Size of Cardiac Ventricles in Experimental Hyperthyroidism in the Rat

Liere, Edward J. Van; Sizemore, David A.; Hunnell, J E

doi:10.3181/00379727-132-34283

Cited by 21 publications

(9 citation statements)

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“…Van Liere et al (36) and, later, Gerdes et al (12) demonstrated that hyperthyroidism in rats causes greater enlargement of right ventricle than of left ventricle, in accordance with our data. In hyperthyroid animals, right ventricular pressure is increased by a much greater percentage than systemic blood pressure (1).…”

Section: Heart Weight-to-body Weight Ratio LV Weight Rv Weight Asupporting

confidence: 93%

Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling

Hu¹,

Benvenuti²,

Liberti³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

105

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-The present study assessed the possible involvement of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) in thyroxine (T 4)-induced cardiac hypertrophy. Hemodynamic parameters, heart weight (HW), ratio of HW to body weight (HW/BW), and myocyte width were evaluated in absence of thyroid hormone (hypothyroidism) and after T 4 administration. Male Wistar rats were used. Some were subjected to thyroidectomies, whereas hyperthyroidism was induced in others via daily intraperitoneal injection of T 4 (25 or 100 g ⅐ 100 g BW Ϫ1 ⅐ day Ϫ1 ) for 7 days. In some cases, T4 administration was combined with the angiotensin I-converting enzyme inhibitor enalapril (Ena), with the angiotensin type 1 (AT1) receptor blocker losartan (Los) or with the ␤-adrenergic blocker propanolol (Prop). Hemodynamics and morphology were then evaluated. Systolic blood pressure (SBP) was not altered by administration of either T4 alone or T4 in combination with the specific inhibitors. However, SBP decreased significantly in hypothyroid rats. An increased heart rate was seen after administration of either T4 alone or T4 in combination with either Los or Ena. Although the higher dose of T 4 significantly increased HW, HW/BW increased in both T 4-treated groups. Ena and Prop inhibited the increase in HW or HW/BW in hyperthyroid rats. Morphologically, both T 4 dose levels significantly increased myocyte width, an occurrence prevented by RAS or SNS blockers. There was a good correlation between changes in HW/BW and myocyte width. These results indicate that T4-induced cardiac hypertrophy is associated with both the SNS and the RAS. cardiac myocytes; thyroid hormone; angiotensin-converting enzyme; angiotensin II receptors CHANGES IN HEMODYNAMIC LOADING appear to be an important stimulus for cardiac growth. However, dissociation between elevated arterial pressure and increased myocardial mass has been demonstrated in hypertensive cardiac hypertrophy in animals and humans (25). This dissociation suggests that, in addition to blood pressure, various stimuli are involved in the development and regression of cardiac hypertrophy (25). Over the past several decades, many neural and hormonal stimuli have been implicated in cardiac muscle growth, including, but not limited to, ␣-and ␤-adrenergic agonists, ANG II, glucocorticoids, insulin, growth hormone, glucagon, and thyroxine (T 4 ) (25).Mechanisms of cardiac hypertrophy produced by elevated T 4 include a direct effect of the hormone on the heart and indirect effects related to stimulation of the adrenergic nervous system or altered left ventricular loading conditions. Decreased systemic vascular resistance and the subsequent increase in cardiac work contribute to this T 4 -induced hypertrophy (15, 25). However, in support of a direct effect of thyroid hormone on heart growth, some authors have observed that T 4 -induced cardiac hypertrophy in isolated heart preparations is accompanied by increased (31) quantity and rate of protein and ribosome synthesis (33).It is well established t...

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Section: Heart Weight-to-body Weight Ratio LV Weight Rv Weight Asupporting

confidence: 93%

Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling

Hu¹,

Benvenuti²,

Liberti³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

105

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“…Both the experimental procedures employed here (surgical stenosis of the abdominal aorta and long-lasting administration of 5'-triiodothyronine) caused heart hypertrophy with a significant increase in the ratio (left ventricular wcight/bedy weight) (+30 %, p < 0.05 in both cases, in agreement with (16,17)). Table 1 shows that in both experimental conditions there are changes in the levels of the adenosine metabolizing enzymes.…”

Section: Changes In the Transmural Distribution Of Enzyme Activities supporting

confidence: 76%

The regional distribution of adenosine-regulating enzymes in the left and right ventricle walls of control and hypertrophic heart

Tata¹,

Gini²,

Simonetti³

et al. 1989

Basic Res Cardiol

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The transmural distribution of the adenosine-generating enzyme 5'-nucleotidase (5'N) and of the adenosine-degrading enzymes adenosine deaminase (ADA), AMP deaminase (AMP-D) and adenosine kinase (Ado-K) were determined across the walls of left and right ventricles of control and hypertrophic rat hearts. The enzyme distribution across the left ventricle wall (but not across the right wall) of normal hearts was not uniform: 5'N activity shows its highest levels in the subepicardial and in the subendocardial regions, whereas all the other enzyme activities show their lowest levels. A similar pattern of transmural distribution was also detected in other mammalian species (ox and pig). In the experimental cardiac hypertrophy, caused by two different types of chronic cardiac overload, the levels and the profiles of transmural distribution of 5'N and ADA enzyme activities may significantly change across the rat left ventricle wall.

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“…After 3 days of triiodothyronine treatment, there was an increase in right ventricular weight (Table 3). The ratios right ventricular weight/heart weight and right ventricular weight/left ventricular weight were elevated slightly, but significantly, demonstrating and confirming a greater proportional increase in right ventricular weight compared to left heart weight (27). Also the RNA content and the RNA/DNA ratio were increased in the right ventricle, the latter being enhanced in the left ventricle as well.…”

Section: Resultsmentioning

confidence: 55%

“…The first is the increase in right ventricular function and metabolism 3 and 16 days after triiodothyronine administration in female Sprague-Dawley rats (Table 2 and 3). It has been noted by other authors that treatment with thyroid hormone for 2 and 10 weeks induced a greater proportional hypertrophy of the right ventricle (8,27). in this context it is worth mentioning that the percent increase in RVSP is more pronounced than the elevation in LVSP (Table 2).…”

Section: Right Ventricular Hypertrophymentioning

confidence: 58%

Right heart catheterization in rats with pulmonary hypertension and right ventricular hypertrophy

et al. 1988

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Using a special Millar ultraminiature catheter pressure transducer, right ventricular functional parameters were measured in anesthetized, closed-chest rats under control conditions, during acute pulmonary hypertension and after induction of right ventricular hypertrophy. Acute i.v. infusion of noradrenaline and a brief period of hypoxia in female Sprague-Dawley rats elicited a marked increase in right ventricular systolic pressure (RVSP) and in the maximal rate of rise in right ventricular pressure (RV dp/dtmax). After 3 and 16 days of daily administrations of triiodothyronine in female Sprague-Dawley rats, all right ventricular hemodynamic parameters were enhanced along with the increase in left ventricular function. The right and left ventricles were hypertrophied, and cardiac output was increased. After 40 and 45 days subsequent to bilateral thorax irradiation of male Brown-Norway rats, RVSP and RV dp/dtmax were increased, the right ventricle was hypertrophied, while the left ventricle did not exhibit appreciable hemodynamic or morphologic alterations. Cardiac output was depressed. Thus, these two experimental models differ considerably as to the mechanism and time course of the development of right ventricular hypertrophy as well as to the participation of the left ventricle and the involvement of volume overload.

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Size of Cardiac Ventricles in Experimental Hyperthyroidism in the Rat

Cited by 21 publications

References 0 publications

Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling

Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling

The regional distribution of adenosine-regulating enzymes in the left and right ventricle walls of control and hypertrophic heart

Right heart catheterization in rats with pulmonary hypertension and right ventricular hypertrophy

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