Problems of High Altitude Medicine and Biology

1. Front Matter

   Pages i-viii

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2. Introduction: 45 Years Of Mountain Medicine

   • James S. Milledge

   Pages 1-9

3. High Altitude Pulmonary Hypertension And Chronic Mountain Sickness-Reappraisal Of The Consensus On Chronic And Subacute High Altitude Diseases

   • Dante Penaloza

   Pages 11-37

4. The Cellular Effects Of Hypoxia In The Pulmonary Circulation

   • Andrew Peacock, Oleg Pak, David Welsh

   Pages 39-55

5. Angiogenesis And Chronic Hypoxic Pulmonary Hypertension

   • Saadia Eddahibi, Bernadette Raffestin, Serge Adnot

   Pages 57-68

6. Tetrahydrobiopterin And Pulmonary Hypertension

   • Lan Zhao, Francis Bahaa, Martin Wilkins

   Pages 69-86

7. Hypoxia-Induced Proliferation Of Human Pulmonary Arterial Smooth Muscle Cells (Pasmc) Is Involved In The Suppression Of Cyclin-Dependent Kinase Inhibitors, P21, P27 And P53

   • T. Ishizaki, S. Mizuno, M. Kadowaki, D. Uesaka, Y. Umeda, M. Morikawa et al.

   Pages 87-99

8. Pulmonary Adaptation To High Altitude In Wild Mammals

   • Akio Sakai, Ishizaki Takeshi, Koizumi Tomonobu, Matsumoto Takayuki

   Pages 101-117

9. The Lung At High Altitude: Between Physiology And Pathology

   • Annalisa Cogo, Federica Campigotto, Valter Fasano, Giovanni Grazzi

   Pages 119-131

10. Sildenafil And Hypoxic Pulmonary Hypertension

    • Baktybek K. Kojonazarov, Mirsaid M. Mirrakhimov, Nicholas W. Morrell, Martin R. Wilkins, Almaz Aldashev

    Pages 133-143

11. The Role Of Antioxidants In Modulation Of Acclimatization Processes

    • Ashyraly Z. Zurdinov

    Pages 145-150

12. Gene Polymorphisms And High Altitude Pulmonary Hypertension

    • Almaz Aldashev

    Pages 151-168

13. Genetic Factors In The Acute Response To Hypoxia In Animals Models

    • Kingman P. Strohl

    Pages 169-184

14. Who Gets High Altitude Pulmonary Edema And Why?

    • Peter Bärtsch, Christoph Dehnert, Heimo Mairbäurl, Marc Moritz Berger

    Pages 185-195

15. Effects Of Inhaled Nitric Oxide And Oxygen In High Altitude Pulmonary Edema

    • Inder S. Anand

    Pages 197-209

16. Altered Autoregulation Of Cerebral Blood Flow In Hypoxia: Relevance To The Pathophysiology Of Acute Mountain Sickness

    • Robert Naeije, Aurelie van Osta

    Pages 211-220

17. Cardiac Limitation To Exercise Capacity At High Altitudes

    • Sandrine Huez, Robert Naeije, Vitalie Faoro

    Pages 221-229

18. Pediatric High Altitude Heart Disease: A Hypoxic Pulmonary Hypertension Syndrome

    • Tianyi Wu

    Pages 231-247

19. Clinical And Functional Features Of Chronic Obstructive Pulmonary Disease In The Highlanders Of Kyrgzstan

    • T. M. Sooronbaev, S. B. Shabykeeva, A. K. Mirzaachmatova, G. K. Kadyraliev, Mirsaid M. Mirrakhimov

    Pages 249-257

20. Monitoring The Morphological And Functional Parameters Of Platelets In Patients With Thrombocytopenic Purpura During High Mountain Treatment

    • Abdukhalim R. Raimjanov, Irina Tsopova, Svetlana Astapova

    Pages 259-262

The major characteristic pathological findings of pulmonary vascular remodelling are increased wall thickening of pulmonary vessels and mus- larization of small arteries. In laboratory animals, decreased ambient oxygen concentrations cause similar pathological findings, including pulmonary smooth muscle hypertrophy and proliferation [22,23]. It has been suggested that proliferation of pulmonary arterial smooth muscle cells (PASMC) is a key component of pulmonary vascular remodelling, and several in vitro studies have also addressed that exposure to hypoxia can stimulate prolife- tion of PASMC [13,4,1]. The proliferation of the PASMC begins when the cells enter into the cell cycle. The most important molecular event necessary for the progress of the cell cycle is phosphorylation of retinoblastoma protein by cyclin-dependent kinase (CDK)-cyclin complexes. The CDK activity can be inhibited by CDK inhibitors and the expression of CDK inhibitor is a major regulator of the transition between each phase of the cell cycle [7]. Previous studies have noted that CDK inhibitor p27 plays an important role in the inhibition of the CDK activity and proliferation in vascular smooth muscle cells [2,3]. The G1 phase in severe hypoxia is suggested to involve the CKI p27, because the expression of p27 increased in several cell-lines when they were exposed to extreme hypoxia [20,5]. Previous reports indicate that hypoxia decreases the p27 expression in the murine lung [23,24] and we found that PGI2 suppresses hypox- induced proliferation of PASMC and maintains p27 in PASMC [20].

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• hypertension

• Kirghiz Institute of Cardiology, Kyrgyz Republic

  Almaz Aldashev

• Free University of Brussels, Belgium

  Robert Naeije

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