Changes in Cell-to-Cell Electrical Coupling Associated With Left Ventricular Hypertrophy

Cooklin, Michael; Wallis, William; Sheridan, Desmond J.; Fry, Christopher

doi:10.1161/01.res.80.6.765

Cited by 107 publications

(105 citation statements)

References 24 publications

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“…In guinea-pig detrusor A is about 1.4 mm which is similar to the value in myocardium, which is a classical electrically coupled functional syncitium. Direct measurement of Ri in detrusor gives a value of about 600 R cm which is very large compared with the value in myocardium of 200 R cm Cooklin et al 1997). …”

Section: H a N G E S I N T H E E L E C T R O P H Y S I O L O G I C mentioning

confidence: 83%

Bladder instability and detrusor smooth muscle function

Fry

Mundy

1999

Experimental Physiology

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Section: H a N G E S I N T H E E L E C T R O P H Y S I O L O G I C mentioning

confidence: 83%

Bladder instability and detrusor smooth muscle function

Fry

Mundy

1999

Experimental Physiology

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“…It has been demonstrated that RV hypertrophy induces electromechanical coupling alterations that could lead to arrhythmias (7,28). However, electromechanical coupling assessment by conventional echocardiography remains difficult (20).…”

Section: Discussionmentioning

confidence: 99%

Doppler tissue imaging in assessment of pulmonary hypertension-induced right ventricle dysfunction

Boissière¹,

Gautier²,

Machet³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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-We aimed to assess the accuracy of Doppler tissue imaging (DTI) in detecting right ventricle (RV) dysfunction and electromechanical coupling alteration following pulmonary hypertension (PHT) in rat. PHT was induced by chronic hypoxia exposure (hypoxic PHT) or monocrotaline treatment (monocrotaline PHT). In both PHT models, we observed transparietal RV pressure increase and remodeling, including hypertrophy and dilation. Conventional echocardiography provided evidence for pulmonary outflow impairment with midsystolic notch and acceleration time decrease in PHT groups (21.7 Ϯ 1.6 and 13.2 Ϯ 2.9 ms in hypoxic and monocrotaline PHT groups vs. 28.1 Ϯ 1.0 ms in control). RV shortening fraction was decreased in the monocrotaline PHT group compared with the hypoxic PHT and control groups. Combining conventional Doppler and DTI was more helpful to detect RV diastolic dysfunction in the monocrotaline PHT group (E/Ea ratio ϭ 17.0 Ϯ 1.4) compared with the hypoxic PHT and control groups (11.5 Ϯ 0.7 and 10.2 Ϯ 0.4, respectively). Tei index measured using DTI highlighted global RV dysfunction in the monocrotaline PHT group (1.36 Ϯ 0.24 vs. 0.92 Ϯ 0.05 and 0.86 Ϯ 0.05 in the hypoxic PHT and control groups, respectively). Q-S m time measured from the onset of Q wave to the onset of DTI S m wave was increased in both PHT groups. PHT-induced electromechanical coupling alteration was confirmed by in vitro activation-contraction delay measurements on isolated RV papillary muscle, and both Q-S m time and activation-contraction delay were correlated with PHT severity. We demonstrated that Q-Sm time measured in DTI was an easily and convenient index to detect early RV electromechanical coupling alteration in both moderate and severe PHT. echocardiography; hypertrophy; right ventricular remodeling CHRONIC ALVEOLAR HYPOXIA, which often occurs in patients suffering from chronic obstructive pulmonary diseases, secondarily induces a sustained increase in pulmonary artery resistance. The subsequent pulmonary artery hypertension (PHT) leads to right ventricle (RV) pressure overload and hypertrophy (22).Conventional transthoracic echocardiography is widely used to detect PHT in humans and animal models (14, 18). The standard parameters are the RV free wall thickening recorded in time-motion (TM) mode, the presence of mild-systolic notch, and the acceleration time decrease in the pulmonary outflow spectrum recorded in pulsed-Doppler mode. Nevertheless, a more extensive assessment of PHT-induced RV dysfunction remains difficult using conventional echocardiography. Indeed, accuracy of RV systolic and diastolic functions assessment is limited by complex anatomy and geometry of the ventricle.The Tei index, which combines both systolic and diastolic parameters, was suggested to determine global myocardial performance (27). It has been used in the assessment of RV dysfunction, especially in PHT (26). In conventional pulsed Doppler, the Tei index derives from both isovolumic contraction and relaxation times (IVCT and IVRT) as well as ejection time of...

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“…hypertrophied left ventricle, factors which may decrease conduction velocity (De Mello, 1994;Cooklin et al 1997). However, the results of Widdop et al (1992) indicate that the major component of a decrease in heart rate following ¬_NAME treatment is mediated through an increase in vagal efferent activity.…”

Section: Discussionmentioning

confidence: 99%

Effect of Captopril in L‐Name‐Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

Bernátová

Pecháňová

Šimko

1999

Experimental Physiology

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summary Long-term administration of N G -nitro-¬_arginine methyl ester (¬_NAME) induces development of hypertension and hypertrophy of the left ventricle in rats. The aim of the present study was to demonstrate the effect of chronic ¬_NAME treatment on DNA and RNA concentration, and protein synthesis in the rat heart, aorta, brain and kidney and to determine the effect of angiotensin converting enzyme (ACE) inhibitor captopril on these potential alterations. Four groups of rats were investigated: control, ¬_NAME (40 mg kg¢ day¢), captopril (100 mg kg¢ day¢), and ¬_NAME (40 mg kg¢ day¢) + captopril (100 mg kg¢ day¢). NO synthase activity in the heart, aorta, brain and kidney was found to be decreased in the ¬_NAME group. In the group of rats treated with ¬_NAME + captopril, captopril did not affect NO synthase inhibition. Captopril, however, completely prevented development of hypertension and left ventricular hypertrophy in this group. In the ¬_NAME group, DNA and RNA concentrations, as well as [14 C]leucine incorporation, were significantly increased in all the tissues investigated. In the ¬_NAME + captopril group, captopril completely prevented the enhancement of DNA and RNA concentrations and [ 14 C]leucine incorporation in all tissues compared to the ¬_NAME group. Moreover, a significant decrease in RNA concentration and [ 14 C]leucine incorporation below control values was found in the captopril group as well as the ¬_NAME + captopril group in all the tissues investigated. We conclude that captopril prevented the development of hypertension and increase in nucleic acid concentration and protein synthesis in the heart, aorta, brain and kidney in rats treated with ¬_NAME + captopril. However, this protective effect of captopril was not associated with increased NO synthase activity in this model of hypertension.

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Changes in Cell-to-Cell Electrical Coupling Associated With Left Ventricular Hypertrophy

Cited by 107 publications

References 24 publications

Bladder instability and detrusor smooth muscle function

Bladder instability and detrusor smooth muscle function

Doppler tissue imaging in assessment of pulmonary hypertension-induced right ventricle dysfunction

Effect of Captopril in L‐Name‐Induced Hypertension on the Rat Myocardium, Aorta, Brain and Kidney

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