Non-invasive echocardiographic studies in mice

Chaves, Alysia; Weinstein, David M.; Bauer, John

doi:10.1016/s0024-3205(01)01123-7

Cited by 72 publications

(69 citation statements)

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“…Compensatory mechanisms in vivo at rest and negative inotropic and chronotropic effects of anesthesia are other possible causes. Echocardiography revealed bradycardia, as previously observed in mice (7,43).…”

Section: Discussionsupporting

confidence: 84%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

243

265

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. Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy. J Appl Physiol 93: 1301-1309. First published May 24, 2002 10.1152/japplphysiol.00231.2002-Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored and call for an effective and wellcharacterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (V O2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent V O2 max with 0.98 test-retest correlation was found at 25°treadmill grade. Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85-90% of V O2 max and 2 min at 50% (adjusted to weekly V O2 max testing) increased V O2 max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both sexes, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased by 19-29 and 12-17% in females and males, respectively, whereas cardiomyocyte dimensions increased by 20-32, and 17-23% in females and males, respectively; skeletal muscle mass increased by 12-18%. Thus the model mimics human responses to exercise and can be used in future studies of molecular mechanisms underlying these adaptations. maximal oxygen uptake; work economy; respiratory exchange ratio; cardiomyocyte; allometric scaling SEVERAL NOVEL SIGNALING PATHWAYS of pathological cardiac hypertrophy have been unveiled in the powerful model of mechanical overloading by thoracic aorta constriction in genetically modified mice (8,22). Thus far, the molecular mechanisms of adaptive cardiac hypertrophy in response to physiological stimuli remain virtually unexplored because of a paucity of effective and well-controlled experimental models in this species. Ideally, the outcome should mimic typical results of exercise training in humans, e.g., increased maximal oxygen uptake (V O 2 max ) and work economy (21). In healthy individuals, increased exercise capacity is dependent on functional and structural adaptations in skeletal muscle, blood vessels, and heart. Cardiac adaptation includes increased ventricular chamber volumes and weights, cardiomyocyte hypertrophy, increased cardiac output, and improved contractile function measured in isolated cardiomyocytes and in the intact heart (2, 3).At present, there are few well-controlled endurance training studies in mice. Training is usually carried out as voluntary exercise regimens, with little control of exercise intensity and the individual's fitness level. Voluntary wheel running is most frequently used. V O 2 max has been shown to increase by 12-30% after a 7-to 12-wk period of free wheel running (11,40). The latter study also demonstrated a 6% decreased respiratory exchange ratio (RER) at V O 2 max in trained mice. Exercise capacity and adaptations have al...

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Section: Discussionsupporting

confidence: 84%

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Kemi

Loennechen

Wisløff

et al. 2002

Journal of Applied Physiology

243

265

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“…In this study, halothane has been used to perform echocardiogram, because it is more convenient and reliable with respect to rate of induction, reversibility, and control of anesthetic depth. 34 In addition, HR is less affected with inhaled anesthetic than with intraperitoneal ones. Although further studies with other anesthetics, such as isoflurane, would be interesting to confirm our findings with halothane, the similarity between our in vivo and in vitro data provides a very strong evidence for a key role of the Ang-(1-7)-Mas axis in heart function.…”

Section: Discussionmentioning

confidence: 99%

“…The anesthetic of choice to make echocardiograms in mice is always a complex issue, because most of them influence HR, which alters cardiac function. 34 Because the mice HR is normally very high, choosing an anesthetic regimen that keeps it near to physiological levels should be an important concern. In this study, halothane has been used to perform echocardiogram, because it is more convenient and reliable with respect to rate of induction, reversibility, and control of anesthetic depth.…”

Section: Discussionmentioning

confidence: 99%

Impairment of In Vitro and In Vivo Heart Function in Angiotensin-(1-7) Receptor Mas Knockout Mice

Santos¹,

Castro²,

Gava³

et al. 2006

Hypertension

214

172

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Abstract-In this study we investigated the effects of the genetic deletion of the angiotensin (Ang)-(1-7) receptor Mas on heart function. Localization of Mas in the mouse heart was evaluated by binding of rhodamine-labeled Ang-(1-7). Cardiac function was examined using isolated heart preparations. Echocardiography was used to confirm the results obtained with isolated heart studies. To elucidate the possible mechanisms involved in the cardiac phenotype observed in Mas Ϫ/Ϫ mice, whole-cell calcium currents in cardiomyocytes and the expression of collagen types I, III, and VI and fibronectin were analyzed. Ang-(1-7) binding showed that Mas is localized in cardiomyocytes of the mouse heart. Isolated heart techniques revealed that Mas-deficient mice present a lower systolic tension (average: 1.4Ϯ0.09 versus 2.1Ϯ0.03 g in Mas ϩ/ϩ mice), ϮdT/dt, and heart rate. A significantly higher coronary vessel resistance was also observed in Mas-deficient mice. Echocardiography revealed that hearts of Mas-deficient mice showed a significantly decreased fractional shortening, posterior wall thickness in systole and left ventricle end-diastolic dimension, and a higher left ventricle end-systolic dimension. A markedly lower global ventricular function, as defined by a higher myocardial performance index, was observed. A higher delayed time to the peak of calcium current was also observed. The changes in cardiac function could be partially explained by a marked change in collagen expression to a profibrotic profile in Mas-deficient mice. These results indicate that Ang-(1-7)-Mas axis plays a key role in the maintenance of the structure and function of the heart. (Hypertension. 2006;47:996-1002.)

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“…Because anesthesia using xylazine can produce significant reduction in cardiac output, 27 xylazine and acepromazine were avoided for these measurements, and the combination of ketamine (100 mg/kg) and diazepam (10 mg/kg) was used. Mean arterial pressure (MAP) was measured by catheterization of the right femoral artery and recorded continuously; the external zero reference was placed at the level of the heart.…”

Section: Hemodynamic Measurementmentioning

confidence: 99%

Venous Identity Is Lost but Arterial Identity Is Not Gained During Vein Graft Adaptation

Kudo

Muto

Maloney

et al. 2007

ATVB

108

116

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Objectives— Ephrin ligands and Eph receptors are signaling molecules that are differentially expressed on arteries and veins during development. We examined whether Eph-B4, a venous marker, and Ephrin-B2, an arterial marker, are regulated during vein graft adaptation in humans and aged rats. Methods and Results— Eph-B4 transcripts and immunodetectable protein are downregulated in endothelial and smooth muscle cells of patent vein grafts in both humans and in aged rats, whereas Ephrin-B2 transcripts and protein are not strongly induced. Other markers of arterial identity, including dll4 and notch-4, are also not induced during vein graft adaptation in aged rats. Because VEGF-A is upstream of the Ephrin–Eph pathway, and expression of VEGF-A is induced only at early time points after exposure of the vein to the arterial environment, we inhibited VEGF-A in vein grafts using an siRNA-based approach. Vein grafts treated with siRNA directed against VEGF-A demonstrated a thicker intima-media containing α-actin, consistent with arterialization, but did not contain Eph-B4 or Ephrin-B2. Conclusions— Venous identity is preserved in the veins of aged animals, but is lost during adaptation to the arterial circulation; arterial markers are not induced. Markers of vessel identity are plastic in adults and their selective regulation may mediate vein graft adaptation to the arterial environment in aged animals and humans.

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Non-invasive echocardiographic studies in mice

Cited by 72 publications

References 0 publications

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Intensity-controlled treadmill running in mice: cardiac and skeletal muscle hypertrophy

Impairment of In Vitro and In Vivo Heart Function in Angiotensin-(1-7) Receptor Mas Knockout Mice

Venous Identity Is Lost but Arterial Identity Is Not Gained During Vein Graft Adaptation

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