Cardiotrophin-1 is a prophylactic against the development of chronic hypoxic pulmonary hypertension in rats Norikazu Nomura, MD, Miki Asano, MD, Takayuki.

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Presentation transcript:

Cardiotrophin-1 is a prophylactic against the development of chronic hypoxic pulmonary hypertension in rats Norikazu Nomura, MD, Miki Asano, MD, Takayuki Saito, MD, Shigeru Sasaki, MD, Hikaru Suzuki, PhD, Tadao Manabe, MD, Akira Mishima, MD The Annals of Thoracic Surgery Volume 76, Issue 1, Pages 237-243 (July 2003) DOI: 10.1016/S0003-4975(03)00339-4

Fig 1 Effect of administering CT-1 on mean PAP (a) and on the ratio of the systolic pressures of the pulmonary and systemic arteries (Pp/Ps) (b), and in rats exposed to chronic hypoxic conditions or ambient air. Treatment with CT-1 under hypoxic conditions significantly reduced mean PAP and Pp/Ps values. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia; ‡p < 0.05 versus hypoxia. (CT-1 = cardiotrophin-1; PAP = pulmonary arterial pressure.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)

Fig 2 Endothelium-dependent relaxation in response to ACh in precontracted rings of intrapulmonary arteries. Data presented as percentage relaxation (% relaxation) to noradrenaline (10−6 M) precontraction. Impairment of endothelium-dependent vasorelaxation was lower in the CT-1+hypoxia group than in the hypoxia group for ACh at a concentration of 10−5 M. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia at same concentration of agonist; ○ = normoxia (n = 6); ▵ = CT-1 + normoxia (n = 5); • = hypoxia (n = 6); X = CT-1 + hypoxia (n = 6). (ACh = acetylcholine; CT-1 = cardiotrophin-1.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)

Fig 3 Endothelium-independent relaxation in response to SNP in precontracted rings of intrapulmonary arteries. Data presented as percentage relaxation (% relaxation) to noradrenaline (10−6 M) precontraction. Percentage relaxation for SNP at a concentration of 10−8 M in the hypoxia group (14.7% ± 16.4%) was significantly lower than in the normoxia group (55.3% ± 18.6%, p = 0.0005) and in the CT-1+normoxia group (53.8% ± 17.4%, p = 0.0012). For SNP at 10−7 M, the decrease in percentage relaxation was significantly greater in the hypoxia group (65.5% ± 9.4%) than in the normoxia group (96.7% ± 6.0%, p < 0.0001) and in the CT-1+normoxia group (97.1% ± 3.1%, p < 0.0001). For SNP at 10−6 M, the percentage relaxation was also significantly lower in the hypoxia group (85.9% ± 9.0%) than in the normoxia group (98.8% ± 2.9%, p = 0.0066) and in the CT-1+normoxia group (100.0% ± 0%, p = 0.005). There was no appreciable difference between the CT-1+hypoxia and hypoxia groups for SNP concentrations ranging from 10−9 M to 10−5 M. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia; ‡p < 0.01 versus CT-1+normoxia at same concentration of agonist; ○ = normoxia (n = 6); ▵ = CT-1+normoxia (n = 5); • = hypoxia (n = 6); X = CT-1+hypoxia (n = 4). (CT-1 = cardiotrophin-1; SNP = sodium nitroprusside.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)

Fig 4 Relation between endothelium-dependent vasorelaxation for ACh at 10−5 M and mean PAP. The increase in mean PAP was suppressed in proportion to the vasodilative response induced by ACh. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia; ‡p < 0.05 versus hypoxia; ○ = normoxia; ▵ = CT-1 + normoxia; • = hypoxia; X = CT-1+hypoxia. (ACh = acetylcholine; CT-1 = cardiotrophin-1; PAP = pulmonary arterial pressure.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)

Fig 5 Changes in body weight in each group. Treatment with CT-1 did not affect body weight in the chronic hypoxic and normoxic groups. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia; ○ = normoxia (n = 21); ▵ = CT-1+normoxia (n = 13); • = hypoxia (n = 30); X = CT-1+hypoxia (n = 20). (CT-1 = cardiotrophin-1.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)

Fig 6 (a) Ratio of the weight of the free wall of the right ventricle to the weight of the left ventricle plus intraventricular septum (RV/[LV+S]), and (b) ratio of the weight of the free wall of the right ventricle to body weight (RV/BW) in each group. Administration of CT-1 inhibited the development of right ventricular hypertrophy induced by chronic hypoxia. *p < 0.01 versus normoxia; †p < 0.01 versus hypoxia; ‡p < 0.05 versus hypoxia. (CT-1 = cardiotrophin-1.) The Annals of Thoracic Surgery 2003 76, 237-243DOI: (10.1016/S0003-4975(03)00339-4)