Development and regression of right heart ventricular hypertrophy: Biochemical and morphological aspects

Schneider, M.; Wiese, Signe; Kunkel, B.; Hauk, Helen Feodora Sweta; Pfeiffer, Barbara

doi:10.1007/978-3-642-85369-2_1

Cited by 5 publications

(3 citation statements)

References 32 publications

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“…Finally, in our study, RV histology findings showed edema infiltrations in both PHT groups as well as red blood cell extravasations in the severe-PHT group, as previously shown (13,23,25). These structural myocardial alterations can explain the electromechanical coupling alterations observed in RV.…”

Section: Discussionsupporting

confidence: 88%

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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Section: Discussionsupporting

confidence: 88%

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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“…In addition, no difference in echocardiographic left ventricular mass was noted between N and CH rats during and after exposure. In previous studies, mammalian left ventricular mass was reported either increased (Genovese et al, 1983;Schneider et al, 1987), unaffected (Hultgren & Miller, 1967), or decreased (Scognamiglio et al, 1991) after chronic exposure to hypoxia. In our animal model, chronic exposure to mild hypoxia slowly increased posterior wall thickness and left ventricular cavity, but only in the first 3 weeks, which could not be therefore related to our HRV measurements made on day 72.…”

Section: Effects Of Cardiac Morphology and Functions On Hrv During Nomentioning

confidence: 96%

Heart Rate Variability in Rats Acclimatized to High Altitude

Melin

Fauchier

Dubuis³

et al. 2003

High Altitude Medicine & Biology

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The aims of this study were to relate heart morphology and functions changes to heart rate variability (HRV) components after acclimatization to high altitude and to define whether preadaptation to hypoxia could modulate HRV responses to acute hypoxic stress. Doppler-echocardiographic studies of the left ventricle were performed in female Wistar rats before, during, and after a 10-week exposure to moderate hypobaric hypoxia (CH rats, approximately 4000 m simulated) or normoxia (N rats, approximately 55 m). Right ventricular morphology and function and pulmonary artery pressure were evaluated using heart catheterization. Spectral analysis of HRV was studied after exposure in conscious unrestrained rats in normoxia and during acute hypoxic stress. Necropsy right ventricular hypertrophy and intraventricular and pulmonary artery hypertension were found in CH rats compared with N rats. Echocardiographic left ventricular morphology and functions were similar between the groups after exposures. Compared to the control group, CH rats had similar heart rates and HRV components when measured in normoxia. During acute hypoxic stress, HRV decreased in all rats, but less in CH rats. These results support the hypothesis that long-term mild hypoxia may moderate sympathetic activation induced by acute hypoxia and that right ventricular hypertrophy cannot be the direct cause of such a shift in sympathovagal nerve interaction during acute hypoxic stress.

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“…All pretreatment reagents were administered by intraperitoneal injection at a dose of 5 mL/kg per day. After the pre‐treatment, except for those in the NS and NG groups, rats in all groups were introduced into a hypobaric chamber that simulated an altitude of 6000 m for 48 h. The HACI model was established by referring to published studies (Lin et al, 2011; Lin et al, 2020; Schneider et al, 1987). The rats were all anesthetized with pentobarbital sodium intraperitoneally according to their body weight (50 mg/kg, dissolved in normal saline).…”

Section: Methodsmentioning

confidence: 99%

Pretreatment with Notoginsenoside R1 attenuates high‐altitude hypoxia‐induced cardiac injury via activation of the ERK1/2‐P90RSK‐Bad signaling pathway in rats

Zhao

Jia

Shen

et al. 2023

Phytotherapy Research

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High‐altitude cardiac injury (HACI) is one of the common tissue injuries caused by high‐altitude hypoxia that may be life threatening. Notoginsenoside R1 (NG‐R1), a major saponin of Panax notoginseng, exerts anti‐oxidative, anti‐inflammatory, and anti‐apoptosis effects, protecting the myocardium from hypoxic injury. This study aimed to investigate the protective effect and molecular mechanism of NG‐R1 against HACI. We simulated a 6000 m environment for 48 h in a hypobaric chamber to create a HACI rat model. Rats were pretreated with NG‐R1 (50, 100 mg/kg) or dexamethasone (4 mg/kg) for 3 days and then placed in the chamber for 48 h. The effect of NG‐R1 was evaluated by changes in Electrocardiogram parameters, histopathology, cardiac biomarkers, oxidative stress and inflammatory indicators, key protein expression, and immunofluorescence. U0126 was used to verify whether the anti‐apoptotic effect of NG‐R1 was related to the activation of ERK pathway. Pretreatment with NG‐R1 can improve abnormal cardiac electrical conduction and alleviate high‐altitude‐induced tachycardia. Similar to dexamethasone, NG‐R1 can improve pathological damage, reduce the levels of cardiac injury biomarkers, oxidative stress, and inflammatory indicators, and down‐regulate the expression of hypoxia‐related proteins HIF‐1α and VEGF. In addition, NG‐R1 reduced cardiomyocyte apoptosis by down‐regulating the expression of apoptotic proteins Bax, cleaved caspase 3, cleaved caspase 9, and cleaved PARP1 and up‐regulating the expression of anti‐apoptotic protein Bcl‐2 through activating the ERK1/2‐P90RSK‐Bad pathway. In conclusion, NG‐R1 prevented HACI and suppressed apoptosis via activation of the ERK1/2‐P90RSK‐Bad pathway, indicating that NG‐R1 has therapeutic potential to treat HACI.

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Development and regression of right heart ventricular hypertrophy: Biochemical and morphological aspects

Cited by 5 publications

References 32 publications

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

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

Heart Rate Variability in Rats Acclimatized to High Altitude

Pretreatment with Notoginsenoside R1 attenuates high‐altitude hypoxia‐induced cardiac injury via activation of the ERK1/2‐P90RSK‐Bad signaling pathway in rats

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