Lactic Acidosis and the Cardiovascular System in the Dog

1983 ◽  
Vol 64 (6) ◽  
pp. 573-580 ◽  
Author(s):  
Allen I. Arieff ◽  
Edward W. Gertz ◽  
Robert Park ◽  
Will Leach ◽  
Virginia C. Lazarowitz
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Lactic Acid ◽  
Lactic Acidosis ◽  
Cardiac Function ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Control Group ◽  
Type B

1. Lactic acidosis is a clinical syndrome characterized by metabolic acidaemia (pH < 7.25) and hyperlactaemia (lactate >5 mmol/l). Many patients with type B lactic acidosis have no evidence of tissue hypoxia or myocardial dysfunction when first evaluated. Although it is considered that cardiac dysfunction is secondary to the systemic effects of lactic acidosis, the reverse may sometimes be true. To evaluate this possibility, studies were carried out in 43 dogs consisting of a control group and three groups which had hyperlactataemia and metabolic acidaemia related to either: (1) phenformin infusion; (2) hepatectomy; (3) lactic acid infusion. Serial studies of cardiac function, as well as measurements of GFR (glomerular filtration rate) and hepatic portal vein (HPV) blood flow, were carried out. 2. in dogs infused with phenformin for 99 min, the arterial pH, lactate, bicarbonate, heart rate and mean blood pressure (BP) were normal. However, there was significant deterioration (P < 0.01) in several indices of cardiac function, including the peak positive dP/dt, cardiac output, LVEDP (left ventricular end-diastolic pressure) and percentage extraction of oxygen and lactate by the heart. After 3 h of phenformin, the blood lactate exceeded 5 mmol/l and there were further significant decrements (P < 0.01) in cardiac output, LVEDP and dP/dt, as well as BP and heart rate. in dogs subjected to hepatectomy, the decrement in cardiac output was similar to that with phenformin infusion. However, in animals infused with lactic acid, despite a similar blood pH and lactate, cardiac output was unaffected. Although percentage myocardial oxygen extraction declined in phenformin-infused animals, there was a concomitant increase in coronary sinus blood flow such that myocardial oxygen utilization was probably unaltered. 3. Thus, in certain types of experimental type B lactic acidosis, myocardial dysfunction may be a primary event, with other associated systemic manifestations being secondary.

scholarly journals Elevated vascular resistance and afterload reduce the cardiac output response to dobutamine in early growth-restricted rats in adulthood

2011 ◽  
Vol 106 (9) ◽  
pp. 1374-1382 ◽  
Author(s):  
Vladislava Zohdi ◽  
M. Jane Black ◽  
James T. Pearson
Keyword(s):  
Cardiac Output ◽  
Cardiac Function ◽  
Peripheral Resistance ◽  
Early Growth ◽  
Left Ventricular ◽  
Growth Restriction ◽  
Protein Diet ◽  
Ventricular Pressure ◽  
Control Group ◽  
Increased Risk

Epidemiological studies have linked intra-uterine growth restriction (IUGR) with an increased risk of CVD later in life. The aim of the present study was to examine the effect of maternal protein restriction on cardiac function in adulthood during dobutamine (DOB) stimulation. IUGR was induced in Wistar Kyoto dams through administration of a low-protein diet (LPD; 8·7 % casein) during pregnancy and lactation; the control group received a normal-protein diet (NPD; 20 % casein). At 14 weeks of age, cardiac function was assessed in male and female NPD (eight females and eight males) and LPD offspring (ten females and ten males) by pressure volumetry using an anaesthetised closed-chest approach. We determined mean arterial pressure (MAP), heart rate and left ventricular pressure–volume indices under baseline conditions and DOB stimulation (2 and 4 μg/kg per min). During β-adrenergic activation in LPD offspring, increases in cardiac output (CO, P < 0·018) and stroke volume (SV, P < 0·005) were attenuated in comparison with NPD offspring, while increases in ejection fraction and the maximal rate of ventricular pressure development were not affected. LPD females maintained a smaller end-diastolic volume (P < 0·017). MAP did not differ between the groups and did not change significantly during DOB infusion. Arterial elastance and total peripheral resistance decreased in all rats but remained significantly elevated in LPD offspring (P < 0·015 and < 0·01). Early growth restriction did not affect ventricular contractility but led to an increased afterload and impaired the ability to increase SV and CO during β-adrenergic stimulation.

scholarly journals Esmolol for cardioprotection during resuscitation with adrenaline in an ischaemic porcine cardiac arrest model

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Hilde Karlsen ◽  
Harald Arne Bergan ◽  
Per Steinar Halvorsen ◽  
Kjetil Sunde ◽  
Eirik Qvigstad ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiac Output ◽  
Single Dose ◽  
Cardiac Function ◽  
Left Ventricular ◽  
Low Flow ◽  
Control Group ◽  
Myocardial Infarct Size ◽  
Tetrazolium Chloride ◽  
Va Ecmo

Abstract Background The effectiveness of adrenaline during resuscitation continues to be debated despite being recommended in international guidelines. There is evidence that the β-adrenergic receptor (AR) effects of adrenaline are harmful due to increased myocardial oxygen consumption, post-defibrillation ventricular arrhythmias and increased severity of post-arrest myocardial dysfunction. Esmolol may counteract these unfavourable β-AR effects and thus preserve post-arrest myocardial function. We evaluated whether a single dose of esmolol administered prior to adrenaline preserves post-arrest cardiac output among successfully resuscitated animals in a novel, ischaemic cardiac arrest porcine model. Methods Myocardial infarction was induced in 20 anaesthetized pigs by inflating a percutaneous coronary intervention (PCI) balloon in the circumflex artery 15 min prior to induction of ventricular fibrillation. After 10 min of untreated VF, resuscitation with veno-arterial extracorporeal membrane oxygenation (VA-ECMO) was initiated and the animals were randomized to receive an injection of either 1 mg/kg esmolol or 9 mg/ml NaCl, prior to adrenaline. Investigators were blinded to allocation. Successful defibrillation was followed by a 1-h high-flow VA-ECMO before weaning and an additional 1-h stabilization period. The PCI-balloon was deflated 40 min after inflation. Cardiac function pre- and post-arrest (including cardiac output) was assessed by magnetic resonance imaging (MRI) and invasive pressure measurements. Myocardial injury was estimated with MRI, triphenyl tetrazolium chloride (TTC) staining and serum concentrations of cardiac troponin T. Results Only seven esmolol and five placebo-treated pigs were successfully resuscitated and available for post-arrest measurements (p = 0.7). MRI revealed severe but similar reductions in post-arrest cardiac function with cardiac output 3.5 (3.3, 3.7) and 3.3 (3.2, 3.9) l/min for esmolol and control (placebo) groups, respectively (p = 0.7). The control group had larger left ventricular end-systolic and end-diastolic ventricular volumes compared to the esmolol group (75 (65, 100) vs. 62 (53, 70) ml, p = 0.03 and 103 (86, 124) vs. 87 (72, 91) ml, p = 0.03 for control and esmolol groups, respectively). There were no other significant differences in MRI characteristics, myocardial infarct size or other haemodynamic measurements between the two groups. Conclusions We observed similar post-arrest cardiac output with and without a single dose of esmolol prior to adrenaline administration during low-flow VA-ECMO in an ischaemic cardiac arrest pig model.

Echocardiographic effects of dexmedetomidine–ketamine in chinchillas (Chinchilla lanigera)

2016 ◽  
Vol 51 (1) ◽  
pp. 89-92 ◽  
Author(s):  
Grayson A Doss ◽  
Christoph Mans ◽  
Rebecca L Stepien
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Function ◽  
Flow Velocity ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Ketamine Anesthesia ◽  
Echocardiographic Parameters ◽  
Fractional Shortening

Alpha2-agonist anesthetic combinations are often used in rodent anesthesia but no information about their effects on cardiac function in chinchillas exists. The purpose of this study was to utilize echocardiography to evaluate the cardiovascular effects of dexmedetomidine–ketamine anesthesia in chinchillas. Echocardiographic examinations were performed in eight adult chinchillas under manual restraint and following dexmedetomidine (0.015 mg/kg) and ketamine (4 mg/kg) administration. Dexmedetomidine–ketamine anesthesia resulted in a significantly decreased heart rate, fractional shortening, cardiac output, and flow velocity across the aortic and pulmonic valves, and significantly increased left ventricular internal diameter in systole. The observed changes in echocardiographic parameters are similar to those previously reported in chinchillas anesthetized with isoflurane.

Alpha 1-adrenergic constriction limits coronary flow and cardiac function in running dogs

1986 ◽  
Vol 250 (6) ◽  
pp. H1117-H1126 ◽  
Author(s):  
P. A. Gwirtz ◽  
S. P. Overn ◽  
H. J. Mass ◽  
C. E. Jones
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Function ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
Adrenergic Blockade

Modulation of coronary blood flow and cardiac function by alpha 1-adrenergic receptors was examined in dogs during strenuous exercise. Fifteen dogs were chronically instrumented to measure left circumflex blood flow, heart rate, regional left ventricular function (systolic shortening, and rate of shortening), and global left ventricular function (left ventricular pressure, and dP/dt). The specific postsynaptic alpha 1-receptor blocker prazosin (0.5 mg) and nonselective alpha-receptor blocker phentolamine (1.0 mg) were injected through an indwelling circumflex artery catheter to produce local adrenergic blockade of the posterior left ventricular region during exercise. Exercise significantly increased heart rate, left ventricular systolic pressure, dP/dt, segment shortening and rate of shortening, and coronary blood flow. Both prazosin and phentolamine caused similar additional increases in dP/dt by 21 +/- 4%, in rate of shortening in the posterior region by 37 +/- 6%, and in myocardial O2 consumption by 26 +/- 11%, which were associated with a 21 +/- 3% increase in coronary flow during exercise but no change in O2 extraction. Similar results were obtained when dogs were beta-blocked with either atenolol (1.0 mg ic) or propranolol (1.0 mg ic) prior to exercise. These data suggest that an alpha 1-vasoconstriction modulates O2 delivery to myocardial tissue and limits both coronary vasodilation and cardiac function during exercise.

Cardiac and Renal Effects of Levosimendan, Arginine Vasopressin, and Norepinephrine in Lipopolysaccharide-treated Rabbits

2005 ◽  
Vol 103 (3) ◽  
pp. 514-521 ◽  
Author(s):  
Valérie Faivre ◽  
Husam Kaskos ◽  
Jacques Callebert ◽  
Marie-Reine Losser ◽  
Paul Milliez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Function ◽  
Arginine Vasopressin ◽  
Myocardial Dysfunction ◽  
Left Ventricular ◽  
Sodium Pentobarbital ◽  
Maximum Acceleration ◽  
Human Sepsis ◽  
Beneficial Effects ◽  
Cardiac Myofilament

Background Because sepsis-induced myocardial dysfunction related to sepsis is at least partially related to a decrease in cardiac myofilament response to calcium, the use of the new myofilament-calcium sensitizer, levosimendan, has been proposed. In addition, arginine vasopressin is increasingly proposed as a vasopressor in septic patients, although data on its effects on cardiac function are still scarce. The aim of the current study was to assess, invasively and noninvasively, whether levosimendan, arginine vasopressin, and norepinephrine, either alone or combined, may modify sepsis-induced myocardial dysfunction and renal hemodynamics. Methods Thirty-six hours after lipopolysaccharide or saline administration, rabbits were studied either after slight sedation for echocardiography or after general anesthesia with sodium pentobarbital for the following measurements: aortic flow velocity and maximum acceleration of blood flow in the ascending aorta and renal macrocirculation and microcirculation. Results Levosimendan improved, within 30 min of administration, both maximum acceleration of blood flow by 20 +/- 12% (n = 8; P &lt; 0.05) and left ventricular shortening fraction by a similar extent. Furthermore, low doses of arginine vasopressin markedly deteriorated cardiac function via an afterload-independent mechanism, even when animals were pretreated with levosimendan, whereas norepinephrine showed no detrimental effects on cardiac function. The study also showed that norepinephrine often improved renal medullary blood flow, whereas arginine vasopressin consistently decreased it. Conclusion Levosimendan and norepinephrine both exert beneficial effects in endotoxemic animals and should be further explored in human sepsis trials.

Effects of naloxone on systemic and regional hemodynamic responses to exercise in dogs

1988 ◽  
Vol 64 (4) ◽  
pp. 1493-1499 ◽  
Author(s):  
N. Imai ◽  
C. K. Stone ◽  
P. D. Woolf ◽  
C. S. Liang
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Normal Saline ◽  
Adrenocorticotropic Hormone ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Moderate Exercise ◽  
Beta Endorphin ◽  
Developed Pressure

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.

Alpha-adrenergic vasoconstriction in normal and hypoperfused myocardium during sympathetic nerve stimulation

1992 ◽  
Vol 263 (6) ◽  
pp. H1682-H1688 ◽  
Author(s):  
J. Westby ◽  
S. Birkeland ◽  
S. E. Rynning ◽  
O. L. Myking ◽  
J. Lekven ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Adrenergic Receptors ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Control Group ◽  
Coronary Perfusion ◽  
Sympathetic Nerve Stimulation

Coronary vasoconstriction mediated by postjunctional alpha 1- and alpha 2-adrenergic receptors was studied in normally perfused (control group) and left coronary hypoperfused (stenosis group) hearts of vagotomized, beta-blocked (propranolol) cats. Cardiac sympathetic nerve stimulation was combined with alpha 1- and subsequent alpha 2-adrenergic antagonism (doxazosin and SK &F 104078). Coronary perfusion pressure and heart rate were kept constant within groups; regional myocardial blood flow and cardiac output were obtained by means of microspheres with concomitant measurement of left ventricular myocardial oxygen consumption (MVO2). alpha 1-Adrenergic antagonism alone did not significantly alter blood flow in any wall layer in either group. Subsequent alpha 2-adrenergic antagonism increased epicardial as well as composite transmural flow in the stenosis group (P < 0.025). The inverse correlation between coronary resistance and MVO2 vanished in the stenosis group following alpha 1- and alpha 2-adrenergic antagonism. Maximal first derivative of the left ventricular pressure-time relation (dP/dt) and cardiac output were reduced simultaneously (P < 0.001). Hence, the significance of alpha 1- and alpha 2-adrenergic stimulation of inotropy and cardiac performance are augmented by myocardial hypoperfusion. Furthermore, alpha 2-adrenergic receptors are responsible for epicardial vasoconstriction in hypoperfused myocardium.

scholarly journals Absence of left ventricular and arterial adaptations to exercise in octogenarians

2004 ◽  
Vol 97 (5) ◽  
pp. 1654-1659 ◽  
Author(s):  
Robert J. Spina ◽  
Timothy E. Meyer ◽  
Linda R. Peterson ◽  
Dennis T. Villareal ◽  
Morton R. Rinder ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Exercise Group ◽  
Left Ventricular ◽  
Applanation Tonometry ◽  
Rate Pressure Product ◽  
Control Group ◽  
Modest Improvement ◽  
Dimensional Echocardiography ◽  
And Function

Recent evidence suggests that octogenarians exhibit attenuated adaptations to training with a small increase in peak O2 consumption (V̇o2) that is mediated by a modest improvement in cardiac output without an increase in arteriovenous O2 content difference. This study was designed to determine whether diminished increases in peak V̇o2 and cardiac output in the octogenarians are associated with absence of left ventricular and arterial adaptations to exercise training. We studied 22 octogenarians (81.9 ± 3.7 yr, mean ± SD) randomly assigned a group that exercised at an intensity of 82.5 ± 5% of peak heart rate for 9 mo and 14 (age 83.1 ± 4.1) assigned to a control group. Peak V̇o2 increased 12% in the exercise group but decreased slightly (−7%) in the controls. The exercise group demonstrated significant but small decreases in the heart rate (6%, P = 0.002) and the rate-pressure product (9%, P = 0.004) during submaximal exercise at an absolute work rate. Training induced no significant changes in the left ventricular size, geometry (wall thickness-to-radius ratio), mass, and function assessed with two-dimensional echocardiography or in arterial stiffness evaluated with applanation tonometry. Data suggest that the absence of cardiac and arterial adaptations may in part account for the limited gain in aerobic capacity in response to training in the octogenarians.

Abstract 20445: Pras40 Prevents Development of Diabetic Cardiomyopathy

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Mirko Volkers ◽  
Shirin Doroudgar ◽  
Christopher Glembotski ◽  
Mark Sussman
Keyword(s):  
Cardiac Function ◽  
Diabetic Cardiomyopathy ◽  
Myocardial Dysfunction ◽  
Serum Glucose ◽  
Left Ventricular ◽  
Control Group ◽  
Diabetic Patients ◽  
Metabolic Function ◽  
Hypertrophic Growth

Introduction: Diabetes is a multi organ disease and diabetic cardiomyopathy can result in heart failure, which is a leading cause of morbidity and mortality in diabetic patients. Defects in mTOR signaling are believed to contribute to metabolic dysfunctions in diabetic liver and hearts, but evidence is missing that mTOR activation is causal to the development of diabetic cardiomyopathy. PRAS40 (Proline Rich Akt Substrate of 40kDa) is a specific component of mTORC1 that interacts with RAPTOR to inhibit mTORC1 kinase activity Methods and Results: The db/db mouse exhibits key characteristics of T2DM, namely hyperinsulinemia, insulin resistance, hyperglycemia, and develops diabetic cardiomyopathy with decreased cardiac function. Selective mTORC1 inhibition in cardiomyocytes from db/db mice in vivo was achieved using PRAS40 delivered via recombinant cardiotropic adeno-associated vector serotype 9 (AAV9) driven by a cardiomyocyte-specific myosin light chain (MLC2v) promoter construct. Myocardial dysfunction was prevented in AAV-PRAS40 treated db/db mice compared to the AAV-Control group, as seen by significantly higher cardiac ejection fraction (EF%), fractional shortening (FS%) measured by serial echocardiography, despite similar increases in body weight, serum glucose levels, and fat deposition in the liver. The effects of PRAS40 were tested in a model of T2DM induced by high fat diet (HFD). AAV-PRAS40 or AAV-Control was injected at 7 weeks of age and mice were fed HFD chow of or standard for an additional 25 weeks. Decreased cardiac function was observed in the HFD control group measured by echocardiography. This preservation of function was associated with decreased left ventricular diastolic dimension (LVID) and improved diastolic function. This phenotype was associated with improved metabolic function, blunted hypertrophic growth, and preserved insulin sensitivity. Conclusions: mTORC1 inhibition with PRAS40 prevents diabetic cardiomyopathy and improves metabolic function in diabetic mice. These findings may open novel avenues for therapeutic strategies using PRAS40 directed against diabetic-related diseases.

Integrated cardiac and peripheral vascular response to atriopeptin 24 in conscious dogs

1986 ◽  
Vol 251 (6) ◽  
pp. H1292-H1297 ◽  
Author(s):  
J. T. Shapiro ◽  
V. M. DeLeonardis ◽  
P. Needleman ◽  
T. H. Hintze
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Blood Flows ◽  
Blood Flow Ratio ◽  
The Right

Little attention has been directed toward the action of atrial peptides on integrated cardiovascular function. In conscious dogs intravenous injection of atriopeptin 24 (10 micrograms/kg) reduced mean arterial pressure (11 +/- 3.2%), mean left atrial pressure (32 +/- 8.6%), left ventricular (LV) end-diastolic pressure (24 +/- 4.3%), and increased heart rate (25 +/- 6.2%). LV dP/dt and stroke volume increased 17 +/- 4.0 and 12 +/- 3.3%, respectively. Cardiac output increased 39 +/- 6.3%. These effects were only acute, lasting less than 10 min. The tachycardia and increase in LV dP/dt were abolished by combined beta-adrenergic and muscarinic cholinergic blocking agents. During an infusion of atriopeptin 24 (10 micrograms X kg-1 X min-1) blood flow, as measured with radioactive microspheres, increased to both the left (101 +/- 35%) and right kidney (122 +/- 37%) and to the spleen (140 +/- 50%). However, blood flow to the stomach, large and small intestine, pancreas, liver, and skeletal muscle did not change, indicating the selectivity of the atriopeptin. Blood flow in the right ventricle, septum, and in all layers of the left ventricle increased slightly, resulting in no change in the endocardial-to-epicardial blood flow ratio most likely due to the changes in myocardial function, i.e., heart rate and stroke volume. Thus, in conscious dogs, atriopeptins increase myocardial performance most likely indirectly secondary to baroreflex unloading after the direct hypotensive effects of atriopeptin 24. This serves to increase cardiac output at a time when renal and splenic blood flows are increased.

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