Adaptation of cardiac myosin and creatine kinase to chronic hypoxia: role of anorexia and hypertension

1997 ◽  
Vol 272 (4) ◽  
pp. H1690-H1695 ◽  
Author(s):  
M. Pissarek ◽  
X. Bigard ◽  
P. Mateo ◽  
C. Y. Guezennec ◽  
J. A. Hoerter
Keyword(s):  
Pulmonary Hypertension ◽  
Creatine Kinase ◽  
Hypobaric Hypoxia ◽  
Chronic Hypoxia ◽  
Specific Activity ◽  
Cardiac Myosin ◽  
Simulated Altitude ◽  
Biochemical Basis ◽  
Threefold Increase

The effects of chronic hypobaric hypoxia (CHH, 28 days, simulated altitude 5,500 m) on the cardiac expression of myosin heavy chain (MHC) and creatine kinase (CK) was studied in rat left (LV) and right (RV) ventricle. To separate the effects of hypoxia from its associated perturbations, anorexia and pulmonary hypertension (resulting in RV hypertrophy), CHH animals were compared with normoxic controls (C) and with rats restricted in food supply (pair fed, PF). In RV, the increased proportion of beta-MHC in CHH (20 +/- 3%) vs. C (7 +/- 2%, P < 0.01) and vs. PF (12 +/- 2%, P < 0.05) rats was mainly attributed to hypertension. In contrast, the higher beta-MHC of CHH (23 +/- 2%) vs. C (13 +/- 2%, P < 0.05) in LV was mainly ascribed to anorexia (PF = 21 +/- 3%, not significant). A major contribution of anorexia was also evidenced in the isozymic profile of CK; anorexia accounted for a 25% decrease in mito-CK specific activity in LV, whereas hypertension partly accounted for the threefold increase in BB-CK in RV. CHH specifically induced a twofold rise in LV BB-CK. This suggests that both the expression of slow myosin, improving the economy of contraction, and the changes in CK isozymic profile could provide a biochemical basis for the CHH resistance to ischemia.

scholarly journals 55th Bowditch Lecture: Effects of chronic hypoxia on the pulmonary circulation: Role of HIF-1

2012 ◽  
Vol 113 (9) ◽  
pp. 1343-1352 ◽  
Author(s):  
Larissa A. Shimoda
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Circulation ◽  
Vascular Remodeling ◽  
Chronic Hypoxia ◽  
Critical Role ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Pulmonary Arterial ◽  
Expression And Activity

When exposed to chronic hypoxia (CH), the pulmonary circulation responds with enhanced contraction and vascular remodeling, resulting in elevated pulmonary arterial pressures. Our work has identified CH-induced alterations in the expression and activity of several ion channels and transporters in pulmonary vascular smooth muscle that contribute to the development of hypoxic pulmonary hypertension and uncovered a critical role for the transcription factor hypoxia-inducible factor-1 (HIF-1) in mediating these responses. Current work is focused on the regulation of HIF in the chronically hypoxic lung and evaluation of the potential for pharmacological inhibitors of HIF to prevent, reverse, or slow the progression of pulmonary hypertension.

Increased lung endothelin-1 production in rats with idiopathic pulmonary hypertension

1992 ◽  
Vol 262 (5) ◽  
pp. L614-L620 ◽  
Author(s):  
T. J. Stelzner ◽  
R. F. O'Brien ◽  
M. Yanagisawa ◽  
T. Sakurai ◽  
K. Sato ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Mrna Expression ◽  
Chronic Hypoxia ◽  
Sprague Dawley ◽  
Northern Blots ◽  
Endothelin 1 ◽  
Right Ventricular Size ◽  
Filter Hybridization ◽  
Idiopathic Pulmonary Hypertension

The role of endogenous circulating or locally produced endothelin-1 (ET-1) in pulmonary hypertensive states is unknown. To investigate this we measured ET-1 levels and preproendothelin-1 (prepro-ET-1) mRNA expression at various ages in control Sprague-Dawley (SDR) rats and in fawn-hooded rats (FHR), a strain which develops idiopathic pulmonary hypertension. Although serum ET-1 levels were similar in SDR and FHR, we found twofold increases in FHR whole lung homogenate ET-1 levels by radioimmunoassay. Coexisting threefold increases in preproET-1 mRNA expression were found in FHR lungs by densitometric analysis of Northern blots and by filter hybridization, suggesting the increase in lung ET-1 was due to enhanced intrapulmonary production of the peptide. To test whether the increase in lung preproET-1 mRNA was primary or secondary to established pulmonary hypertension, we compared preproET-1 mRNA expression prior to development of pulmonary hypertension in fetal (19 day gestation) and neonatal (5 day old) FHR and SDR. Despite similar right ventricular size in SDR and FHR, preproET-1 mRNA was already elevated in neonatal FHR lungs. Furthermore, we found no increase in lung preproET-1 mRNA or ET-1 levels in adult SDR with an equivalent degree of pulmonary hypertension due to chronic hypoxia, implying that the increases in ET-1 production in FHR were not a common consequence of all pulmonary hypertensive states. The functional significance of these observations remains unclear but raises the possibility of a role for ET-1 in the pathophysiology of pulmonary hypertension in the FHR.

Role of calcitonin gene-related peptide (CGRP) in chronic hypoxia-induced pulmonary hypertension in the mouse

2002 ◽  
Vol 108 (2-3) ◽  
pp. 129-133 ◽  
Author(s):  
Trinity J Bivalacqua ◽  
Albert L Hyman ◽  
Philip J Kadowitz ◽  
Nazareno Paolocci ◽  
David A Kass ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene

scholarly journals NFATc3 is required for chronic hypoxia‐induced pulmonary hypertension: role of BKα and β subunits

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Ryann Bierer ◽  
Sergio Frutos ◽  
Carlos H Nitta ◽  
Thomas C Resta ◽  
Jessica Friedman ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Chronic Hypoxia

scholarly journals Reactive Oxygen Species Production in the Early and Later Stage of Chronic Ventilatory Hypoxia

2012 ◽  
pp. 145-151 ◽  
Author(s):  
D. HODYC ◽  
E. JOHNSON ◽  
A. SKOUMALOVÁ ◽  
J. TKACZYK ◽  
H. MAXOVÁ ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Reactive Oxygen ◽  
No Production ◽  
Oxygen Species ◽  
Air Plasma ◽  
Species Production ◽  
Specific Timing

Pulmonary hypertension resulting from chronic hypoxia is at least partly caused by the increased production of reactive oxygen species (ROS). The goal of the presented study was to investigate the dynamics and the site of production of ROS during chronic hypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (FiO2=0.1), while controls stayed in normoxia. We compared NO production in expired air, plasma and perfusate drained from isolated rat lungs and measured superoxide concentration in the perfusate. We also detected the presence of superoxide products (hydrogen peroxide and peroxynitrite) and the level of ROS-induced damage expressed as the concentration of lipid peroxydation end products. We found that the production and release of ROS and NO during early phase of chronic hypoxia has specific timing and differs in various compartments, suggesting the crucial role of ROS interaction for development of hypoxic pulmonary hypertension.

Possible role of pulmonary blood volume in chronic hypoxic pulmonary hypertension

1993 ◽  
Vol 74 (6) ◽  
pp. 3020-3026 ◽  
Author(s):  
L. C. Ou ◽  
G. L. Sardella ◽  
N. S. Hill ◽  
C. D. Thron
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Blood Volume ◽  
Ventricular Hypertrophy ◽  
Chronic Hypoxia ◽  
Right Ventricular Hypertrophy ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Blood Volume

Chronic hypoxia increases the total blood volume (TBV) and pulmonary arterial blood pressure (Ppa) and induces pulmonary vascular remodeling. The present study was undertaken to assess how the pulmonary blood volume (PBV) changes during hypoxia and the possible role of PBV in chronic hypoxic pulmonary hypertension. A novel method has been developed to measure the TBV, PBV, and Ppa in conscious rats. The method consists of chronic implantation of a loose ligature around the ascending aorta and pulmonary artery, so that when the ligature is drawn tightly, it traps the blood in the pulmonary vessels and left heart and simultaneously kills the rat. The pulmonary veins are then ligated to separate the left ventricular blood volume from the PBV. This surgical approach, together with chronic catheterization of the pulmonary artery and the use of 51Cr-labeled red blood cells, allows measurement of TBV, PBV, and Ppa. This method has been used to analyze the relationships between TBV and PBV and between Ppa or right ventricular hypertrophy and PBV in two rat strains with markedly different TBV and Ppa responses to chronic hypoxia. PBV per given lung weight did not increase and even decreased during hypoxia despite marked increases in TBV. There was a close correlation between Ppa or right ventricular hypertrophy and PBV in the two strains of chronically hypoxic animals, suggesting that a greater PBV plays a significant role in the development of severe chronic hypoxic pulmonary hypertension in the altitude-susceptible Hilltop rats.

The role of cytochrome c oxidase subunit 4 isoform 2 (Cox4i2) in chronic hypoxia induced pulmonary hypertension

Pneumologie ◽  
2016 ◽  
Vol 70 (S 01) ◽  
Author(s):  
F Jonas ◽  
C Veith-Berger ◽  
S Kraut ◽  
K Quanz ◽  
M Gierhardt ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Chronic Hypoxia ◽  
Oxidase Subunit
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