Supplementation of Creatine and Ribose Prevents Apoptosis and Right Ventricle Hypertrophy in Hypoxic Hearts

2013 ◽  
Vol 19 (39) ◽  
pp. 6873-6879 ◽  
Author(s):  
Anna Caretti ◽  
Paola Bianciardi ◽  
Marina Marini ◽  
Provvidenza Abruzzo ◽  
Alessandra Bolotta ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

scholarly journals TETRALOGI FALLOT DAN ATRESIA PULMONAL

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Alice I. Supit ◽  
Erling D. Kaunang
Keyword(s):  
Patent Ductus Arteriosus ◽  
Right Ventricle ◽  
Tetralogy Of Fallot ◽  
Congenital Heart ◽  
Heart Diseases ◽  
Ductus Arteriosus ◽  
Ventricle Hypertrophy ◽  
The Right ◽  
Right Ventricle Hypertrophy ◽  
Patent Ductus

Abstract: Congenital heart disease is a structural defect due to the malformation of the heart, aorta, and or great blood vessels. It is the most frequent congenital malformation in newborn babies. Tetralogy of Fallot is one of the congenital heart diseases (CHD) with central cyanosis, and covers 5-10% of all CHD. We reported a boy of one year old with Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The diagnosis was based on anamnesis, physical examination, and other supporting examinations. The chest X-ray showed a normal sized heart (CTR 57%) with coer-en-sabot shape, and right and left parahilar infiltration, which resulted in bronchopneumonia and ToF. The electrocardiography showed a right deviation of axis and a hypertrophy of the right ventricle; the echocardiography showed a right ventricle hypertrophy, an over-riding aorta, a large malalignment of the ventricular septal defect, no visualization of pulmonar artery, and no visualization of patent ductus arteriosus (PDA). Conclusion: Based on all the tests performed, the diagnosis of this patient was Tetralogy of Fallot and pulmonal atresia (ToF-PA), associated with bronchopneumonia. The prognosis related to bronchopneumonia in this case was good due to the use of antibiotics. Keywords: tetralogy of Fallot, pulmona atresia, bronchopneumonia.  Abstrak: Penyakit jantung bawaan (PJB) ialah kelainan struktural akibat malformasi jantung, aorta dan atau pembuluh darah besar, dan merupakan kelainan kongenital tersering pada bayi baru lahir. Tetralogi Fallot merupakan salah satu PJB dengan sianosis sentral, dan mencakup 5-10% dari seluruh PJB. Kami melaporkan kasus seorang anak laki-laki berusia satu tahun dengan Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Diagnosis ditegakkan melalui anamnesis, pemeriksaan fisik, dan pemeriksaan penunjang. Hasil ekspertisi foto toraks AP memperlihatkan ukuran jantung normal (CTR 57%) berbentuk coer-en-sabot, dan pada paru-paru terlihat infiltrat parahilar kanan dan kiri serta corakan vaskular paru berkurang yang menunjukkan suspek bronkopneumonia dan ToF. Elektrokardiografi memperlihatkan deviasi aksis ke kanan dan hipertrofi ventrikel kanan, dan pada ekokardiografi tampak right ventricle hypertrophy, overriding aorta, VSD malalignment besar, tidak tampak visualisasi arteri pulmonal, dan tidak tampak patent ductus arteriosus (PDA) dengan hasil Tetralogi Fallot dan atresia pulmonal. Simpulan: Berdasarkan hasil pemeriksaan yang dilakukan, diagnosis pasien ini ialah Tetralogi Fallot dan atresia pulmonal (ToF-PA) disertai bronkopneumonia. Prognosis bronkopenumonia pada kasus ini baik yang dapat diatasi dengan antibiotika.Kata kunci: tetralogi Fallot, atresia pulmonal, bronkopneumonia.  

scholarly journals Resistance training prevents right ventricle hypertrophy in rats exposed to secondhand cigarette smoke

PLoS ONE ◽  
2020 ◽  
Vol 15 (8) ◽  
pp. e0236988
Author(s):  
Ana Caroline Rippi Moreno ◽  
Gisele Alborghetti Nai ◽  
Caroline Pancera Laurindo ◽  
Karen Cristina Rego Gregorio ◽  
Tiago Olean-Oliveira ◽  
...  
Keyword(s):  
Resistance Training ◽  
Right Ventricle ◽  
Cigarette Smoke ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

scholarly journals Ethyl 4-(4′-heptanoyloxyphenyl)-6-methyl-3,4-dihydropyrimidin-2-one-5-carboxylate Prevents Progression of Monocrotaline-induced Pulmonary Arterial Hypertension in Rats

2017 ◽  
Vol 3 (1) ◽  
pp. 31
Author(s):  
S. M. Malik ◽  
Satyanarayan Deep ◽  
Rahul Ranjan ◽  
A. K. Prasad ◽  
Dipti N Prasad ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Pulmonary Vasculature ◽  
Treatment Groups ◽  
Future Drug ◽  
Wet Weight ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

<p>Therapies to prevent onset and progression of pulmonary arterial pressure are not very effective yet. This study was designed to investigate the effects of a novel dihydropyrimidinone, ethyl 4-(4′-heptanoyloxyphenyl)-6-methyl-3,4-dihydropyrimidin-2-one-5-carboxylate (H-DHPM) on pathogenesis of monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH). For the same purpose, rats were injected intraperitoneally (i.p.) a single dose (60 mg/kg) of MCT which led to development of PAH in 21 days. MCT insult caused high mortality, pulmonary vascular and parenchymal remodelling. Since the course of PAH pathogenesis is characterised by an early onset and progression phases, H-DHPM was administered i.p. at 30 mg/kg dosage in MCT pre-injected animals either from day 0 through day 21 or day 14 though day 21 of MCT injection in two separate treatment groups. H-DHPM significantly improved survival, prevented remodelling of pulmonary vasculature and parenchyma and subsequently ameliorated PAH pathogenesis. Moreover, we observed significant decrease in right ventricle hypertrophy, measured by wet weight of right ventricle (RV) divided by wet weight of left ventricle plus septum (LV+S), in H-DHPM treated groups as compared to MCT injected animals. These findings suggest H-DHPM not only prevented development of PAH but also treated the PAH pathogenesis in progressive phase. In conclusion, our data determines H-DHPM, might be a future drug for the prevention of PAH.</p>

Pulmonary hypertension is attenuated and ventilation-perfusion matching is maintained during chronic hypoxia in deer mice native to high altitude

2021 ◽  
Author(s):  
Claire M. West ◽  
Oliver H. Wearing ◽  
Rod G. Rhem ◽  
Graham R. Scott
Keyword(s):  
Pulmonary Hypertension ◽  
Smooth Muscle ◽  
Right Ventricle ◽  
High Altitude ◽  
Chronic Hypoxia ◽  
Pulmonary Arteries ◽  
Deer Mice ◽  
Maladaptive Response ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

Hypoxia at high altitude can constrain metabolism and performance, and can elicit physiological adjustments that are deleterious to health and fitness. Hypoxic pulmonary hypertension is a particularly serious and maladaptive response to chronic hypoxia, which results from vasoconstriction and pathological remodeling of pulmonary arteries, and can lead to pulmonary edema and right ventricle hypertrophy. We investigated whether deer mice (Peromyscus maniculatus) native to high altitude have attenuated this maladaptive response to chronic hypoxia, and whether evolved changes or hypoxia-induced plasticity in pulmonary vasculature might impact ventilation-perfusion (V-Q) matching in chronic hypoxia. Deer mouse populations from both high and low altitudes were born and raised to adulthood in captivity at sea level, and various aspects of lung function were measured before and after exposure to chronic hypoxia (12 kPa O2, simulating the O2 pressure at 4300 m) for 6-8 weeks. In lowlanders, chronic hypoxia increased right ventricle systolic pressure (RVSP) from 14 to 19 mmHg (P = 0.001), in association with thickening of smooth muscle in pulmonary arteries and right ventricle hypertrophy. Chronic hypoxia also impaired V-Q matching in lowlanders (measured at rest using SPECT-CT imaging), as reflected by increased log SD of the perfusion distribution (log SDQ) from 0.55 to 0.86 (P = 0.031). In highlanders, chronic hypoxia had attenuated effects on RVSP and no effects on smooth muscle thickness, right ventricle mass, or V-Q matching. Therefore, evolved changes in lung function help attenuate maladaptive plasticity and contribute to hypoxia tolerance in high-altitude deer mice.

scholarly journals Cyclosporin A Inhibits Hypoxia-induced Pulmonary Hypertension and Right Ventricle Hypertrophy

2006 ◽  
Vol 174 (6) ◽  
pp. 699-705 ◽  
Author(s):  
Nathalie Koulmann ◽  
Valérie Novel-Chaté ◽  
André Peinnequin ◽  
Rachel Chapot ◽  
Bernard Serrurier ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Cyclosporin A ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

Activation of the GLP-1 Receptor by Liraglutide Increases ACE2 Expression, Reversing Right Ventricle Hypertrophy, and Improving the Production of SP-A and SP-B in the Lungs of Type 1 Diabetes Rats

Endocrinology ◽  
2015 ◽  
Vol 156 (10) ◽  
pp. 3559-3569 ◽  
Author(s):  
Marina Romaní-Pérez ◽  
Verónica Outeiriño-Iglesias ◽  
Christian M. Moya ◽  
Pilar Santisteban ◽  
Lucas C. González-Matías ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Right Ventricle ◽  
Rat Model ◽  
Renin Angiotensin System ◽  
Surfactant Protein ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Ventricle Hypertrophy ◽  
Right Ventricle Hypertrophy

Diabetes alters microvascular function in the vascular beds of organs, including the lungs. Cardiovascular complications of pulmonary vascular affectation may be a consequence of the overactivation of the vasoconstrictive and proliferative components of the renin-angiotensin system. We previously reported that pulmonary physiology and surfactant production is improved by the glucagon-like peptide 1 receptor (GLP-1R) agonist liraglutide (LIR) in a rat model of lung hypoplasia. Because we hypothesized that streptozotocin-induced diabetes rats would show deficiencies in lung function, including surfactant proteins, and develop an imbalance of the renin-angiotensin system in the lungs. This effect would in turn be prevented by long-acting agonists of the GLP-1R, such as LIR. The induction of diabetes reduced the surfactant protein A and B in the lungs and caused the vasoconstrictor component of the renin-angiotensin system to predominate, which in turn increased angiotensin II levels, and ultimately being associated with right ventricle hypertrophy. LIR restored surfactant protein levels and reversed the imbalance in the renin-angiotensin system in this type 1 diabetes mellitus rat model. Moreover, LIR provoked a strong increase in angiotensin-converting enzyme 2 expression in the lungs of both diabetic and control rats, and in the circulating angiotensin(1–7) in diabetic animals. These effects prompted complete reversion of right ventricle hypertrophy. The consequences of LIR administration were independent of glycemic control and of glucocorticoids, and they involved NK2 homeobox 1 signaling. This study demonstrates by first time that GLP-1R agonists, such as LIR, might improve the cardiopulmonary complications associated with diabetes.

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