Effect of altered thyroid status on in vitro cardiac performance in rats

1987 ◽  
Vol 252 (4) ◽  
pp. H788-H795 ◽  
Author(s):  
K. H. McDonough ◽  
V. Chen ◽  
J. J. Spitzer
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Cardiac Output ◽  
Thyroid Hormone ◽  
Systolic Pressure ◽  
Heart Weight ◽  
The Difference ◽  
Altered Thyroid ◽  
Similar Body

Effect of a chronic excess or deficit of thyroid hormone on intrinsic myocardial performance in rats was assessed. Animals were thyroidectomized or treated with thyroid hormone or vehicle 6-7 wk before the study. Body weight and heart weight were decreased in the hypothyroid group, and heart weight was elevated in the hyperthyroid group. Hearts were removed from thyroidectomized, euthyroid or thyroid-treated animals and studied as isolated, perfused working heart preparations. Ventricular function curves were generated by increasing left atrial filling pressure, whereas outflow resistance was not varied. Coronary flow, aortic outflow (and thus cardiac output), heart rate, and peak aortic systolic pressure were measured as a function of preload. These studies showed that performance of hearts from hyperthyroid animals was similar to that of euthyroid controls. Hearts from hypothyroid rats had decreased rate, pressure, and cardiac output but normal stroke volume. Since heart weight was 55% lower than control, normalization of volume work to dry heart weight reversed the difference in cardiac output. Comparison of hearts from hypothyroid animals to control rats of similar weight showed minimal differences in pump function. Thus hyperthyroidism did not result in altered in vitro cardiac output or peak systolic pressure as a function of changing preload when compared with age-matched euthyroid controls, hypothyroidism resulted in a decreased in vitro heart rate but greater cardiac output normalized to heart weight when compared with age-matched controls and hyperthyroid animals; external pacing of hypothyroid hearts yielded myocardial work parameters that were comparable to euthyroid control rats of similar body weight; and cardiac efficiency was significantly greater in hypothyroid hearts than in hyperthyroid hearts.(ABSTRACT TRUNCATED AT 250 WORDS)

T3 treatment does not prevent myocardial dysfunction in chronically diabetic rats

1988 ◽  
Vol 254 (2) ◽  
pp. H265-H273
Author(s):  
R. W. Barbee ◽  
R. E. Shepherd ◽  
A. H. Burns
Keyword(s):  
Heart Rate ◽  
Cardiac Function ◽  
Myocardial Dysfunction ◽  
Systolic Pressure ◽  
Cardiac Pacing ◽  
Diabetic Rats ◽  
Heart Weight ◽  
Citrate Buffer ◽  
Heart Preparation

The isolated working heart preparation was used to investigate the effect of continuous triiodothyronine (T3) administration on cardiac function and metabolism of rats rendered diabetic for a period of 4 wk with streptozocin (STZ). T3 controlled-release pellets were implanted 1 wk after STZ (70 mg/kg) injection. Rats injected with citrate buffer without STZ received T3 pellets 1 and/or 2 wk later. A comparable number of rats received placebo pellets. Untreated diabetic rats exhibited a decrease in spontaneous heart rate and myocardial cytochrome c concentrations concurrent with depressed plasma T3 values compared with untreated controls. T3 treatment did not improve in vitro cardiac performance (assessed as cardiac output times peak systolic pressure per gram dry heart weight) in hearts from diabetic rats perfused with glucose alone. Addition of octanoate reversed this depression and improved cardiac function to a greater extent in treated than in untreated diabetic animals. However, these differences between treated and untreated diabetic animals disappeared when heart rate was controlled by cardiac pacing. Furthermore, T3 treatment of controls and diabetics did not alter the oxidation of octanoate or the cardiac responsiveness to isoproterenol. These results suggest that experimental diabetic cardiomyopathy is partly attributable to a substrate deficiency and is not due entirely to hypothyroidism.

Dissociation of Direct and Indirect Effects of Angiotensin II on the Heart

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 683-684
Author(s):  
Jorge P van Kats ◽  
David W Silversides ◽  
Timothy L Reudelhuber
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Renin Angiotensin System ◽  
Cardiac Cells ◽  
Heart Weight ◽  
Ang Ii ◽  
Direct Stimulation ◽  
Beneficial Effects

33 Cardiac angiotensin II (Ang II), either derived from the circulation or locally synthesized, is often suggested to be involved in the structural adaptations occurring in the heart in hypertension and following myocardial infarction. However, it is debated whether the proven beneficial effects of renin-angiotensin system blockade in these pathologies are related to an inhibition of the direct cardiac actions of the peptide. The objective of the present study was to investigate which of the effects of cardiac Ang II are due to direct stimulation of cardiac cells by Ang II. To test for cardiac specific functions of Ang II, transgenic mice were developed that express an Ang II-releasing fusion protein (J Biol Chem 1997;272:12994-99) exclusively in cardiomyocytes. Blood pressure, heart rate, cardiac and plasma Ang II content, Ang II receptor binding and organ morphology were monitored in transgenic (TG) and non-transgenic littermate mice (control). Cardiac Ang II levels in TG mice were 20-40 fold higher than in hearts of control mice (15±3 pg/100 mg ww). In 3 independent founder lines of TG mice, plasma Ang II concentration was not altered as compared to control (119±20 vs. 127±20 pg/mL). The heart weight to body weight ratio in TG mice (4.0±0.1 mg/g) was not different from controls (3.8±0.1 mg/g), neither was systolic pressure (137±4 and 138±7 mm Hg respectively) or heart rate (618±13 and 662±15 bpm respectively). Microscopic inspection of TG hearts did not reveal any differences with control regarding size and number of cardiomyocytes and organization of extracellular matrix proteins. TG mice had not become less sensitive for Ang II signaling since Ang II receptor number was not altered in TG mice (Bmax = 23±3 fmol/mg protein) as compared to control (22±2 fmol/mg protein). Our data show that very high Ang II levels in hearts of TG mice do not lead to myocardial enlargement or affect cardiovascular physiology. We conclude that elevated Ang II in the heart has no direct effects on cardiac cells and we hypothesize that effects of cardiac Ang II become apparent upon altered hemodynamic loading.

Control circulatory values of morphinepentobarbitalized dogs

1960 ◽  
Vol 199 (5) ◽  
pp. 797-799 ◽  
Author(s):  
S. Deavers ◽  
E. L. Smith ◽  
R. A. Huggins
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Cell Volume ◽  
Blood Volume ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Control Data ◽  
Plasma Protein Concentration

Mean control data on a series of 100 dogs are presented. Cell volume, measured with Cr51-tagged red cells and plasma volume determined simultaneously by T-1824 dye was 33.5 ± 0.74 cc/kg and 50.2 ± 1.11 cc/kg, respectively. The venous hematocrit was 45.2% and the circulatory/venous hematocrit ratio was 0.89 ± 0.01 for the group. The plasma protein concentration of these animals was 6.25 ± 0.07 gm/100 cc. No difference in blood volume per unit of body weight was found between large (12.6 kg) and small (5.8 kg) dogs. The femoral mean systolic pressure was 139.0 ± 2.53 mm Hg, the diastolic pressure 65.6 ± 1.46 mm Hg and the heart rate 85.9 ± 2.86/min.

Pulsatile Flow Characteristics in a Stenotic Aortic Valve Model: An In Vitro Experimental Study

2019 ◽  
Author(s):  
Ruihang Zhang ◽  
Yan Zhang
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Pulsatile Flow ◽  
Heart Diseases ◽  
Flow Characteristics ◽  
Aortic Valve Area ◽  
Heart Rates ◽  
Valvular Heart Diseases

Abstract Aortic stenosis (AS) is one of the most common valvular heart diseases around the globe. The accurate assessment of AS severity is important and strongly associated with accurate interpretation of the hemodynamic parameters across the stenotic valve. In this study, we conducted in vitro fluid dynamic experiments to investigate the pulsatile flow characteristics of a stenotic aortic valve as a function of heart rate. An in vitro cardiovascular flow simulator was used to generate pulsatile flow with a prescribed waveform (40% systolic period and 4L/min cardiac output) under varied heart rates (50 bpm, 75 bpm and 100 bpm). The stenotic valve was constructed by molding silicone into three-leaflet aortic valve geometries wrapping around thin fabrics which increases its stiffness and tensile strength. Two-dimensional phase-locked particle image velocimetry (PIV) was employed to quantify the flow field characteristics of the stenotic valve. Pressure waveforms were recorded to evaluate the severity of the stenosis via the Gorlin and Hakki equations. Results suggest that as the heart rate increases, the peak pressure gradient across the stenotic aortic valve increases significantly under the same cardiac output. Analysis also shows the estimated aortic valve area (AVA) decreases as the heart rate increases under the same cardiac output using Gorlin equation estimation, while the trend is reversed using Hakki equation estimation. Under phase-locked conditions, quantitative flow characteristics, such as phase-averaged flow velocity, turbulence kinetic energy (TKE) for the stenotic aortic valve were analyzed based on the PIV data. Results suggest that the peak systolic jet velocity downstream of the valve increases as the heart rate increases, implying a longer pressure recovery distance as heart rate increases. While the turbulence at peak systole is higher under the slower heart rate, the faster heart rate contributes to a higher turbulence during the late systole and early diastole phases. Based on the comparison with no-valve cases, the differences in TKE was mainly related to the dynamics of leaflets under different heart rates. Overall, the results obtained in this study demonstrate that the hemodynamics of a stenotic aortic valve is complex and the assessment of AS could be significantly affected by the pulsating rate of the flow.

scholarly journals Allylmethylsulfide, a Sulfur Compound Derived from Garlic, Attenuates Isoproterenol-Induced Cardiac Hypertrophy in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Soheb Anwar Mohammed ◽  
Bugga Paramesha ◽  
Yashwant Kumar ◽  
Ubaid Tariq ◽  
Sudheer Kumar Arava ◽  
...  
Keyword(s):  
Body Weight ◽  
Cardiac Hypertrophy ◽  
Weight Ratio ◽  
Chronic Administration ◽  
The Body ◽  
Heart Weight ◽  
Serum Biochemical ◽  
Enalapril Treatment ◽  
Histopathological Investigation

Allylmethylsulfide (AMS) is a novel sulfur metabolite found in the garlic-fed serum of humans and animals. In the present study, we have observed that AMS is safe on chronic administration and has a potential antihypertrophic effect. Chronic administration of AMS for 30 days did not cause any significant differences in the body weight, electrocardiogram, food intake, serum biochemical parameters, and histopathology of vital organs. Single-dose pharmacokinetics of AMS suggests that AMS is rapidly metabolized into Allylmethylsulfoxide (AMSO) and Allylmethylsulfone (AMSO2). To evaluate the efficacy of AMS, cardiac hypertrophy was induced by subcutaneous implantation of ALZET® osmotic minipump containing isoproterenol (~5 mg/kg/day), cotreated with AMS (25 and 50 mg/kg/day) and enalapril (10 mg/kg/day) for 2 weeks. AMS and enalapril significantly reduced cardiac hypertrophy as studied by the heart weight to body weight ratio and mRNA expression of fetal genes (ANP and β-MHC). We have observed that TBARS, a parameter of lipid peroxidation, was reduced and the antioxidant enzymes (glutathione, catalase, and superoxide dismutase) were improved in the AMS and enalapril-cotreated hypertrophic hearts. The extracellular matrix (ECM) components such as matrix metalloproteinases (MMP2 and MMP9) were significantly upregulated in the diseased hearts; however, with the AMS and enalapril, it was preserved. Similarly, caspases 3, 7, and 9 were upregulated in hypertrophic hearts, and with the AMS and enalapril treatment, they were reduced. Further to corroborate this finding with in vitro data, we have checked the nuclear expression of caspase 3/7 in the H9c2 cells treated with isoproterenol and observed that AMS cotreatment reduced it significantly. Histopathological investigation of myocardium suggests AMS and enalapril treatment reduced fibrosis in hypertrophied hearts. Based on our experimental results, we conclude that AMS, an active metabolite of garlic, could reduce isoproterenol-induced cardiac hypertrophy by reducing oxidative stress, apoptosis, and stabilizing ECM components.

Experimental hyperthyroidism in dogs and effect of salivariectomy

1961 ◽  
Vol 201 (4) ◽  
pp. 723-728 ◽  
Author(s):  
Dorothy A. Piatnek ◽  
Robert E. Olson
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Oxygen Consumption ◽  
Thyroid Hormone ◽  
Body Temperature ◽  
Caloric Intake ◽  
Clinical Signs ◽  
Turnover Rates ◽  
Laboratory Findings ◽  
Thyroid State

A hyperthyroid state was induced and maintained in 17 dogs for 2–10 months by the administration of massive amounts of thyroid hormone. The great tolerance of this species to such large doses was striking. The clinical signs characteristic of hyperthyroidism in other mammals were observed including significantly increased caloric intake, oxygen consumption, heart rate, and body temperature. The laboratory findings included polycythemia, markedly increased levels of protein-bound iodide (PBI), increased turnover rates of l-thyroxine, and a decreased urinary excretion of inorganic iodide. Unlike other species the hyperthyroid dogs did not demonstrate marked reductions in body weight or serum cholesterol. Salivariectomy neither hastened nor enhanced the onset of exogenous hyperthyroidism in the dog. Measurements of the rate of disappearance of I131 l-thyroxine from the plasma and the rate of appearance of radioactive iodide in the urine indicated that the salivary glands in the intact dog are effective sites of deiodination and iodide excretion. This activity, however, is not the sole regulator of the level of circulating thyroid hormone and thus of the thyroid state.

A study of the physiological consequences of sympathetic denervation of the heart caused by the arterial switch procedure

2010 ◽  
Vol 20 (2) ◽  
pp. 150-158 ◽  
Author(s):  
Cecilia Falkenberg ◽  
Stefan Hallhagen ◽  
Krister Nilsson ◽  
Boris Nilsson ◽  
Ingegerd Östman-Smith
Keyword(s):  
Heart Rate ◽  
Coronary Flow ◽  
Arterial Switch Operation ◽  
Sympathetic Nerves ◽  
Heart Weight ◽  
Maximal Heart Rate ◽  
Response Curves ◽  
Arterial Switch

AbstractBackgroundThe arterial switch operation is the corrective operation for transposition of the great arteries, defined as the combination of concordant atrioventricular and discordant ventriculo–arterial connections, but there have been concerns about silent subendocardial ischaemia on exercise and coronary artery growth. The arterial switch divides the majority of the sympathetic nerves entering the heart; we have studied the effects of coronary flow and sensitivity to catecholamine stimulation in an animal model.MethodsA total of 10 piglets were operated on cardiopulmonary bypass with section and resuturing of aortic trunk, pulmonary artery and both coronary arteries, with 13 sham-operated controls. After 5–7 weeks of recovery, seven simulated switch survivors and 13 controls were studied.ResultsBasal heart rate was significantly higher in switch piglets: in vivo mean (standard deviation) 112 (12) versus sham 100 (10) beats per minute, (p = 0.042); in vitro (Langendorff preparation): 89 (9) versus sham 73 (8) beats per minute (p = 0.0056). In vivo maximal heart rate in response to epinephrine was increased in switch piglets, 209 (13) versus 190 (17) beats per minute (p = 0.044). In vitro dose–response curves to norepinephrine were shifted leftward and upwards (p = 0.0014), with an 80% increase in heart rate induced by 0.095 (0.053) norepinephrine micromole per litre perfusate in switch hearts versus 0.180 (0.035) norepinephrine micromole per litre (p = 0.023). Increase in coronary flow on norepinephrine stimulation and maximal coronary flow were significantly reduced in switch hearts: 0.3 (0.2) versus 0.8 (0.4) millilitre per gram heart weight (p = 0.045) and 2.5 (0.4) versus 3.1 (0.4) millilitre per gram heart (p = 0.030), respectively.ConclusionsA combination of increased intrinsic heart rate, increased sensitivity to chronotropic actions of norepinephrine, and a decreased maximal coronary flow creates potential for a mismatch between perfusion and energy demands.

Fluid replacement and glucose infusion during exercise prevent cardiovascular drift

1991 ◽  
Vol 71 (3) ◽  
pp. 871-877 ◽  
Author(s):  
M. T. Hamilton ◽  
J. Gonzalez-Alonso ◽  
S. J. Montain ◽  
E. F. Coyle
Keyword(s):  
Heart Rate ◽  
Body Weight ◽  
Cardiac Output ◽  
Rectal Temperature ◽  
Prolonged Exercise ◽  
Blood Glucose Concentration ◽  
Fluid Replacement ◽  
O2 Uptake ◽  
Trained Subjects ◽  
Cardiovascular Drift

This study examined the influence of both hydration and blood glucose concentration on cardiovascular drift during exercise. We first determined if the prevention of dehydration during exercise by full fluid replacement prevents the decline in stroke volume (SV) and cardiac output (CO) during prolonged exercise. On two occasions, 10 endurance-trained subjects cycled an ergometer in a 22 degrees C room for 2 h, beginning at 70 +/- 1% maximal O2 uptake (VO2max) and in a euhydrated state. During one trial, no fluid (NF) replacement was provided and the subject's body weight declined 2.09 +/- 0.19 kg or 2.9%. During the fluid replacement trial (FR), water was ingested at a rate that prevented body weight from declining after 2 h of exercise (i.e., 2.34 +/- 0.17 1/2 h). SV declined 15% and CO declined 7% during the 20- to 120-min period of the NF trial while heart rate (HR) increased 10% and O2 uptake (VO2) increased 6% (all P less than 0.05). In contrast, SV was maintained during the 20- to 120-min period of FR while HR increased 5% and thus CO actually increased 7% (all P less than 0.05). Rectal temperature, SV, and HR were similar during the 1st h of exercise during NF and FR. However, after 2 h of exercise, rectal temperature was 0.6 degree C higher (P less than 0.05) and SV and CO were 11–16% lower (P less than 0.05) during NF compared with FR.(ABSTRACT TRUNCATED AT 250 WORDS)

Crystalloid and perfluorochemical perfusates in an isolated working rabbit heart preparation

1985 ◽  
Vol 249 (2) ◽  
pp. H285-H292 ◽  
Author(s):  
J. M. Chemnitius ◽  
W. Burger ◽  
R. J. Bing
Keyword(s):  
Cardiac Output ◽  
Coronary Flow ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Rabbit Heart ◽  
Left Ventricular ◽  
Heart Weight ◽  
Perfused Heart ◽  
Heart Preparation ◽  
Perfused Hearts

Krebs-Henseleit buffer (KH) and a perfluorochemical (FC-43) were compared as perfusates in an isolated working rabbit heart preparation. Both perfusates were oxygenated in an identical manner using an infant bubble oxygenator. After 60 min of perfusion, no difference could be detected in the ratio of wet to dry heart weight between KH- and FC-43-perfused hearts (KH, 6.25 +/- 0.3; FC-43, 5.99 +/- 0.20). Left ventricular systolic pressure, maximal rate of left ventricular pressure rise, mean aortic systolic pressure, cardiac output, aortic flow, left ventricular power, and myocardial O2 consumption (MVO2) were significantly higher in FC-43-perfused hearts throughout the time of perfusion. However, there were no differences in resistance to cardiac output and heart rate. In KH- and FC-43-perfused hearts, MVO2 and left ventricular power were closely correlated (KH, r = 0.793; FC-43, r = 0.831). Significantly higher coronary flow of KH-perfused hearts could be attributed to the lower viscosity of KH (1.05 Pa . s) compared with FC-43 (1.91 Pa . s). Increased O2 extraction during KH perfusion could not compensate for low O2-carrying capacity of KH buffer (345 compared with 705 nmol O2 X ml-1 in FC-43 emulsion). A postischemic increase of coronary flow was observed only in FC-43-perfused hearts (28%). These results demonstrate a different response of perfused heart preparations to FC-43 and KH buffer.

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