls. The results suggest differential changes in the viable left and right ventricles with respect to adenylyl cyclase activities during the development of congestive heart failure due to myocardial infarction.

Left ventricular failure induced by myocardial infarction. II. Tissue morphometry

1985 ◽  
Vol 248 (6) ◽  
pp. H883-H889 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Volume Fraction ◽  
Volume Ratio ◽  
Left Ventricular ◽  
Tissue Growth ◽  
Left And Right ◽  
The Right ◽  
And Diffusion

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.

Regulation of K+ and Ca2+ channels in experimental cardiac failure

1991 ◽  
Vol 261 (6) ◽  
pp. H1979-H1987 ◽  
Author(s):  
M. Gopalakrishnan ◽  
D. J. Triggle ◽  
A. Rutledge ◽  
Y. W. Kwon ◽  
J. A. Bauer ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Cardiac Failure ◽  
Radioligand Binding ◽  
Weight Ratio ◽  
Left Ventricular ◽  
Coronary Artery Ligation ◽  
Artery Ligation ◽  
The Right

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.

Plasma Levels of Adrenomedullin in Patients with Acute Myocardial Infarction

1998 ◽  
Vol 94 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Yuji Yoshitomi ◽  
Toshio Nishikimi ◽  
Shunichi Kojima ◽  
Morio Kuramochi ◽  
Shuichi Takishita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Congestive Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Right Atrium ◽  
Plasma Levels ◽  
The Right

1. Adrenomedullin, a newly identified vasorelaxant peptide, participates in the regulation of the cardiovascular system. To investigate the pathophysiological significance of adrenomedullin in patients with acute myocardial infarction, we measured plasma levels of adrenomedullin. 2. Cardiac catheterization was performed on admission, after 1 day, and after 4 weeks in 36 patients with acute myocardial infarction. We measured plasma levels of adrenomedullin, atrial natriuretic peptide and brain natriuretic peptide in the right atrium, pulmonary artery and aorta. 3. Plasma levels of adrenomedullin in the right atrium (mean ± SEM) were significantly increased on admission (4.2 ± 2.6 h) in patients with acute myocardial infarction (10.6 ± 1.0 pmol/l) compared with controls (5.2 ± 0.3 pmol/l, P < 0.01). In addition, plasma levels of adrenomedullin were further elevated in patients with congestive heart failure (12.3 ± 1.4 pmol/l) compared with patients without congestive heart failure (7.8 ± 0.6 pmol/l, P < 0.01). In patients with congestive heart failure, plasma adrenomedullin on admission significantly correlated with atrial natriuretic peptide and brain natriuretic peptide. 4. These results suggest that plasma adrenomedullin increases in the early phase of acute myocardial infarction and that volume expansion may be one of the additional stimuli for the release of adrenomedullin in patients with acute myocardial infarction complicated by congestive heart failure.

Alterations in ventricular excitability in conscious dogs during development of chronic heart failure

1986 ◽  
Vol 250 (6) ◽  
pp. H1022-H1029 ◽  
Author(s):  
C. W. White ◽  
M. J. Mirro ◽  
D. D. Lund ◽  
D. J. Skorton ◽  
N. G. Pandian ◽  
...  
Keyword(s):  
Heart Failure ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Time Course ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Maximum Increase ◽  
Electrophysiological Properties ◽  
Cycle Lengths ◽  
The Right

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.

Sarcolemmal calcium transport in congestive heart failure due to myocardial infarction in rats

1992 ◽  
Vol 262 (5) ◽  
pp. H1387-H1394 ◽  
Author(s):  
I. M. Dixon ◽  
T. Hata ◽  
N. S. Dhalla
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Calcium Transport ◽  
Left Coronary Artery ◽  
Diastolic Pressure ◽  
Abdominal Cavity ◽  
Left Ventricular ◽  
Maximal Velocity ◽  
Negative Change

Because Na(+)-Ca2+ exchange and Ca2+ pump are thought to play a role in sarcolemmal Ca2+ movements, we examined the Na(+)-dependent Ca(2+)-uptake and ATP-dependent Ca(2+)-uptake activities in failing heart after myocardial infarction in rats. The left coronary artery was ligated, and the viable left ventricle was used 4, 8, and 16 wk later; sham-operated animals served as controls. Increased left ventricular diastolic pressure and decreased positive and negative change in pressure over time were observed in experimental animals at 4, 8, and 16 wk; these changes were associated with accumulation of fluid in the abdominal cavity. The sarcolemmal Na(+)-dependent Ca2+ uptake was depressed in 4-, 8-, and 16-wk experimental hearts. The decrease in sarcolemmal Na(+)-dependent Ca2+ uptake in failing hearts was seen when the activity was assayed either as a function of time or Ca2+ concentration; a depression of maximal velocity without any change in activity constant for Ca2+ was observed. No alteration in the Ca2+ pump (ATP-dependent Ca2+ accumulation and Ca(2+)-stimulated adenosinetriphosphatase) activities was evident in the 4-, 8-, and 16-wk experimental groups. These data suggest that changes in the Na(+)-dependent Ca2+ handling by the sarcolemmal membrane may be associated with contractile abnormalities in this model of congestive heart failure.

Differential Alterations in Left and Right Ventricular G-Proteins in Congestive Heart Failure due to Myocardial Infarction

1998 ◽  
Vol 30 (11) ◽  
pp. 2153-2163 ◽  
Author(s):  
Rajat Sethi ◽  
Vijayan Elimban ◽  
Donald Chapman ◽  
Ian M.C. Dixon ◽  
Naranjan S. Dhalla
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Congestive Heart Failure ◽  
Right Ventricular ◽  
G Proteins ◽  
Left And Right

Difficulties in diagnosing the myocardial infarction of the left ventricle inferior wall involving the right ventricle

2021 ◽  
Vol 19 (1) ◽  
pp. 82-85
Author(s):  
S. D. Mayanskaya ◽  
◽  
A. A. Gilmanov ◽  
T. V. Rudneva ◽  
M. M. Mangusheva ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Left Ventricular ◽  
Inferior Wall ◽  
Jugular Veins ◽  
St Segment Elevation ◽  
St Segment ◽  
The Right ◽  
Negative Predictor

The article presents a clinical observation of myocardial infarction (MI) of the inferior wall of the left ventricle (LV) with ST-segment elevation in combination with damage to the right ventricle (RV). Unfortunately, there is often a delay in the timely diagnosis of RV involvement in the process. This is because, at the beginning of the symptoms, it may not differ clinically from the typical manifestations of MI of the inferior-diaphragmatic region of the LV. However, the combination of LV inferior wall MI with RV MI is an important, negative predictor of increased mortality in these patients. In this case, RV MI was diagnosed after stenting of the right coronary artery, only when signs of hypotension and increased pressure of the jugular veins appeared. Based on the analysis of this clinical case, the authors discuss the need to record an ECG of the right heart in most patients with inferior MI, especially in the presence of hypotension without signs of acute left ventricular failure.

Parasympathetic control of the heart. I. An interventriculo-septal ganglion is the major source of the vagal intracardiac innervation of the ventricles

2004 ◽  
Vol 96 (6) ◽  
pp. 2265-2272 ◽  
Author(s):  
Tannis A. Johnson ◽  
Alrich L. Gray ◽  
Jean-Marie Lauenstein ◽  
Stephen S. Newton ◽  
V. John Massari
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Left Ventricular ◽  
Anterior Surface ◽  
Ventricular Performance ◽  
Neuronal Marker ◽  
Left And Right ◽  
Intracardiac Ganglia ◽  
The Right

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 ± 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.

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