Noninvasive Evaluation of the Time Course of Change in Cardiac Function in Spontaneously Hypertensive Rats by Echocardiography

Kokubo, Manabu; Uemura, Arata; Matsubara, Tatsuaki; Murohara, Toyoaki

doi:10.1291/hypres.28.601

Cited by 76 publications

(73 citation statements)

References 40 publications

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“…This problem had been previously reported (42) and prevented us from determining diastolic function. Although we could not measure cardiac output, the normalization of telediastolic left ventricular diameter and the improvement of intramyocardial vasculature support that heart function is probably improved by treatment.…”

Section: Discussionmentioning

confidence: 79%

Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR

Conde

González

Quintana‐Villamandos³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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Conde MV, Gonzalez MC, Quintana-Villamandos B, Abderrahim F, Briones AM, Condezo-Hoyos L, Regadera J, Susin C, de Diego JJ, Delgado-Baeza E, Diaz-Gil JJ, Arribas SM. Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR. Am J Physiol Heart Circ Physiol 301: H1153-H1165, 2011. First published June 3, 2011 doi:10.1152/ajpheart.00886.2010.-Liver growth factor (LGF) is an endogenous albumin-bilirubin complex with antihypertensive effects in spontaneously hypertensive rats (SHR). We assessed the actions of LGF treatment on SHR mesenteric resistance and intramyocardial arteries (MRA and IMA, respectively), heart, and vascular smooth muscle cells (VSMC). SHR and Wistar-Kyoto (WKY) rats treated with vehicle or LGF (4.5 g LGF/rat, 4 ip injections over 12 days) were used. Intra-arterial blood pressure was measured in anesthetized rats. The heart was weighted and paraffinembedded. Proliferation, ploidy, and fibronectin deposition were studied in carotid artery-derived VSMC by immunocytochemistry. In MRA, we assessed: 1) geometry and mechanics by pressure myography; 2) function by wire myography; 3) collagen by sirius red staining and polarized light microscopy, and 4) elastin, cell density, nitric oxide (NO), and superoxide anion by confocal microscopy. Heart sections were used to assess cell density and collagen content in IMA. Left ventricular hypertrophy (LVH) regression was assessed by echocardiography.LGF reduced blood pressure only in SHR. LGF in vitro or as treatment normalized the alterations in proliferation and fibronectin in SHR-derived VSMC with no effect on WKY cells. In MRA, LGF treatment normalized collagen, elastin, and VSMC content and passive mechanical properties. In addition, it improved NO availability through reduction of superoxide anion. In IMA, LGF treatment normalized perivascular collagen and VSMC density, improving the wall-to-lumen ratio. Paired experiments demonstrated a partial regression of SHR LVH by LGF treatment. The effective cardiovascular antifibrotic and regenerative actions of LGF support its potential in the treatment of hypertension and its complications. intramyocardial arteries; mesenteric resistance arteries; nitric oxide; vascular remodeling; left ventricular hypertrophy LIVER GROWTH FACTOR (LGF) was first described as an endogenous factor with mitogenic properties in liver (21).LGF is not detected in physiological conditions, but it increases in plasma in situations of hepato-biliary disorders, both in humans and rats (21,24). The chemical analysis of LGF obtained from human and rat plasma has revealed that it is a covalently bound albumin-bilirubin complex (24,25). The regenerative effects of LGF, initially described in hepato-biliary disorders (22,23,26), have been recently extended to other diseases, such as Parkinson's disease (35, 52), testicular degeneration (51), and pulmonary fibrosis (47).LGF treatment also has cardiovascular effects as previously shown in rodent models of hype...

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Section: Discussionmentioning

confidence: 79%

Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR

Conde

González

Quintana‐Villamandos³

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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“…Systolic cardiac function has been shown to be altered in SHR, with some reports showing systolic function to be decreased (24,42), increased (6), or unchanged (47) early in the course of hypertension. In the present study, E s was significantly lower in SHR compared with WKY.…”

Section: Discussionmentioning

confidence: 99%

“…We also established whether training altered cardiac performance to a Starling challenge in normotensive and hypertensive hearts. The Wistar-Kyoto rat (WKY) and SHR models were utilized for these experiments on the basis that SHR mimic well the clinical course of untreated essential hypertension in humans and are well documented to show left ventricular (LV) chamber enlargement by 6 -12 mo of age (1,6,11,16,24).…”

mentioning

confidence: 99%

Exercise training improves systolic function in hypertensive myocardium

Libonati

Sabri

Xiao

et al. 2011

Journal of Applied Physiology

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Libonati JR, Sabri A, Xiao C, MacDonnell SM, Renna BF. Exercise training improves systolic function in hypertensive myocardium. J Appl Physiol 111: 1637-1643, 2011. First published September 15, 2011 doi:10.1152/japplphysiol.00292.2011The general purpose of this study was to test the effect of exercise training on the left ventricular (LV) pressure-volume relationship (LV/PV) and apoptotic signaling markers in normotensive and hypertensive hearts. Four-month-old female normotensive Wistar-Kyoto rats (WKY; n ϭ 37) and spontaneously hypertensive rats (SHR; n ϭ 38) were assigned to a sedentary (WKY-SED, n ϭ 21; SHR-SED, n ϭ 19) or treadmilltrained (WKY-TRD, n ϭ 16; SHR-TRD, n ϭ 19) group (ϳ60% V O2 peak, 60 min/day, 5 days/wk, 12 wk). Ex vivo LV/PV were established in isovolumic Langendorff-perfused hearts, and LV levels of Akt, phosphorylated Akt (Akt Pi), Bad, phosphorylated Bad (BadPi) c-IAP, x-IAP, calcineurin, and caspases 3, 8, and 9 were measured. Heart-to-body weight ratio was increased in SHR vs. WKY (P Ͻ 0.05), concomitant with increased calcineurin mRNA (P Ͻ 0.05). There was a rightward shift in the LV/PV (P Ͻ 0.05) and a reduction in systolic elastance (E s) in SHR vs. WKY. Exercise training corrected E s in SHR (P Ͻ 0.05) but had no effect on the LV/PV in WKY. Caspase 3 was increased in SHR-SED relative to WKY-SED, while Bad Pi, c-IAP, and x-IAP were significantly lower in SHR relative to WKY (P Ͻ 0.05). Exercise training increased BadPi in both WKY and SHR but did not alter caspase 9 activity in either group. While caspase 3 activity was increased with training in WKY (P Ͻ 0.05), it was unchanged with training in SHR. We conclude that moderate levels of regular aerobic exercise attenuate systolic dysfunction early in the compensatory phase of hypertrophy, and that a differential phenotypical response to moderate-intensity exercise exists between WKY and SHR.

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“…Conventional transthoracic echocardiography transducers often do not provide enough resolution. However, high-frequency transducers (7.5-15 MHz) are now available to monitor morphometric and functional changes in small animals in vivo [25] . Hemodynamics monitoring is one of the reliable methods to evaluate left ventricle performance by invasive catheterization.…”

Section: Discussionmentioning

confidence: 99%

Ouabain induces cardiac remodeling in rats independent of blood pressure

Xing

Ren

Lü

2007

Acta Pharmacologica Sinica

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Aim: To investigate the ouabain's effects on cardiac remodeling in rats. Methods: Male Sprague‐Dawley rats were treated with ouabain. Systolic blood pressure (SBP) was recorded weekly. After 4 and 6 weeks, echocardiography were performed, hemodynamic parameters were measured by invasive cardiac catheterization, changes in cardiac ultrastructure were analyzed using transmission electron microscopy, the collagen fraction of the left ventricle was assessed with Picrosirius red stain, and RT‐PCR was applied to evaluate the mRNA level of myosin heavy chain‐α and ‐β in the left ventricle. Results: Having been treated with ouabain for 4 weeks, there was no significant difference in the mean SBP of the two groups. However, left ventricular hypertrophy, myocardial ultrastructure deterioration, and extracellular matrix remodeling were induced by ouabain treatment; meanwhile, cardiac systolic and diastolic performance were both worsened. Moreover, the cardiac MHC‐β mRNA was upregulated by ouabain treatment, whereas MHC‐α mRNA was downregulated. After 4 weeks, the mean SBP in the ouabain group began to increase and was significantly higher than that in control group after 6 weeks (P<0.01); the rats' cardiac structure and function were worsened. Conclusion: These results suggested that ouabain induces alterations in cardiac structure and function, and the effects happened before the increase of blood pressure. The results indicated that ouabain induced cardiac remodeling in rats independent of blood pressure.

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Noninvasive Evaluation of the Time Course of Change in Cardiac Function in Spontaneously Hypertensive Rats by Echocardiography

Cited by 76 publications

References 40 publications

Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR

Liver growth factor treatment restores cell-extracellular matrix balance in resistance arteries and improves left ventricular hypertrophy in SHR

Exercise training improves systolic function in hypertensive myocardium

Ouabain induces cardiac remodeling in rats independent of blood pressure

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