Antioxidant and oxidative stress changes in experimental cor pulmonale

Although right heart failure (RHF) contributes to 20% of all cardiovascular complications, most of the information available on RHF in general is based on the experiences with left heart failure. This study on RHF investigates changes in antioxidants and oxidative stress which are suggested to play a role in the transition from hypertrophy to failure. RHF subsequent to pulmonary hypertension was produced in rats by a single injection of monocrotaline (MCT, 60 mg/kg, i.p.). Based on hemodynamic, clinical and histopathologic observations, the animals were grouped in three functional stages at 1-, 2- and 6-week post-injection periods. In the 1-week group, RV pressure overload and hypertrophy, and a mild increase in antioxidant enzymes was seen. In the 2-week group, compensated HF, a significant increase in antioxidant enzymes, an increase in septal (IVS) wall thickness and leftward displacement of IVS without change in LV free wall were seen. In the 6-week group, lung and liver congestion, RVF and dilation, a decrease in antioxidant enzyme activities, increase in lipid peroxidation and severe bulging of the IVS into the left ventricle were seen. These changes in the hemodynamic, biochemical and histopathologic characteristics suggest that in early stages of MCT-induced pulmonary hypertension at 1 and 2 weeks, RV hypertrophy was accompanied by sustained hemodynamic function and an increase in antioxidant reserve. In the later stage at 6 weeks, clinical RHF was associated with abnormalities of the right heart systolic and diastolic function along with a decrease in antioxidant reserve. These biphasic changes in RV antioxidant enzymes, i.e. an increase during hypertrophy and a decrease in failure may suggest a role of oxidative stress in the pathogenesis of right ventricular dysfunction.     

Antioxidant and oxidative stress changes in experimental cor pulmonale

Although right heart failure (RHF) contributes to 20% of all cardiovascular complications, most of the information available on RHF in general is based on the experiences with left heart failure. This study on RHF investigates changes in antioxidants and oxidative stress which are suggested to play a role in the transition from hypertrophy to failure. RHF subsequent to pulmonary hypertension was produced in rats by a single injection of monocrotaline (MCT, 60 mg/kg, i.p.). Based on hemodynamic, clinical and histopathologic observations, the animals were grouped in three functional stages at 1-, 2- and 6-week post-injection periods. In the 1-week group, RV pressure overload and hypertrophy, and a mild increase in antioxidant enzymes was seen. In the 2-week group, compensated HF, a significant increase in antioxidant enzymes, an increase in septal (IVS) wall thickness and leftward displacement of IVS without change in LV free wall were seen. In the 6-week group, lung and liver congestion, RVF and dilation, a decrease in antioxidant enzyme activities, increase in lipid peroxidation and severe bulging of the IVS into the left ventricle were seen. These changes in the hemodynamic, biochemical and histopathologic characteristics suggest that in early stages of MCT-induced pulmonary hypertension at 1 and 2 weeks, RV hypertrophy was accompanied by sustained hemodynamic function and an increase in antioxidant reserve. In the later stage at 6 weeks, clinical RHF was associated with abnormalities of the right heart systolic and diastolic function along with a decrease in antioxidant reserve. These biphasic changes in RV antioxidant enzymes, i.e. an increase during hypertrophy and a decrease in failure may suggest a role of oxidative stress in the pathogenesis of right ventricular dysfunction.     

Spontaneous cor pulmonale in laboratory beagles

Right heart failure associated with postmortem evidence of pulmonary hypertension (cor pulmonale) was observed in nearly 1% of the young beagles of a large research colony. During the past 18 years, 176 dogs with cor pulmonale were observed. Most cases occurred between September and April of each year. Nearly equal numbers of males and females were involved, and some siblings were affected. Ninety-six percent of known affected dogs died, and 85% of the deaths occurred by 5 weeks of age. Clinically, most dogs were stunted and exhibited ascites, subcutaneous edema, hypothermia, dyspnea, cyanosis, and systolic murmur. Radiography revealed cardiomegaly, and electrocardiography revealed right axis deviation and an enlarged right atrium. Postmortem evidence of cor pulmonale included subcutaneous edema, ascites, hydrothorax, mediastinal and mesenteric edema, splenomegaly, centrolobular hepatic congestion and necrosis, right ventricular hypertrophy, interstitial pneumonia, and medial hypertrophy of pulmonary arteries and arterioles. The specific cause of the disease was not determined.     

Portable oxygen and exercise tolerance in patients with chronic hypoxic cor pulmonale.

Breathing 30% oxygen during exercise alleviated arterial hypoxaemia and reduced minute ventilation in patients with severe chronic bronchitis. A similar level of oxygen (2 or 4 litres of oxygen/minute) from nasal prongs also increased their exercise tolerance, as assessed by the distance that they could walk on the level in 12 minutes. Nevertheless, a single-blind controlled study showed that the effort of carrying their portable supply of liquid oxygen, in the Union Carbide Oxygen Walker, abolished this gain in exercise tolerance. The improvement in walking distance was restored when oxygen on exercise was provided by wheeling the oxygen walker on a light-weight shopping trolley.