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.

Measurement of left and right ventricular volume from implanted radiopaque markers

1981 ◽  
Vol 240 (6) ◽  
pp. H896-H900
Author(s):  
W. P. Santamore ◽  
R. Carey ◽  
D. Goodrich ◽  
A. A. Bove
Keyword(s):  
Standard Deviation ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Ventricular Volumes ◽  
Radiopaque Markers ◽  
Left And Right ◽  
The Right

To better understand biventricular mechanics, an algorithm was developed to simultaneously calculate right and left ventricular volumes from randomly placed subendocardial radiopaque markers. Mathematically, the ventricle is represented as a stack of circular discs. The radius R of each disc is calculated as the distance from the subendocardial radiopaque marker to a computer generated base-to-apex line, and the height H of each disc is determined by the projected distance between radiopaque markers along the base-to-apex line. Accordingly, the volume (V) is calculated as V = pi . sigma Hi . Ri2. The validity of this algorithm was tested on 10 canine left ventricular casts, on 10 human right ventricular casts, and in five experiments. For the left ventricle, the regression line between the casts (VT) and calculated (VC) volumes was VC = 0.55 VT + 6.6, with r = 0.95, standard error of estimate (Sy) = 1.9 ml, and the standard deviation of percent error = 12.6%. For the right ventricle, VC = 1.75 VT = 42.5, with r = 0.86, Sy = 16.2 ml, and the standard deviation of percent error = 24.8%. In five animal experiments, radiopaque markers were implanted into the endocardium of the left and right ventricles and comparisons were made between angiographic- and marker-determined ventricular volumes. For the five experiments, the mean correlation coefficient, relating the marker volumes to the angiographic volumes, were 0.92 +/- 0.01 for the left ventricle and 0.89 +/- 0.02 for the right ventricle. The results, which are similar to other volume-determination methods, indicate that this method can be applied to determine right and left ventricular volume. Once implanted, fluoroscopy of these markers provides a noninvasive means of calculating ventricular volume.

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.

scholarly journals D-Shaped Left Ventricle, Anatomic, and Physiologic Implications

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Eder Hans Cativo Calderon ◽  
Tuoyo O. Mene-Afejuku ◽  
Rachna Valvani ◽  
Diana P. Cativo ◽  
Devendra Tripathi ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Interventricular Septum ◽  
Pressure Overload ◽  
Volume Overload ◽  
Left Ventricular ◽  
Transthoracic Echocardiogram ◽  
Elderly Male ◽  
In Series ◽  
The Right

Right ventricular loading/pressure influences left ventricular function because the two ventricles pump in series and because they are anatomically arranged in parallel, sharing the common ventricular septum. Flattening of the interventricular septum detected during echocardiographic examination is called D-shaped left ventricle. We present a case of an elderly male of African descent, who presented with increased shortness of breath. Transthoracic echocardiogram showed flattening and left sided deviation of interventricular septum causing a decreased size in left ventricle, secondary to volume/pressure overload in the right ventricle. While patient received hemodialysis therapy and intravascular volume was removed, patient blood pressure was noted to increase, paradox. Repeated transthoracic echocardiogram demonstrated less left deviation of interventricular septum compared with previous echocardiogram. We consider that it is important for all physicians to be aware of the anatomic and physiologic implication of D-shaped left ventricle and how right ventricle pressure/volume overload affects its function and anatomy.

scholarly journals Difference in Thickness Between Right Ventricle and Left Ventricle of Adult Human Heart: A Cadaveric Study

2021 ◽  
Vol 9 (4) ◽  
pp. 8116-8119
Author(s):  
Kalpana Thounaojam ◽  
◽  
Keisam Anupama Devi ◽  
Joyce Tunglut ◽  
◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Human Heart ◽  
Interventricular Septum ◽  
Posterior Wall ◽  
Left Ventricular ◽  
Wall Thickening ◽  
Cross Sectional ◽  
Adult Human ◽  
The Right

Background: The left ventricle is longer and narrower than the right ventricle, extending from its base in the plane of the atrioventricular groove to the cardiac apex. The wall of the left ventricle is three times thicker (8-12 mm) than those of right ventricle. The wall of the right ventricle is relatively thin (3–5 mm), the ratio of the thickness of the two ventricular walls usually being 1:3. Hypertrophic cardiomyopathy is characterized by myocardial wall thickening, particularly a disproportionate thickening of the interventricular septum in comparison with the posterior wall. An athlete’s heart may physiologically hypertrophy but in a uniform fashion. The objective of the study is to determine the thickness of wall of right and left ventricle of adult human heart and ratio of thickness of right and left ventricle. Materials and Methods: Adult human hearts were procured from the specimens preserved in Anatomy Department of Jawaharlal Nehru Institute of Medical Sciences. A cross-sectional study was conducted on forty- four specimen of adult heart. The measurement of the right and left ventricular wall was done with digital vernier caliper. The measurements were done at three levels in both right and left ventricle: upper, middle and lower part. Result and Conclusion: The ratio of the thickness of the wall of right and left ventricle is well known as 1:3. However, in our study we found the ratio as 1:1.4. We found the thickness of the right ventricle thicker than the normal thickness reported in previous studies. We wish to continue the study with a larger sample size. KEY WORDS: Heart, Right ventricle, left ventricle, Thickness Ratio, Myocardium.

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.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

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.

Cat heart acetylcholine: structural proof and distribution

1976 ◽  
Vol 231 (3) ◽  
pp. 781-785 ◽  
Author(s):  
OM Brown
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Left Atrium ◽  
Right Atrium ◽  
Interventricular Septum ◽  
Pyrolysis Product ◽  
Heart Tissue ◽  
Choline Esters ◽  
The Right ◽  
Cat Heart

The distribution of acetylcholine (ACh) in the cat heart was investigated by a pyrolysis-gas chromatography (PGC) method. The hearts were dissected into various regions and homogenized in acetonitrile in the presence of propionylcholine, internal standard. Following extraction with toluene and hexane, the choline esters were precipitated as the enneaiodide complex. The isolated choline esters were analyzed by PGC, and the peak corresponding to ACh was quantified. The compound extracted from heart tissue that eluted with the retention time of authentic ACh was identified by mass spectrometry as dimethylaminoethylacetate, the pyrolysis product of ACh. ACh concentrations were found to be higher in the atria than the ventricles. In both the atria and the ventricles, a higher content of ACh was found in the right than the left portions: right ventricle, 5.0 compared to left ventricle, 2.0 nmol/g; and right atrium, 16.8 compared to left atrium, 11.3 nmol/g. Some cats were subjected to a bilateral cervical vagotomy 3 wk before removal and analysis of heart tissue. Hearts from vagotomized cats contained less ACh than controls in the right ventricle (-31%), right atrium (-54%), SA node (-42%), and papillary muscle (-53%), but no decreases were found in the left ventricle, left atrium, or interventricular septum.

scholarly journals Left Ventricular Performance During By-Pass or Distension of the Right Ventricle

1965 ◽  
Vol 17 (6) ◽  
pp. 484-491 ◽  
Author(s):  
SPYRIDON D. MOULOPOULOS ◽  
ARIS SARCAS ◽  
STAMATOS STAMATELOPOULOS ◽  
EVANGELOS AREALIS
Keyword(s):  
Right Ventricle ◽  
Left Ventricular ◽  
Left Ventricular Performance ◽  
Ventricular Performance ◽  
The Right

scholarly journals Genomic modulation of mitochondrial respiratory genes in the hypertrophied heart reflects adaptive changes in mitochondrial and contractile function

2007 ◽  
Vol 293 (5) ◽  
pp. H2819-H2825 ◽  
Author(s):  
Makhosazane Zungu ◽  
Maria Pilar Alcolea ◽  
Francisco José García-Palmer ◽  
Martin E. Young ◽  
M. Faadiel Essop
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Respiratory Function ◽  
Hypobaric Hypoxia ◽  
Contractile Function ◽  
Left Ventricular ◽  
Transcript Levels ◽  
Mitochondrial Number ◽  
The Right ◽  
Mitochondrial Respiratory

We hypothesized the coordinate induction of mitochondrial regulatory genes in the hypertrophied right ventricle to sustain mitochondrial respiratory capacity and contractile function in response to increased load. Wistar rats were exposed to hypobaric hypoxia (11% O2) or normoxia for 2 wk. Cardiac contractile and mitochondrial respiratory function were separately assessed for the right and left ventricles. Transcript levels of several mitochondrial regulators were measured. A robust hypertrophic response was observed in the right (but not left) ventricle in response to hypobaric hypoxia. Mitochondrial O2 consumption was increased in the right ventricle, while proton leak was reduced vs. normoxic controls. Citrate synthase activity and mitochondrial DNA content were significantly increased in the hypertrophied right ventricle, suggesting higher mitochondrial number. Transcript levels of nuclear respiratory factor-1, peroxisome proliferator-activated receptor-γ-coactivator-1α, cytochrome oxidase (COX) subunit II, and uncoupling protein-2 (UCP2) were coordinately induced in the hypertrophied right ventricle following hypoxia. UCP3 transcript levels were significantly reduced in the hypertrophied right ventricle vs. normoxic controls. Exposure to chronic hypobaric hypoxia had no significant effects on left ventricular mitochondrial respiration or contractile function. However, COXIV and UCP2 gene expression were increased in the left ventricle in response to chronic hypobaric hypoxia. In summary, we found coordinate induction of several genes regulating mitochondrial function and higher mitochondrial number in a model of physiological right ventricular hypertrophy, linking the efficiency of mitochondrial oxidative phosphorylation and respiratory function to sustained contractile function in response to the increased load.

Delayed enhancement imaging in a contemporary patient cohort following correction of tetralogy of Fallot

2014 ◽  
Vol 25 (7) ◽  
pp. 1268-1275 ◽  
Author(s):  
Uta Preim ◽  
Philipp Sommer ◽  
Janine Hoffmann ◽  
Jana Kehrmann ◽  
Lukas Lehmkuhl ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Tetralogy Of Fallot ◽  
Nyha Class ◽  
Left Ventricular ◽  
Delayed Enhancement ◽  
Volume Index ◽  
Delayed Enhancement Imaging ◽  
The Right ◽  
Myocardial Scars

AbstractObjectiveTo test the hypothesis that myocardial scars after repair of tetralogy of Fallot are related to impaired cardiac function and adverse clinical outcome.MethodsA total of 53 patients were retrospectively analysed after repair of tetralogy of Fallot. The median patient age was 20 years (range 2–48).Cardiac MRI with a 1.5 T magnet included cine sequences to obtain volumes and function, phase-sensitive inversion recovery delayed enhancement imaging to detect myocardial scars, and flow measurements to determine pulmonary regurgitation fraction. In addition, clinical parameters were obtained.ResultsAn overall 83% of patients were in NYHA class I. All patients with the exception of 2 (96%) had pulmonary insufficiency. Mean ejection fraction and end-diastolic volume index were 46% and 128 ml/m2 for the right ventricle and 54% and 82 ml/m2 for the left ventricle, respectively. Excluding enhancement of the septal insertion and prosthetic patches, delayed enhancement was seen in 11/53 cases (21%). Delayed enhancement of the right ventricle was detected in 6/53 patients (11%) and of the left ventricle in 5/53 patients (9%). The patient group with delayed enhancement was significantly older (p=0.003), had later repair (p=0.007), and higher left ventricular myocardial mass index (p=0.009) compared with the group without delayed enhancement.ConclusionsThis study reveals that scarring is common in patients after surgical repair of tetralogy of Fallot and is associated with older age and late repair. However, there was no difference in right ventricular function, NYHA class, or occurrence of clinically relevant arrhythmias between patients with and those without myocardial scars.

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