Regression Of Cardiac Hypertrophy Research Articles

Reversal of changes in myocardial beta-receptors and inotropic responsiveness with regression of cardiac hypertrophy in renal hypertensive rats (RHR).

Our previous studies, in vivo and in vitro, have shown reduced inotropic responsiveness to isoproterenol of hypertrophied hearts in renovascular hypertensive rats. In the present study, we have investigated, in the same model, the effects of treatment either by nephrectomy or captopril on the inotropic responsiveness to isoproterenol and on the number and affinity of ventricular beta-receptors. Isoproterenol infusion of isolated hearts from renovascular hypertensive rats 12-18 weeks post-clipping produced lower inotropic responses (delta peak dP/dt) than age-matched sham-operated normotensive rats (P less than 0.001). Quantitative assessment of beta-adrenergic receptors in the same hearts showed a significant decrease in renovascular hypertensive rats ventricular receptor numbers, whether calculated per milligram membrane protein (22.3 +/- 2.66 fmol/mg vs. 37.9 +/- 4.34, P less than 0.005) or per gram wet ventricular weight (1.43 +/- 0.14 pmol/g vs. 2.2 +/- 0.21, P less than 0.005), with no significant change in Kd. Control of hypertension by either nephrectomy or captopril led to regression of hypertrophy 6 weeks after stabilization of blood pressure (12-18 weeks post-clipping) and returned both the ventricular receptor density and inotropic responsiveness toward normal. The improvement in inotropic responsiveness to isoproterenol in regressed hearts correlated with both the reduction in ventricular weight and the decrease of blood pressure. Regression of hypertrophy did not alter the relationship between inotropic response, receptor density, and ventricular weight. These results indicate that the increase in cardiac mass associated with renovascular hypertension may interfere with adrenergic support to the heart, and that proper control of hypertension and regression of hypertrophy could reverse that impairment and restore its responsiveness to adrenergic stimulation.

Effects of the cessation of training on left ventricular function in the racing greyhound

Exercise-induced cardiac hypertrophy has been associated with normal resting left ventricular function and, after cessation of training, variable degrees of regression. The racing greyhound is an animal with cardiac hypertrophy said to be part congenital and part exercise-induced. Racing greyhounds underwent serial cardiac catheterization three times during an 8-month period after cessation of racing/training to determine the functional consequences of the cessation of training. At the end of 8 months of inactivity the animals' hearts were excised and weighed in order to compare heart weight/body weight (HW/BW) ratios with those obtained in a group of racing greyhounds killed within one month, 19 +/- 16 days (mean +/- SD), of the cessation of training. Comparison of HW/BW ratios failed to reveal a significant difference between the serially studied group, 12.1 +/- 1.9 g/kg (mean +/- SD), and the more recently exercising group, 12.7 +/- 1.4 g/kg (mean +/- SD) of dogs. After 2 months of inactivity, 9 of 12 greyhounds in the serially studied group showed increases in max dP/dt and dP/dt normalized to a pressure of 50 mmHg. Modified pre-ejection period and peak negative dP/dt also increased significantly (p less than .004) during this same period. No further changes in these variables were found at the final 8-month study. Our failure to demonstrate a difference in HW/BW ratios between these two groups of dogs suggests that the exercise-induced component of cardiac hypertrophy in the trained racing greyhound is probably very small and, if it exists, regresses very early (less than 1 month). Changes in contractility indices that were observed occurred after this time period (between 1 and 2 months) and are therefore probably not due to regression of cardiac hypertrophy.

Regression of cardiac hypertrophy experimental animal model

Regression of cardiac hypertrophy has been proven to occur in experimental animals following some types of antihypertensive therapy. However, no direct and necessary correlation can be found between hypertension and cardiac hypertrophy. The effect of different antihypertensive drugs on regression of cardiac hypertrophy varies despite the same degree of reduction in arterial pressure in hypertensive control subjects. Therapy with α-methyldopa resulted in reversal of hypertrophy with effective blood pressure control, whereas treatment with vasodilators, namely hydralazine and minoxidil, either did not alter (hydralazine) degree of myocardial hypertrophy or increase it (minoxidil) despite normalization of blood pressure. The biochemical profile of the myocardium after regression of hypertrophy following antihypertensive therapy is not homogeneous; for example, reversal with α-methyldopa is associated with increased collagen content, whereas reversal with Captopril did not alter collagen content of the heart. Adrenergic factors seem to play an important role in the modulation of myocardial structure to variations in arterial pressure. Furthermore, in each type of hypertrophy in hypertension, a combination of different factors might be responsible, and it may not be correct to assume that the same factors must be involved in the regression of all types of myocardial hypertrophy.

Regression of left ventricular hypertrophy by medical treatment: Present status and possible implications

Actual regression of left ventricular hypertrophy was shown to occur following some types of antihypertensive therapy both in experimental models and in human subjects with arterial hypertension. This regression was linked to blood pressure control but was not entirely dependent on it; there is growing evidence that adrenergic factors play an important role in modulating the response of the heart to measures lowering arterial pressure. However, generalization would be premature because of the differences reported between various experimental types of hypertension and of the interindividual variations noticed among hypertensive patients receiving similar models of therapy. The reduction in ventricular mass has not been associated with a diminution in overall cardiac performance; in studies of isolated papillary muscle the return of contractility to normal with reversal of hypertrophy has been reported. More investigations are still needed, however, to determine the regressed heart's performance under stress. In that regard, regression of hypertrophy has been associated with normalization of inotropic responsiveness of the heart to adrenergic stimuli. Of particular importance in hypertensive diseases, but as yet incompletely defined, is the extent to which regression of vascular hypertrophy parallels regression of cardiac hypertrophy.

Regression of thyroid hormone induced cardiac hypertrophy: Effect on cardiac beta receptors and adenyl cyclase activity

Adrenergic mechanisms may be important in the symptomatic manifestations of hyperthyroidism. The chronic administration of thyroid hormone also results in cardiac hypertrophy and increased numbers of beta-adrenergic receptors in cardiac membranes. The roles of adrenergic mechanisms in the initiation and perpetuation of this hypertrophy has been open to speculation. Rats treated chronically with L-thyroxin were sacrificed after 7 days of treatment and 1–4 days after cessation of treatment. Hearts were removed and weighed and norepinephrine measured. In other groups of identically treated rats, membranes were prepared from the left ventricle for invitro measurements of beta-adrenergic receptor characteristics and adenyl cyclase activity. Regression of cardiac hypertrophy with a decrease in receptor number to control values was seen as early as 2 days after stopping thyroxine. Cardiac norepinephrine concentrations had also returned to control values at this time. Displacement of bound [H 3] dihydroalprenolol by isoproterenol was not changed from control. Basal and isoproterenol stimulated adenyl cyclase activity was not changed by thyroxine administration or its cessation. The rapid reversal of the increased beta-adrenergic receptor number and cardiac hypertrophy raises the possibility that thyroid hormone may play a regulatory role in cardiac function. Although the enhancement of myocardial contractility by thyroid hormone may be mediated through cardiac hypertrophy this effect of thyroid hormone is independent of the catecholamine sensitive adenyl cyclase system.

Polyamine levels and diamine oxidase activity in hypertrophic heart of spontaneously hypertensive rats and of rats treated with isoproterenol

Polyamine levels and diamine oxidase (EC 1.4.3.6) activity were studied in hypertrophic heart of spontaneously hypertensive rats as well as in the heart of Wistar rats during the development and regression of cardiac hypertrophy induced by isoproterenol administration. In spontaneously hypertensive rats, putrescine content and diamine oxidase activity were higher than those found in normotensive Kyoto-Wistar control rats. During the development of cardiac hypertrophy induced by isoproterenol, there was an increase in polyamine content and diamine oxidase activity. The administration of cycloheximide or actinomycin D prevented the increase in diamine oxidase activity during the first 24 h after isoproterenol administration, demonstrating that the rise in diamine oxidase activity was due to synthesis of new enzyme. Following the cessation of isoproterenol treatment, cardiac hypertrophy regressed and polyamine levels and diamine oxidase activity diminished toward control values. The administration of aminoguanidine to isoproterenol-treated rats caused in the heart an inhibition of diamine oxidase activity that led to an increase in putrescine level beyond the values found in animals given isoproterenol alone. The results suggest that the enhancement of diamine oxidase activity plays a role in the regulation of putrescine level in hypertrophic heart.

Prevention of the development of heart failure and the regression of cardiac hypertrophy by captopril in the spontaneously hypertensive rat.

The spontaneously hypertensive rat (SHR) exhibits both a compensated phase of cardiac hypertrophy in which forward output is maintained despite persistently elevated systemic arterial pressures and a decompensated phase in which cardiac performance has deteriorated in spite of further hypertrophic growth. To determine whether chronic antihypertensive therapy prevents the development of heart failure and the progression of cardiac hypertrophy in SHR with advanced hypertension, captopril (2 g/l of drinking water), a converting enzyme inhibitor, was administered to 14 month old female SHR and normotensive American Wistar rats (NWR) for 10 months. The severe left ventricular hypertrophy of the 24 month old untreated SHR (4.37 +/- 0.2 mg/g v. 2.50 +/- 0.06 mg/g, untreated NWR) was markedly reduced (P less than 0.02) by captopril (3.01 +/- 0.1 mg/g). Chronic therapy prevented the reduction of both baseline and maximal cardiac indices in SHR, but did not alter blood flow in NWR. Left ventricular dilatation was present in 24 month old SHR and, as peak stroke volume index was diminished, the ejection fraction index of the SHR was reduced. Captopril restored this index in SHR to normal. The relation of ejection fraction index and afterload (peak systolic wall stress) was depressed in untreated SHR, but was normal in treated SHR. Thus, chronic therapy with captopril prevented the development of severe cardiac dysfunction and produced a marked regression of cardiac hypertrophy in SHR with advanced hypertensive heart disease.

Regression of left ventricular hypertrophy and prevention of left ventricular dysfunction by captopril in the spontaneously hypertensive rat.

To determine whether chronic antihypertensive therapy prevents the progression of cardiac hypertrophy and the deterioration in cardiac performance observed in spontaneously hypertensive rats (SHR) with long-term hypertension, 14-month-old female SHR and normotensive American Wistar rats (NWR) were treated for 10 months with an inhibitor of angiotensin I-converting enzyme, captopril (2 g/liter of drinking water). Captopril reduced the marked left ventricular hypertrophy of 24-month-old SHR (untreated, 4.37 +/- 0.2 mg/g of body weight; treated, 3.01 +/- 0.1 mg/g; P less than 0.02) to levels observed in 6-month-old SHR. Treatment prevented the reductions in baseline and maximal aortic blood flows that occurred in SHR between ages 12 and 24 months yet had no effect on the blood flows of NWR. The diminished maximal stroke volume of untreated SHR was ejected from a significantly increased left ventricular end-diastolic volume, so that the ejection-fraction index was markedly reduced (24-month-old untreated NWR, 84 +/- 3%; untreated SHR, 56 +/- 5%; P less than 0.001). Therapy restores this index in SHR to normal (77 +/- 4%). The relationship between ejection-fraction index, and afterload was also normal in treated SHR. Thus, chronic therapy with captopril produced a marked regression of cardiac hypertrophy and prevented the deterioration of cardiac performance in SHR with long-standing hypertension.

Alterations in the electrocardiogram of spontaneously hypertensive rats by chronic antihypertensive therapy with captopril.

To determine whether the electrocardiogram (ECG) could detect a reduction in ventricular mass with chronic antihypertensive therapy, ECGs were obtained in two year old female normotensive (NR) and spontaneously hypertensive rats (SHR) following nine months of treatment with captopril or water. The ECG of untreated SHR was considerably different than that of age- and sex-matched NR. The notable differences were the increased voltage, left axis deviation, a delay in the intrinsicoid deflection, and the increased frequency of left atrial abnormalities. Chronic captopril therapy produced a substantial reduction in left ventricular mass in the SHR (NR, 0.63 +/- 0.01; SHR, 1.08 +/- 0.03; captopril SHR, 0.80 +/- 0.04 g). The ECG reflected this regression of left ventricular hypertrophy since the voltage and axis of the treated SHR were no longer different than those of NR. Thus, the ECG may be effective in evaluating the regression of cardiac hypertrophy in response to chronic therapy in experimental hypertension.

Effect of antihypertensive therapy on calcium transport by cardiac sarcoplasmic reticulum of SHRs.

Cardiac hypertrophy develops during the course of blood pressure elevation in spontaneously hypertensive rats (SHRs) and is associated with defective calcium transport by cardiac sarcoplasmic reticulum (SR). AT 20 weeks of age, calcium uptake is reduced in SHRs (42 +/- 1.3 vs 64 +/- 1.6 nmol X mg-1 X min-1 in age-matched normotensive Wistar-Kyoto rats, P less than 0.01), while Ca2+ ATPase activity is enhanced (44 +/- 1.1 vs 35 +/- 0.7 nmol X mg-1 X min-1 in WKYs, P = 0.02); this results in low stoichiometry between calcium uptake and ATP hydrolysis in SHRs. The steady-state levels of the phosphoprotein intermediate [EP] of the transport ATPase are higher in normotensive rats (0.97 +/- 0.1 vs 0.67 +/- 0.08 nmol X mg-1 in SHRs, P less than 0.01) but the Ca2+- and ATP-dependency are similar in the two groups. In order to study the relative roles of hypertension and cardiac hypertrophy in the depression of SHR function, 20-week old SHRs and normotensive rats were treated for 10 weeks with either hydralazine (100 mg X litre-1) or alpha-methyldopa (8 g X litre-1). Both therapeutic regimens resulted in near normalisation of blood pressure of SHRs (hydralazine: 18.1 +/- 0.5 kPa [136 +/- 4 mmHg]; alpha-methyldopa 17.6 +/- kPa [132 +/- 3 mmHg]). Regression of cardiac hypertrophy, however, was seen only in the alpha-methyldopa-treated group, as judged by changes in left ventricular weight, RNA/DNA ratio, and hydroxyproline content. Furthermore, improvement in calcium transport capacity by the SHR, as reflected in higher calcium uptake and stoichiometric ratio between uptake and ATP hydrolysis, was found after alpha-methyldopa, but not hydralazine treatment. These results indicate that reversal of cardiac hypertrophy is required for improvement in calcium transport by cardiac SR after antihypertensive therapy of SHRs.

Lysosomal enzymes in the development and regression of myocardial hypertrophy induced by systemic hypertension

Left ventricular hypertrophy was induced in unilaterally-nephrectomized rats by excess dietary salt intake, with or without injections of deoxycorticosterone (DOCA). No changes occurred in the cardiac activities or distribution of several lysosomal enzymes (cathepsin D, acid phosphatase, β-acetylglucosaminidase). Similarly, regression of hypertrophy after return to normal salt intake and cessation of DOCA was unaccompanied by any changes in the enzymes. These results suggest that significant changes in lysosomal function are not an important feature of the development or regression of cardiac hypertrophy induced by systemic hypertension.

Heart volume and myocardial connective tissue during development and regression of thyroxine-induced cardiac hypertrophy in rats.

To determine whether development and regression of cardiac hypertrophy are accompanied by changes in heart volume and to learn whether a change in heart volume is associated with changes in the myocardial connective tissue, cardiac hypertrophy was induced in rats by administration of thyroxine. Rats were given L-thyroxine for 4 weeks. Heart volume was estimated radiologically in vivo at the start of the experiment and at 1- or 2-week intervals for 7 weeks. At each of these stages a number of rats were killed, their hearts were weighed and determinations were made of the myocardial contents of DNA, of collagen measured as hydroxyproline, and of glycosaminoglycans, measured as uronic acid. After thyroxine treatment the ratio of left heart ventricle weight to body weight and of heart volume to body weight rose significantly. The increase in heart weight was greater than the increase in heart volume. At the same time, there was a significant decrease in the concentration of hydroxyproline. After discontinuation of thyroxine treatment heart volume, heart weight and the concentration of myocardial collagen returned to normal within 2 weeks. However, the total amount of myocardial collagen was still less than normal at 2 weeks. The results suggest that the decrease in the amount of myocardial collagen associated with thyroxine-induced cardiac hypertrophy--because it results in a weakening of the supporting properties of the myocardial connective tissue framework--might contribute to a slight increase in in vivo heart volume.

Rat myocardial mechanics during pressure-induced hypertrophy development and reversal.

Moderate cardiac hypertrophy (CH) was produced in rats by abdominal aorta constriction for 5, 8, 15, 21, and 28 days. Aortic constriction release after 5, 8, and 15 days led to CH regression, which was complete within 15 days. A study of left ventricular papillary muscle mechanics during CH development demonstrated an early but transitory decrease in both maximum isometric force (Po) and maximum muscle shortening velocity (max V); in addition, the time-to-peak tension increased, and there was a decrease in isometric relaxation rate and in force-frequency relationship (negative staircase.) After CH regression, isometric relaxation and negative staircase were similar to controls, whereas the prolonged duration of contraction persisted. After release of the aortic constriction at 8 and 15 days, Po and max V were normal; however, after the earlier release (5 days), Po was higher than control, when muscle thickness was taken into consideration. These findings suggest 1) that an alteration in muscle mechanics may be related to the hypertrophy itself; 2) that anomalous excitation-contraction coupling might persist after CH regression.

A method for producing reversible long-term pressure overload of the cat right ventricle.

ArticleA method for producing reversible long-term pressure overload of the cat right ventricle.G Cooper 4th, and R M SatavaG Cooper 4th, and R M SatavaPublished Online:01 Nov 1974https://doi.org/10.1152/jappl.1974.37.5.762MoreSectionsPDF (708 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmailWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByTime course of right ventricular pressure-overload induced myocardial fibrosis: relationship to changes in fibroblast postsynthetic procollagen processingCatalin F. Baicu, Jiayu Li, Yuhua Zhang, Harinath Kasiganesan, George Cooper†, Michael R. Zile, and Amy D. Bradshaw1 November 2012 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 303, No. 9Rapamycin treatment augments both protein ubiquitination and Akt activation in pressure-overloaded rat myocardiumRebecca K. Harston, John C. McKillop, Phillip C. Moschella, An Van Laer, Lakeya S. Quinones, Catalin F. Baicu, Sundaravadivel Balasubramanian, Michael R. Zile, and Dhandapani Kuppuswamy1 May 2011 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 300, No. 5Hypertrophic Stimulation Increases β-actin Dynamics in Adult Feline Cardiomyocytes12 July 2010 | PLoS ONE, Vol. 5, No. 7Microtubule-dependent distribution of mRNA in adult cardiocytesDimitri Scholz, Catalin F. Baicu, William J. Tuxworth, Lin Xu, Harinath Kasiganesan, Donald R. Menick, and George Cooper1 March 2008 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 294, No. 3Phenotypic consequences of β1-tubulin expression and MAP4 decoration of microtubules in adult cardiocytesMasaru Takahashi, Hirokazu Shiraishi, Yuji Ishibashi, Kristie L. Blade, Paul J. McDermott, Donald R. Menick, Dhandapani Kuppuswamy, and George Cooper1 November 2003 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 285, No. 5c-Raf/MEK/ERK Pathway Controls Protein Kinase C-mediated p70S6K Activation in Adult Cardiac Muscle CellsJournal of Biological Chemistry, Vol. 277, No. 25Differential Activation of p70 and p85 S6 Kinase Isoforms during Cardiac Hypertrophy in the Adult MammalJournal of Biological Chemistry, Vol. 273, No. 38Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.Circulation, Vol. 89, No. 1Electrophysiological effects of left ventricular hypertrophy. Effect of calcium and potassium channel blockade.Circulation, Vol. 83, No. 6The Regression of Cardiac Hypertrophy: Functional, Anatomic, and Hemodynamic ConsiderationsComplete reversibility of cat right ventricular chronic progressive pressure overload.Circulation Research, Vol. 54, No. 3Basic Methods of Investigative Cardiovascular Radiology More from this issue > Volume 37Issue 5November 1974Pages 762-4 https://doi.org/10.1152/jappl.1974.37.5.762PubMed4279897History Published online 1 November 1974 Published in print 1 November 1974 Metrics

Protein metabolism in hypertrophied heart muscle.

The following aspects of protein metabolism in myocardium are discussed: (1) The kinetics of labeling of aminoacyl-transfer ribonucleic acid (tRNA) and the intracellular free amino acid pool. The specific activity of leucyl-tRNA correlates closely with that of the extracellular leucine during the first 15 minutes after intravenous injection of (/sup 3/H)leucine. Equilibrium of the leucyl-tRNA with total intracellular leucine is reached at a later time. (2) Determination of the fractional rate constant (k) of myosin synthesis with leucyl-tRNA as precursor. For a period between 15 and 30 minutes after intravenous injection, the k value was approximately 0.1 day/sup -1/(t/2 approximately = 6 days). (3) Synthesis and degradation of mitochondrial components in hypertrophied heart. Cardiac cytochrome c increases faster than the remainder of cellular proteins in the first day after aortic constriction. The results of labeling with delta-aminolevulinic acid indicate increased rate of synthesis and decreased rate of degradation of cytochrome c. (4) Role of lysosomes in regression of cardiac hypertrophy. During the period of rapid fall in cardiac mass and RNA after removal of the constricting band, the activities of cathepsin D and ribonuclease were found unchanged. (5) Properties of calcium-activated neutral protease (CAF), which specifically removes Z lines frommore » myofibrils. It was shown that CAF treatment of myofibrils results in the disappearance of a single protein, ..cap alpha..-actinin.« less

Effects of prolonged treatment with adrenergic beta-receptor antagonists on blood pressure, cardiovascular design and reactivity in spontaneously hypertensive rats (SHR).

AbstractYoung “prehypertensive” SHR were treated with two kinds of β‐adrenergic receptor antagonists from 2 1 / 2 up to 8 months of age. Arterial pressure largely remained at prehypertensive levels and acute cardiovascular responses to “stress” were considerably modified compared to untreated SHR. Quantitative hemodynamic analyses revealed that resistance vessel design exhibited only slight hypertensive changes when related to untreated controls, while the development of left ventricular hypertrophy was far less influenced by the treatment. In part of the group, pressure was followed for another 6 months after treatment, showing only a delayed and modest pressure rise compared with untreated, matched SHR. When instead adult SHR, with “established” hypertension, were similarly treated from 8 up to 10 months of age, resting arterial pressure remained unaffected and the resistance vessels exhibited only modest regression of the hypertensive changes, with signs of a largely preserved increase of vascular wall/lumen ratio, and with negligible regression of cardiac hypertrophy. The results indicate that early, “preventive” treatment of SHR with β‐receptor blockers is of considerable value whichever their exact modes of action, though some regression of vascular changes can be achieved also in established hypertension, particularly in females (Weiss 1974).

Normal myocardial function and energetics after reversing pressure-overload hypertrophy.

ARTICLESNormal myocardial function and energetics after reversing pressure-overload hypertrophyG Cooper 4th, RM Satava, CE Harrison, and Coleman HN 3rdG Cooper 4th, RM Satava, CE Harrison, and Coleman HN 3rdPublished Online:01 May 1974https://doi.org/10.1152/ajplegacy.1974.226.5.1158MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe Right Ventricle in Left Heart Failure13 September 2014Myocardial Growth and the Development and Regression of Increased Ventricular MassCytoskeletal networks and the regulation of cardiac contractility: microtubules, hypertrophy, and cardiac dysfunctionGeorge Cooper1 September 2006 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 291, No. 3Passive Load and Angiotensin II Evoke Differential Responses of Gene Expression and Protein Synthesis in Cardiac MyocytesCirculation Research, Vol. 78, No. 5High blood pressure, oxygen radicals and antioxidants: Etiological relationshipsMedical Hypotheses, Vol. 46, No. 4Regional myosin heavy chain expression in volume and pressure overload induced cardiac hypertrophyActa Physiologica Scandinavica, Vol. 155, No. 4Current issues in advanced heart failureMedical Clinics of North America, Vol. 76, No. 5Function of the Hypertrophic Right and Left Ventricles in Experimental ConditionsAlterations in collagen cross-linking impair myocardial contractility in the mouse heart.Circulation Research, Vol. 65, No. 6Load responsiveness of protein synthesis in adult mammalian myocardium: role of cardiac deformation linked to sodium influx.Circulation Research, Vol. 64, No. 1Influence of aortic valve disease on systolic stiffness of the human left ventricular myocardium.Circulation, Vol. 75, No. 5Myocardial Hypertrophy and Cardiac Failure: A Complex InterrelationshipThe Regression of Cardiac Hypertrophy: Functional, Anatomic, and Hemodynamic ConsiderationsControl of myocardial tissue components and cardiocyte organelles in pressure-overload hypertrophy of the cat right ventricleAmerican Journal of Anatomy, Vol. 177, No. 1Reversibility of the structural effects of pressure overload hypertrophy of cat right ventricular myocardiumThe Anatomical Record, Vol. 214, No. 2Myocardial hypertrophy in rats exposed to simulated high altitude26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 93, No. 4Complete reversibility of cat right ventricular chronic progressive pressure overload.Circulation Research, Vol. 54, No. 3Cardiac Hypertrophy and Altered Cellular Electrical Activity of the MyocardiumRegression of left ventricular hypertrophy by medical treatment: Present status and possible implicationsThe American Journal of Medicine, Vol. 75, No. 3Biochemical, structural and mechanical defects of the failing myocardiumPharmacology & Therapeutics, Vol. 22, No. 2Development and regression of increased ventricular massThe American Journal of Cardiology, Vol. 50, No. 3Selective effects of alpha-methyldopa on myocardial cell components independent of cell size in normotensive and genetically hypertensive rats.Hypertension, Vol. 4, No. 4Load regulation of the structure, composition, and function of mammalian myocardium.Circulation Research, Vol. 50, No. 6Morphological changes in the mechanically unloaded myocardial cellThe Anatomical Record, Vol. 200, No. 3Reversal of Cardiac Hypertrophy by Antihypertensive TherapyThe diagnosis and management of acute left-sided valvular regurgitationCurrent Problems in Cardiology, Vol. 4, No. 9Cardiac size and function in acromegaly.Circulation, Vol. 56, No. 5Effects of intermittent pressure loading on the development of ventricular hypertrophy in the cat.Circulation Research, Vol. 40, No. 5Recuperative potential of cardiac muscle following relief of pressure overload hypertrophy and right ventricular failure in the cat.Circulation Research, Vol. 40, No. 1 More from this issue > Volume 226Issue 5May 1974Pages 1158-1165 Copyright & PermissionsCopyright © 1974 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1974.226.5.1158PubMed4274811History Published online 1 May 1974 Published in print 1 May 1974 Metrics

Regression of altitude-produced cardiac hypertrophy.

The rate of regression of cardiac hypertrophy with time has been determined in adult male albino rats. The hypertrophy was induced by intermittent exposure to simulated high altitude. The percentage hypertrophy was much greater (46%) in the right ventricle than in the left (16%). The regression could be adequately fitted to a single exponential function with a half-time of 6.73 plus or minus 0.71 days (90% CI). There was no significant difference in the rates of regression for the two ventricles.

Regression of cardiac hypertrophy following experimental hyperthyroidism in rats.

SummaryHyperthyroidism was induced in male, albino rats by subcutaneous injection of T3 daily for 2 weeks. The day following the last injection, groups of control and experimental animals were killed; the hearts were removed, weighed, and the average amount of cardiac hypertrophy was determined. The hearts were then partitioned and the ventricles were weighed separately. To determine when the hearts returned to normal size, groups of rats were killed at about 5-day intervals up to 35 days. The data were subjected to linear regression analysis. It was observed that the hearts returned to normal size in 13 days; this also held approximately for each ventricle despite the fact that the right ventricle was hypertrophied significantly more, proportionally, than the left ventricle.