Increase In Cardiac Weight Research Articles

Cardioprotective effects of <i>Dan-Yang-Fu-Xin</i> decoction on chronic heart failure in rats

Purpose: To evaluate the cardioprotective effects and possible mechanisms of Dan-Yang-Fu-Xin decoction (DYFX) in a rat chronic heart failure (CHF).Methods: A CHF rat model induced by ligation of the left anterior descending coronary artery was used to investigate the cardioprotective effects of DYFX. After intragastric administration for 8 weeks, several functional cardiac indices, including fractional shortening (FS), ejection fraction (EF), heart rate (HR) and cardiac output (CO) were assessed by ultrasound examination. Subsequently, inflammatory markers, viz, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), myocardial enzymes, namely, lactate dehydrogenase (LDH) and creatine kinase (CK), were also assessed by enzyme-linked immunosorbent assay (ELISA).Results: Intragastric administration of DYFX (200, 400 and 600 mg/kg) significantly reversed the decrease in body weight and increase in cardiac weight (p < 0.05) induced by CHF. Treatment with DYFX also significantly reversed EF, FS, HR, and CO changes in CHF rats. In addition, DYFX inhibited the two inflammatory cytokines (TNF-α and IL-6) and myocardial enzymes (CK and LDH), suggesting that these effects may include the mechanisms of cardioprotectiion involved in attenuation of CHF.Conclusion: DYFX possesses cardioprotective effects involving CHF. The protective mechanisms may include the suppression of expression of inflammatory mediators and myocardial enzymes.Keywords: Dan-Yang-Fu-Xin decoction, Cardioprotection, Chronic heart failure, Inflammatory mediators, Myocardial enzymes

Protective role of endogenous cardiac natriuretic peptide/GC-A system on the maternal heart during the postpartum period

Volume overload during pregnancy results in transient and reversible cardiac hypertrophy in pregnant females. Endogenous atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) acts through the common receptor, guanylyl cyclase-A (GC-A) to lower blood pressure, induce diuresis/natriuresis, and dilate blood vessels. Although the roles of endogenous natriuretic peptides/GC-A system on the cardiovascular system have been well investigated, those on the puerperal period have not been elucidated. The aim of this study was to investigate the physiological role of endogenous natriuretic peptides/GC-A system in the puerperal period by comparing pregnant wild-type (WT) and GC-A knockout (GC-A-KO) mice. Although blood pressure in GC-A-KO mice was not changed during pregnancy or after delivery, there was a dramatic postpartum increase in cardiac weight. Interestingly, the cardiac hypertrophy and interstitial fibrosis in GC-A-KO were dramatically accelerated by repeated pregnancy/lactation cycles (Figure ​(Figure1).1). Moreover, a significant decline in cardiac function, as well as up-regulation of fetal cardiac genes, was observed in the multiparous GC-A-KO heart. Importantly, the hypertrophic change in GC-A-KO heart was observed not during gestation, but during lactation. Furthermore, the lactation-induced cardiac hypertrophy in GC-A-KO was significantly suppressed by avoiding the breast feeding. Our results suggest that the defect in endogenous cardiac natriuretic peptide/GC-A system promotes cardiomyopathy during puerperal period, especially during lactation. Figure 1 Significant cardiac hypertrophy was observed in GC-A-knockout mice during the puerperal period.

Premature death and age-related cardiac dysfunction in male eNOS-knockout mice

The aims of our study were to determine mortality, and age- and genotype-related cardiac phenotype in endothelial nitric oxide synthase (NOS) knockout (–/–) and wild-type (+/+) mice. Male and female (–/–) and male and female (+/+) conscious mice were studied at different ages by echocardiography and tail-cuff blood pressure (BP) measurement. Only 50% male (–/–) mice lived longer than 21 months whereas 89% (+/+) mice were still alive after 24 months ( P < 0.005). There was little mortality in female mice of either genotype. Both (–/–) and (+/+) male mice have normal cardiac dimensions and function at 5.5 months. However, (–/–) mice developed cardiac dilation and dysfunction at 21 months as evidenced by a significant increase ( P < 0.05) in left ventricular (LV) end-diastolic diameter from 2.69 ± 0.13 to 3.13 ± 0.09 mm, LV end-systolic diameter from 1.28 ± 0.11 to 1.86 ± 0.12 mm, LV end-diastolic cavity volume from 21 ± 2.8 to 31 ± 2.5 μl and LV mass from 19 ± 2.5 to 27 ± 1.9 mg/10 g and a significant decrease ( P < 0.05) in ejection fraction (from 65 ± 3.3% to 41 ± 4.6%), shortening fraction (from 53 ± 2.2% to 41 ± 3.4%), LV posterior wall thickening (from 27 ± 2% to 12 ± 4%) and septum thickening (from 27 ± 2% to 12 ± 4%) compared with those at 5.5 months. There was a clear increase in cardiac weight and cardiac dilation by hematoxylin and eosin in male (–/–) mice at 21 months. BP in male (–/–) mice fell with the cardiac dysfunction, whereas female (–/–) mice were hypertensive even at 21 months. The level of mRNA for neuronal NOS and inducible NOS was greater in all females compared to males. These results indicate that male (–/–) mice have a significantly shorter lifespan than (+/+) or female mice, and male (–/–) mice develop cardiac dysfunction with age.

Decreased protein kinase C-epsilon expression in hypertrophied cardiac ventricles induced by triiodothyronine treatment in the rat

To examine the effect of thyroid hormone-induced cardiac hypertrophy on PKC expression, changes in the expression of PKC isoforms were studied in hypertrophied cardiac ventricles induced by triiodothyronine (T3) injection in the rat. Injection with T3 for 8 days induced 49% increase in cardiac weight compared to controls. Immunoblot analysis of cardiac ventricular extracts showed the expression of PKC-δ, -ε, and -ζ in both control and T3-treated groups. The expression of PKC-ε decreased by 40% in hyperthyroid rat cardiac ventricles, while PKC-δ and -ζ expressions were barely affected. PKC-ε immunoreactivity decreased in both cytosol and membrane fractions. On the contrary, PKC-ε expression did not decrease in the extract of hypertrophied cardiac ventricles produced by aortic banding or aortocaval shunt. These results indicate that thyroid hormone down regulates PKC-ε expression in the hyperthyroid-mediated cardiac hypertrophy.

Extracellular matrix deposition in hypertensive hearts antifibrotic effects of ramipril.

Hypertension induced in rats by suprarenal banding has a blood pressure elevating effect that is accompanied by the occurrence of cardiac hypertrophy and fibrosis. This phenomenon is already present at 2 weeks after banding and persists up to 1.5 years. The increase in cardiac weight is mostly due to the development of fibrosis, since myocytes are only slightly increased in size. The fibrotic tissue consists mainly of fibronectin and collagen and contains numerous cellular elements. The occurrence of fibrosis can be completely inhibited by the administration of the specific ACE inhibiting drug, ramipril, which indicated that angiotensin II may directly stimulate fibroblasts to produce fibronectin and collagen. The antifibrotic effect of ramipril was also present in a low dosage that did not lower blood pressure, confirming the hypothesis that angiotensin II has a direct effect on connective tissue cells and their ability to produce extracellular matrix proteins. The direct effect of the renin-angiotensin system on the activity of interstitial cells was further proven by molecular biology techniques showing an upregulation of transcription for collagen I and III which is prevented by ACE inhibition.

Sensitivity of cardiac tissues with moderate and advanced hypertrophy to calcium ions

1. 1. Prolonged existence of hypertension is known to induce a compensatory increase in cardiac weight, later followed by a loss of functional responsiveness to biological stimuli. 2. 2. It was the aim of the present study to investigate the functional responses of hypertrophied hearts to rising levels of intracellular calcium. The experiments were performed using two different degrees of cardiac hypertrophy, the first as obtained in spontaneously hypertensive rats (SHR) of 18–20 weeks old, the second by using rats, 32–34 weeks old, with a surgically induced stenosis of the thoracic aorta (ASR). The ASR, which showed signs of overt heart failure, may be presented as a model for hypertension-induced end-stage cardiac hypertrophy. Age-matched normotensive Wistar-Kyoto rats (WKY) and sham-operated Wistar rats served as respective controls. 3. 3. Different methods were employed such as increasing the extracellular Ca 2+concentration, stimulation of calcium influx by means of the calcium entry promoter Bay K 8644, or altering the sodium-calcium exchange by means of the sodium ionophore monensin. 4. 4. The inotropic responses induced by increasing the extracellular Ca 2+concentration or provoked by the calcium entry promoter Bay K 8644 proved more pronounced in hearts taken from SHR of 18 weeks old than in those from normotensive control rats, whereas the response to monensin was found to be the same in both types of hearts. In the hearts of ASR, however, the inotropic responses to Ca 2+, Bay K 8644 and monensin were strongly impaired. 5. 5. These data demonstrate that in functional experiments the sensitivity to Ca 2+, which represents the main pathway in establishing a contraction, is strongly reduced in advanced cardiac hypertrophy.

Cardiac Hypertrophy and Salt Status in Chronic Myocardial Infarction in the Rat

The effects of salt restriction and the ACE inhibitor enalapril were compared in a model of chronic myocardial infarction in the rat. Total exchangeable sodium was measured by an isotopic dilution technique to quantitate the effects of the low salt diet and ACE inhibitor on body sodium and extracellular fluid. Rats with infarction developed a marked increase in cardiac weight (4.29 +/- 0.18 mg/g body weight) compared with control rats (3.64 +/- 0.08 mg/g, p less than 0.01). There was hypertrophy of both left and right ventricles. Salt restricted rats with infarction developed identical cardiomegaly (4.30 +/- 0.11 mg/g), although total exchangeable body sodium fell by 10% (p less than 0.001). In contrast, rats with infarction receiving enalapril developed significantly less cardiomegaly (3.97 +/- 0.10 mg/g) while body sodium remained unchanged. Rats with infarction had a significant increase in lung weight which was not changed by salt restriction but which was abolished by enalapril. These results suggest that salt restriction does not prevent the progression of cardiomegaly in chronic left heart failure. In contrast our results confirm the ability of ACE inhibitors to prevent progressive cardiomegaly and left heart failure without affecting long-term changes in sodium balance.

Failure of swimming exercise to improve capillarization in cardiac hypertrophy of renal hypertensive rats.

Female Sprague-Dawley rats were made hypertensive by the two kidney/one clip Goldblatt procedure, while control animals were sham-operated. One week later, half of the animals were subjected to a moderate swimming exercise and the other half remained sedentary. Thus, four experimental groups, each consisting of 14 rats, were formed: control animals that were exercised or kept sedentary and corresponding renal hypertensive animals either exercised or sedentary. In hypertensive rats, a significantly increased left ventricular weight and reduced coronary reserve were found. Cardiac hypertrophy in hypertensive rats was characterized by a lower number of capillaries on a tissue cross-section, larger heterogeneity of the capillary net, and a less uniform orientation of capillaries in space. Total length of capillaries in the hypertrophic hearts increased significantly, but less than the increase in cardiac weight, resulting in reduced capillary length density. Chronic swimming for 2 hr/day for a period of 6 weeks, subsequent to a 4-week acclimation period, did not significantly influence any of the investigated indexes of capillaries from hypertrophic hearts. In the normotensive rats, chronic swimming resulted only in a moderate increase in total capillary length associated with a small increase in the left ventricular weight of similar degree. Thus, chronic exercise in normotensive rats induced a moderate increase in total capillary length per left ventricle, while it did not alleviate impaired capillarization of hypertrophic hearts from hypertensive rats.

Frequency analysis of first heart sound for the elderly.

Frequency analysis of first heart sound in elderly and expired cases was performed to reveal changes of the cardiovascular system accompanying aging. The vibration was analyzed for isometric contraction phase or 0.06 seconds following the main vibration of first sound by means of fast Fourier transform technique, and main frequency was compared. Mean main frequencies were 43.0 +/- 15.4 cps (mean +/- SD) in 21 cases from 54 years to 69 years, 41.4 +/- 12.6 cps in 34 cases from 70 years to 79 years, 40.0 +/- 14.4 cps in 19 cases from 80 years to 89 years, and 44.2 +/- 4.5 cps in 4 cases from 90 years to 94 years. It was 44.4 +/- 8.0 cps in 6 cases with left ventricular hypertrophy (LVH) on ECG, and 37.2 +/- 7.5 cps in 18 cases without LVH. It was 35.7 +/- 6.5 cps in 9 cases who expired and 32.6 +/- 5.8 cps in cases of those who died within a year. Though mean main frequencies were almost equal in these groups, it is higher than that of younger subjects, which suggests stiffness of the cardiovascular system of the aged. It was suggested that the stiffness of the cardiovascular system is greater than the increase in cardiac weight of elderly subjects with LVH. Mean main frequency was low in subjects who dies within a year, which may be due to cardiomegaly.

Morphometry and ultrastructure of heart hypertrophy induced by chronic volume overload (aorto-caval fistula in the rat)

Heart hypertrophy due to chronic volume overload was produced in adult female rats by experimental aorto-caval fistula. Animals were sacrificed 5 days, 1 and 6 months after the operation. Morphology of cardiac myocytes from the left ventricle was studied in light and electron microscope. Cardiac weight of operated rats almost doubled the normal heart weight during the first month, while later the rate of cardiac growth was similar in both operated and control animals. Cell length increased to the same extent as the cell width, indicating harmonious growth. Increase in the cell volume was more pronounced in the subendocardial region than in the midwall layers. Similarly, degenerative changes were found more often in the subendocardium. Average increase in the cell volume was similar to the increase in cardiac weight, which seems to suggest hypertrophic growth. Cytological features of active cell growth were found not only in the early stages of pathological growth (5 days and 1 month) but also 6 months after the operation. This observation is consonant with the persistence of increased proteosynthesis not only in the period of the stable hypertrophy but also in the later stages, often associated with cardiac failure.

Myocardial chromatin activation in experimental hyperthyroidism in rats. Role of nuclear non-histone proteins.

HomeCirculation ResearchVol. 42, No. 3Myocardial chromatin activation in experimental hyperthyroidism in rats. Role of nuclear non-histone proteins. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBMyocardial chromatin activation in experimental hyperthyroidism in rats. Role of nuclear non-histone proteins. C J Limas and C Chan-Stier C J LimasC J Limas Search for more papers by this author and C Chan-StierC Chan-Stier Search for more papers by this author Originally published1 Mar 1978https://doi.org/10.1161/01.RES.42.3.311Circulation Research. 1978;42:311–316 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Moussavi R (1990) Neonatal hyperthyroidism enhances growth of the heart but not of skeletal muscle, Mechanisms of Ageing and Development, 10.1016/0047-6374(90)90140-B, 52:1, (1-10), Online publication date: 1-Mar-1990. Zimmer H, Seesko R, Zierhut W and Pechan I (1987) Cardiac Effects of ß-Adrenergic Blockers in Combination with Metabolic Interventions Pharmacological Aspects of Heart Disease, 10.1007/978-1-4613-2057-9_19, (233-247), . Zimmer H and Peffer H (1986) Metabolic aspects of the development of experimental cardiac hypertrophy Controversial issues in cardiac pathophysiology, 10.1007/978-3-662-11374-5_13, (127-137), . Limas C (1984) Subcellular Changes in Compensated and Failing Hypertrophied Hearts Functional Aspects of the Normal, Hypertrophied, and Failing Heart, 10.1007/978-1-4613-3825-3_10, (151-170), . Morkin E, Flink I and Goldman S (1983) Biochemical and physiologic effects of thyroid hormone on cardiac performance, Progress in Cardiovascular Diseases, 10.1016/0033-0620(83)90004-X, 25:5, (435-464), Online publication date: 1-Mar-1983. Limas C (1982) Enhanced myocardial RNA synthesis in spontaneously hypertensive rats Possible role of high-mobility group non-histone proteins, Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression, 10.1016/0167-4781(82)90007-0, 696:1, (37-43), Online publication date: 1-Jan-1982. Lester L, Sodt P, Rich B, Lucky A, Hutcheon N and Arcilla R (1982) Cardiac abnormalities in children with hyperthyroidism, Pediatric Cardiology, 10.1007/BF02332112, 2:3, (215-223), Online publication date: 1-Sep-1982. Limas C (1981) Phosphorylation of myocardial nuclei enhances their susceptibility to deoxyribonuclease I, Biochemical and Biophysical Research Communications, 10.1016/0006-291X(81)91972-0, 100:3, (1347-1352), Online publication date: 1-Jun-1981. Zak R (1981) Contractile Function as a Determinant of Muscle Growth Cell and Muscle Motility, 10.1007/978-1-4684-8196-9_1, (1-33), . Smallridge R (1980) Thyroid Hormone Effects on the Heart Hearts and Heart-Like Organs, 10.1016/B978-0-12-119402-4.50009-9, (93-160), . Zak R, Kizu A and Bugaisky L (1979) Cardiac hypertrophy: Its characteristics as a growth process, The American Journal of Cardiology, 10.1016/0002-9149(79)90226-1, 44:5, (941-946), Online publication date: 1-Oct-1979. March 1, 1978Vol 42, Issue 3 Advertisement Article InformationMetrics Copyright © 1978 by American Heart Associationhttps://doi.org/10.1161/01.RES.42.3.311 Originally publishedMarch 1, 1978 PDF download Advertisement