Effects of Bupivacaine on Mitochondrial Energy Metabolism in Heart of Rats following Exposure to Chronic Hypoxia

2002 ◽  
Vol 97 (6) ◽  
pp. 1507-1511 ◽  
Author(s):  
Karine Nouette-Gaulain ◽  
François Forestier ◽  
Monique Malgat ◽  
Roger Marthan ◽  
Jean-Pierre Mazat ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Left Ventricle ◽  
Adenosine Triphosphate ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Left Ventricular ◽  
Mitochondrial Energy Metabolism ◽  
Hypoxic Heart ◽  
The Right

Background Adaptation to chronic exposure to hypoxia alters energy metabolism in the heart, particularly in the left ventricle, which undergoes a loss in oxidative capacity. Highly lipophilic local anesthetics interfere with mitochondrial energy metabolism. The purpose of this study was to compare the effects of bupivacaine on mitochondrial energy metabolism in heart of rats subjected to normoxic or hypoxic environments. Methods Male Wistar rats (n = 10) were subjected to hypobaric hypoxia (simulated altitude = 5,000 m, 380 mmHg) for 2 weeks. Control rats (n = 10) were maintained in an ambient normoxic environment. Mitochondrial metabolism (oxygen consumption and adenosine triphosphate synthesis) was assessed using saponin-skinned ventricular fibers. Bupivacaine (0-5 mM) was tested on both left and right ventricles of normoxic or hypoxic heart. Results In animals exposed to hypobaric hypoxia for 14 days, cardiac mass significantly increased, and the right-to-left ventricular ratio was approximately twofold (0.48 +/- 0.11 vs. 0.22 +/- 0.04, P < 0.05). Oxygen consumption and adenosine triphosphate synthesis were significantly lower in the hypoxic left ventricles but not in the right ones. The uncoupling effect of bupivacaine was more pronounced in the left ventricle from hypoxic heart than in the right ventricle; the bupivacaine-induced decrease in the adenosine triphosphate synthesis rate and in the adenosine triphosphate-to-oxygen ratio was significantly greater in the hypoxic left ventricle than in the normoxic one. Conclusions Chronic hypoxia impairs cardiac energy metabolism in left ventricles and enhances the depressant effects of bupivacaine on mitochondrial functions.

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.

Comparison of the Effects of Bupivacaine and Ropivacaine on Heart Cell Mitochondrial Bioenergetics 

1998 ◽  
Vol 88 (5) ◽  
pp. 1340-1349 ◽  
Author(s):  
Francois Sztark ◽  
Monique Malgat ◽  
Philippe Dabadie ◽  
Jean-Pierre Mazat
Keyword(s):  
Oxygen Consumption ◽  
Energy Metabolism ◽  
Adenosine Triphosphate ◽  
Respiratory Chain ◽  
Local Anesthetics ◽  
Metabolic Effects ◽  
Lipid Solubility ◽  
Mitochondrial Bioenergetics ◽  
Mitochondrial Energy Metabolism ◽  
Isolated Mitochondria

Background High lipophilic local anesthetics interfere with mitochondrial energy metabolism. These metabolic effects could in part explain some of the toxic effects of local anesthetics, such as bupivacaine-induced myocardial depression. The aim of this study was to compare the bioenergetic effects of the local anesthetics bupivacaine and ropivacaine. Methods The effects of both local anesthetics on mitochondrial energy metabolism were studied in rat heart isolated mitochondria and in saponin-skinned left ventricle fibers. Oxygen consumption, adenosine triphosphate synthesis, and enzymatic activities of the complexes of the respiratory chain were measured. Results Bupivacaine and ropivacaine acted, in isolated mitochondria, as uncouplers between oxygen consumption and phosphorylation of adenosine diphosphate. Further, an inhibitory effect of mitochondrial respiration was evidenced with both anesthetics during maximal respiration and was assigned to a direct inhibition of complex I of the respiratory chain. Mitochondrial adenosine triphosphate synthesis was decreased by both mechanisms. However, both in isolated mitochondria and in permeabilized heart fibers, ropivacaine was less potent than bupivacaine. Adenosine triphosphate synthesis was completely suppressed at 3 mM (approximately 0.1%) bupivacaine, whereas 3 mM ropivacaine induced only about a 40% inhibition. Conclusions Ropivacaine disturbs mitochondrial energy metabolism less than bupivacaine does. The lower lipid solubility of ropivacaine may be responsible for the lesser dose-dependent effects of this drug on mitochondrial bioenergetics.

Clinical and Experimental Analysis of 201Thallium Uptake of the Heart

1978 ◽  
Vol 17 (04) ◽  
pp. 142-148
Author(s):  
U. Büll ◽  
S. Bürger ◽  
B. E. Strauer
Keyword(s):  
Oxygen Consumption ◽  
Left Ventricle ◽  
Muscle Mass ◽  
Myocardial Oxygen Consumption ◽  
Animal Experiments ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Ventricular Wall ◽  
Flow Measurements ◽  
Myocardial Flow

Studies were carried out in order to determine the factors influencing myocardial 201T1 uptake. A total of 158 patients was examined with regard to both 201T1 uptake and the assessment of left ventricular and coronary function (e. g. quantitative ventriculography, coronary arteriography, coronary blood flow measurements). Moreover, 42 animal experiments (closed chest cat) were performed. The results demonstrate that:1) 201T1 uptake in the normal and hypertrophied human heart is linearly correlated with the muscle mass of the left ventricle (LVMM);2) 201T1 uptake is enhanced in the inner (subendocardial) layer and is decreased in the outer (subepicardial) layer of the left ventricular wall. The 201T1 uptake of the right ventricle is 40% lower in comparison to the left ventricle;3) the basic correlation between 201T1 uptake and LVMM is influenced by alterations of both myocardial flow and myocardial oxygen consumption; and4) inotropic interventions (isoproterenol, calcium, norepinephrine) as well as coronary dilatation (dipyridamole) may considerably augment 201T1 uptake in accordance with changes in myocardial oxygen consumption and/or myocardial flow.It is concluded that myocardial 201T1 uptake is determined by multiple factors. The major determinants have been shown to include (i) muscle mass, (ii) myocardial flow and (iii) myocardial oxygen consumption. The clinical data obtained from patient groups with normal ventricular function, with coronary artery disease, with left ventricular wall motion abnormalities and with different degree of left ventricular hypertrophy are correlated with quantitated myocardial 201T1 uptake.

scholarly journals Hemodynamic Support Using Percutaneous Transfemoral Impella 5.0 and Impella RP for Refractory Cardiogenic Shock

2019 ◽  
Vol 2019 ◽  
pp. 1-6 ◽  
Author(s):  
Pratik K. Dalal ◽  
Amy Mertens ◽  
Dinesh Shah ◽  
Ivan Hanson
Keyword(s):  
Left Ventricle ◽  
Pulmonary Artery ◽  
Cardiogenic Shock ◽  
Ventricular Function ◽  
Standard Of Care ◽  
Left Ventricular ◽  
Biventricular Failure ◽  
Ventricular Support ◽  
The Right ◽  
Flow Pump

Acute myocardial infarction (AMI) resulting in cardiogenic shock continues to be a substantial source of morbidity and mortality despite advances in recognition and treatment. Prior to the advent of percutaneous and more durable left ventricular support devices, prompt revascularization with the addition of vasopressors and inotropes were the standard of care in the management of this critical population. Recent published studies have shown that in addition to prompt revascularization, unloading of the left ventricle with the placement of the Impella percutaneous axillary flow pump can lead to improvement in mortality. Parameters such as the cardiac power output (CPO) and pulmonary artery pulsatility index (PAPi), obtained through pulmonary artery catheterization, can help ascertain the productivity of right and left ventricular function. Utilization of these parameters can provide the information necessary to escalate support to the right ventricle with the insertion of an Impella RP or the left ventricle with the insertion of larger devices, which provide more forward flow. Herein, we present a case of AMI complicated by cardiogenic shock resulting in biventricular failure treated with the percutaneous insertion of an Impella RP and Impella 5.0 utilizing invasive markers of left and right ventricular function to guide the management and escalation of care.

scholarly journals Left ventricular noncompaction—a rare cause of triad: heart failure, ventricular arrhythmias, and systemic embolic events: a case report 

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Despina Toader ◽  
Alina Paraschiv ◽  
Petrișor Tudorașcu ◽  
Diana Tudorașcu ◽  
Constantin Bataiosu ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Left Ventricle ◽  
Ventricular Arrhythmias ◽  
Left Ventricular ◽  
Left Ventricular Ejection ◽  
Left Ventricular Noncompaction ◽  
Ventricular Noncompaction ◽  
The Right

Abstract Background Left ventricular noncompaction is a rare cardiomyopathy characterized by a thin, compacted epicardial layer and a noncompacted endocardial layer, with trabeculations and recesses that communicate with the left ventricular cavity. In the advanced stage of the disease, the classical triad of heart failure, ventricular arrhythmia, and systemic embolization is common. Segments involved are the apex and mid inferior and lateral walls. The right ventricular apex may be affected as well. Case presentation A 29-year-old Caucasian male was hospitalized with dyspnea and fatigue at minimal exertion during the last months before admission. He also described a history of edema of the legs and abdominal pain in the last weeks. Physical examination revealed dyspnea, pulmonary rales, cardiomegaly, hepatomegaly, and splenomegaly. Electrocardiography showed sinus rhythm with nonspecific repolarization changes. Twenty-four-hour Holter monitoring identified ventricular tachycardia episodes with right bundle branch block morphology. Transthoracic echocardiography at admission revealed dilated left ventricle with trabeculations located predominantly at the apex but also in the apical and mid portion of lateral and inferior wall; end-systolic ratio of noncompacted to compacted layers > 2; moderate mitral regurgitation; and reduced left ventricular ejection fraction. Between apical trabeculations, multiple thrombi were found. The right ventricle had normal morphology and function. Speckle-tracking echocardiography also revealed systolic left ventricle dysfunction and solid body rotation. Abdominal echocardiography showed hepatomegaly and splenomegaly. Abdominal computed tomography was suggestive for hepatic and renal infarctions. Laboratory tests revealed high levels of N-terminal pro-brain natriuretic peptide and liver enzymes. Cardiac magnetic resonance evaluation at 1 month after discharge confirmed the diagnosis. The patient received anticoagulants, antiarrhythmics, and heart failure treatment. After 2 months, before device implantation, he presented clinical improvement, and echocardiographic evaluation did not detect thrombi in the left ventricle. Coronary angiography was within normal range. A cardioverter defibrillator was implanted for prevention of sudden cardiac death. Conclusions Left ventricular noncompaction is rare cardiomyopathy, but it should always be considered as a possible diagnosis in a patient hospitalized with heart failure, ventricular arrhythmias, and systemic embolic events. Echocardiography and cardiac magnetic resonance are essential imaging tools for diagnosis and follow-up.

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.

scholarly journals Age-associated Decline in Phosphorylated Connexin 43 Protein Expression in the Left Ventricular Tissue of Wister Rats

2019 ◽  
pp. 1-8
Author(s):  
Donatus Onukwufor Onwuli ◽  
Sandra A. Jones
Keyword(s):  
Left Ventricle ◽  
Western Blot ◽  
Cardiac Arrhythmia ◽  
Connexin 43 ◽  
The Elderly ◽  
Left Ventricular ◽  
Cardiac Impulse ◽  
Ventricular Tissue ◽  
Connexin Proteins ◽  
The Right

Cardiac arrhythmia affects ~ 6% in those over 65 years of age (old), but with 0.2% occurrence in those of 45 years and below (young). Arrhythmia can result from dysregulation of the cardiac impulse generation and its conduction. Connexin proteins are responsible for cardiac impulse conduction, and phosphorylation of connexin 43 determines its functional ability. In this study, Phosphorylated connexin 43, density and expression were assessed in ventricular tissues from young (6 months old) and old (24 months old) Wister rats, using the techniques of western blot and immunohistochemistry. Results show that phosphorylated Cx43 in the left ventricle of 24 months old rats significantly declined (P=0.04 & 0.01) by method of western blot and immunohistochemistry respectively, but did not differ in the right ventricle. The left ventricle is known to be responsible for cardiac output. This data suggest an age-associated decline in the expression of phosphorylated connexin 43 in the left ventricle, which may play a significant role in the development of cardiac arrhythmia in the elderly.

Isolated left ventricular apical hypoplasia in a young child

2021 ◽  
Vol 14 (1) ◽  
pp. e239297
Author(s):  
H Ravi Ramamurthy ◽  
Onkar Auti ◽  
Vimal Raj ◽  
Kiran Viralam
Keyword(s):  
Left Ventricle ◽  
Left Ventricular ◽  
Long Term Outcomes ◽  
Wave Inversion ◽  
St Segment ◽  
Cardiac Apex ◽  
The Right ◽  
First Time ◽  
Left Lead

A 16-month-old, healthy, asymptomatic male child presented with a diagnosis of dilated cardiomyopathy. Cardiovascular examination and chest radiograph were normal. ECG revealed sinus rhythm, and the augmented vector left lead showed raised ST segment, T wave inversion and q waves. Echocardiography showed a globular left ventricle with notched cardiac apex, abnormal echogenicity in the left ventricular apical myocardium, single papillary muscle and normal biventricular function. Cardiac MRI scan revealed a globular left ventricle with fibrofatty changes and retraction of the apex, the papillary muscles closely approximated, and the right ventricle wrapping around the apex of the left ventricle. This is described as isolated left ventricular apical hypoplasia. Diagnosis of this rare entity can be made by MRI, and it has been diagnosed largely in adults. The pathophysiology and long-term outcomes are unknown. We characterise the echocardiography findings of this rare anomaly in a child for the first time in the literature.

scholarly journals Heart anatomy of Giraffa camelopardalis rothschildi: a case report

2008 ◽  
Vol 53 (No. 3) ◽  
pp. 165-168 ◽  
Author(s):  
W. Perez ◽  
M. Lima ◽  
G. Pedrana ◽  
F. Cirillo
Keyword(s):  
Case Report ◽  
Coronary Artery ◽  
Left Ventricle ◽  
Left Coronary Artery ◽  
Left Ventricular ◽  
Left Auricle ◽  
Papillary Muscles ◽  
Atrioventricular Valve ◽  
Heart Anatomy ◽  
The Right

In the present study the most outstanding anatomical findings of the heart of a giraffe are described. Two papillary muscles were found in the right ventricle, namely magnus and subarterial. There were no papillary parvi muscles. The supraventricular crest gave insertion to various tendinous chords. These chords fixed the angular cusp of the right atrioventricular valve. The pectinate muscles were better developed in the left auricle than in the right one. Within the left ventricle two big papillary muscles were found as well as a notorious septomarginal trabecula. The left coronary artery irrigated the majority of the heart’s territory. It gave origin to the interventricular paraconal branch and to the circumflex branch. The latter gave off the branch of the left ventricular border and the interventricular subsinosal branch.

Sign in / Sign up

Export Citation Format

Share Document