2011PubMedRequires access

[Determination of pulmonary vascular resistance by improved right heart catheter in rat].

Ping Yuan, Wenhui Wu, Dong Liu, Rui Zhang, Zhi‐Cheng Jing

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Abstract

OBJECTIVE: To establish an easy and repeatable method for determination of pulmonary vascular resistance in normal and pulmonary arterial hypertension (PAH) rats. METHODS: Forty-five Sprague-Dawley rats were randomly assigned into three groups: control group, low dose monocrotaline (MCT) group (50 mg/kg) and high dose MCT group (60 mg/kg). Rats in PAH groups received single subcutaneous injection of MCT. We measured pulmonary artery pressure by right heart catheterization using an improved hand-made PE-50 catheter. Cardiac output was calculated through thermodilution method. Pulmonary vascular resistance equals the mean pulmonary artery pressure divided by cardiac output. RESULTS: The total percentages of success to detect pulmonary artery pressure, cardiac output and pulmonary vascular resistance were 98%, 100% and 96% respectively in 3 groups. Twenty-one days after MCT injection, mean pulmonary artery pressure significantly increased in MCT group compared to control group [(43.1 ± 0.8), (54.8 ± 2.2) vs. (17.4 ± 1.0) mm Hg (1 mm Hg = 0.133 kPa), P < 0.001], and the mPAP was also significantly higher in high dose MCT group than in low dose MCT group (P < 0.001). Cardiac output was significantly lower in PAH rats than in control rats [(77.5 ± 6.9), (71.0 ± 6.7) vs. (126.8 ± 3.9) ml/min, P < 0.001]. Pulmonary vascular resistance was significantly increased in PAH rats compared with control rats [(0.56 ± 0.06), (0.76 ± 0.08) vs. (0.13 ± 0.01) mm Hg×min(-1)×ml(-1), P < 0.001]. There were significant differences in both MCT-treated groups (P = 0.01). CONCLUSIONS: Pulmonary vascular resistance in rats could be reliably detected using the improved hand-made PE-50 right heart catheter.

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What this paper is about

OBJECTIVE: To establish an easy and repeatable method for determination of pulmonary vascular resistance in normal and pulmonary arterial hypertension (PAH) rats. METHODS: Forty-five Sprague-Dawley rats were randomly assigned into three groups: control group, low dose monocrotaline (MCT) group (50 mg/kg) and high dose MCT group (60 mg/kg). Rats in PAH groups received single subcutaneous injection of MCT. We measured pulmonary artery pressure by right heart catheterization using an improved hand-made PE-50 catheter. Cardiac output was calculated through thermodilution method. Pulmonary vascular resistance equals the mean pulmonary artery pressure divided by cardiac output. RESULTS: The total percentages of success to detect pulmonary artery pressure, cardiac output and pulmonary vascular resistance were 98%, 100% and 96% respectively in 3 groups. Twenty-one days after MCT injection, mean pulmonary artery pressure significantly increased in MCT group compared to control group [(43.1 ± 0.8), (54.8 ± 2.2) vs. (17.4 ± 1.0) mm Hg (1 mm Hg = 0.133 kPa), P < 0.001], and the mPAP was also significantly higher in high dose MCT group than in low dose MCT group (P < 0.001). Cardiac output was significantly lower in PAH rats than in control rats [(77.5 ± 6.9), (71.0 ± 6.7) vs. (126.8 ± 3.9) ml/min, P < 0.001]. Pulmonary vascular resistance was significantly increased in PAH rats compared with control rats [(0.56 ± 0.06), (0.76 ± 0.08) vs. (0.13 ± 0.01) mm Hg×min(-1)×ml(-1), P < 0.001]. There were significant differences in both MCT-treated groups (P = 0.01). CONCLUSIONS: Pulmonary vascular resistance in rats could be reliably detected using the improved hand-made PE-50 right heart catheter.

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Available abstract

OBJECTIVE: To establish an easy and repeatable method for determination of pulmonary vascular resistance in normal and pulmonary arterial hypertension (PAH) rats. METHODS: Forty-five Sprague-Dawley rats were randomly assigned into three groups: control group, low dose monocrotaline (MCT) group (50 mg/kg) and high dose MCT group (60 mg/kg). Rats in PAH groups received single subcutaneous injection of MCT. We measured pulmonary artery pressure by right heart catheterization using an improved hand-made PE-50 catheter. Cardiac output was calculated through thermodilution method. Pulmonary vascular resistance equals the mean pulmonary artery pressure divided by cardiac output. RESULTS: The total percentages of success to detect pulmonary artery pressure, cardiac output and pulmonary vascular resistance were 98%, 100% and 96% respectively in 3 groups. Twenty-one days after MCT injection, mean pulmonary artery pressure significantly increased in MCT group compared to control group [(43.1 ± 0.8), (54.8 ± 2.2) vs. (17.4 ± 1.0) mm Hg (1 mm Hg = 0.133 kPa), P < 0.001], and the mPAP was also significantly higher in high dose MCT group than in low dose MCT group (P < 0.001). Cardiac output was significantly lower in PAH rats than in control rats [(77.5 ± 6.9), (71.0 ± 6.7) vs. (126.8 ± 3.9) ml/min, P < 0.001]. Pulmonary vascular resistance was significantly increased in PAH rats compared with control rats [(0.56 ± 0.06), (0.76 ± 0.08) vs. (0.13 ± 0.01) mm Hg×min(-1)×ml(-1), P < 0.001]. There were significant differences in both MCT-treated groups (P = 0.01). CONCLUSIONS: Pulmonary vascular resistance in rats could be reliably detected using the improved hand-made PE-50 right heart catheter.

Key concepts: Pulmonary artery, Vascular resistance, Cardiac output, Medicine, Pulmonary hypertension, Cardiac catheterization, Internal medicine, Cardiology

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