The autonomic nervous system at high altitude Roger Hainsworth,1 Mark J. Drinkhill,1 and Maria Rivera-Chira2 1Institute for Cardiovascular Research, University of Leeds, Leeds, LS2 9JT UK 2Depto. Academico Ciencias, Biologicas y Fisiologicas, UPCH, Lima, Peru Roger Hainsworth, Phone: +44-113/3434-821, Fax: +44-113/3434-803, Email: r.hainswo...@leeds.ac.uk. Corresponding author. Received January 2, 2007; Accepted January 3, 2007. Abstract The effects of hypobaric hypoxia in visitors depend not only on the actual elevation but also on the rate of ascent. Sympathetic activity increases and there are increases in blood pressure and heart rate. Pulmonary vasoconstriction leads to pulmonary hypertension, particularly during exercise. The sympathetic excitation results from hypoxia, partly through chemoreceptor reflexes and partly through altered baroreceptor function. High pulmonary arterial pressures may also cause reflex systemic vasoconstriction. Most permanent high altitude dwellers show excellent adaptation although there are differences between populations in the extent of the ventilatory drive and the erythropoiesis. Some altitude dwellers, particularly Andeans, may develop chronic mountain sickness, the most prominent characteristic of which being excessive polycythaemia. Excessive hypoxia due to peripheral chemoreceptor dysfunction has been suggested as a cause. The hyperviscous blood leads to pulmonary hypertension, symptoms of cerebral hypoperfusion, and eventually right heart failure and death. Keywords: altitude, mountain sickness, hypoxia, polycythemia, respiration, chemoreceptors, baroreceptors, autonomic nervous system Clin Auton Res. 2007 February; 17(1): 13–19. Published online 2007 January 30. doi: 10.1007/s10286-006-0395-7. PMCID: PMC1797062
Pulmonary hypertension may lead to "cor pulmonale". In this disorder, the right ventricle, which pumps blood to the lungs, becomes enlarged,eventually resulting in right sided heart failure.
Marcus Aurelius wrote: > Pulmonary hypertension may lead to "cor pulmonale". In this disorder, > the right ventricle, which pumps blood to the lungs, > becomes enlarged,eventually resulting in right sided heart failure.
The enlargement of the right-ventricle occurs to compensate for its weakening from the chronic pressure overload of pulmonary hypertension.
This is in accord with Starling's law.
May you and other dear neighbors, friends, and brethren have a blessedly wonderful 2008th year since the birth of our LORD Jesus Christ as our Messiah, the Son of Man ...
On Jul 4, 4:59 pm, "Andrew B. Chung, MD/PhD" <lov...@thetruth.com> wrote:The enlargement of the right-ventricle occurs to compensate for its weakening from the chronic pressure overload of pulmonary hypertension. <<
"Chronic pressure overload of pulmonary hypertension"
This can be caused by erythrocytosis / polycythaemia .. which .. coincidentally .. HAPPENS .. in this incidence.
Therefore in theory erythrocytosis / increased red blood cell production could BE THE **cause** OF pulmonary hypertension down here amongst those normally residing at sea level.
Spoor.
Increased red blood cells happens only in a few ways.
> This is in accord with Starling's law. > Marcus Aurelius wrote: > > Pulmonary hypertension may lead to "cor pulmonale". In this disorder, > > the right ventricle, which pumps blood to the lungs, > > becomes enlarged,eventually resulting in right sided heart failure.
> The enlargement of the right-ventricle occurs to compensate for its > weakening from the chronic pressure overload of pulmonary > hypertension.
> This is in accord with Starling's law.
> May you and other dear neighbors, friends, and brethren have a > blessedly wonderful 2008th year since the birth of our LORD Jesus > Christ as our Messiah, the Son of Man ...
On Jul 4, 6:19 pm, ironjustice <ironjust...@cashette.com> wrote: "Chronic pressure overload of pulmonary hypertension" This can be caused by erythrocytosis / polycythaemia <<
" Hemoglobin had a direct effect on Pulmonary Arterial Pressure"
Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary Vascular Resistance in Patients with Chronic Emphysema Akira Nakamuraa, Norio Kasamatsua, Ikko Hashizumea, Takushi Shiraia, Suguru Hanzawab, Shigeru Momikib, Kazuyoshi Sasakib, Masao Kinoshitab, Osamu Okadac, Koichiro Tatsumic, Takayuki Kuriyamac
Departments of aRespiratory Medicine and bThoracic Surgery, Hamamatsu Medical Center, Hamamatsu, and cDepartment of Chest Medicine, Chiba University, Chiba, Japan
Background: The increase in viscosity caused by secondary polycythemia is thought to be one of the major causes of pulmonary hypertension secondary to chronic emphysema. However, very few clinical studies considered the relation between pulmonary hypertension and polycythemia in the case of chronic obstructive pulmonary disease. Objective: The purpose of this study is to elucidate the relative contribution of an increase in hemoglobin level (Hb) to mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR). Methods: We retrospectively investigated 41 patients with chronic emphysema who had undergone a right heart catheterization. Multiple-regression analysis and F test were performed to investigate both direct effects of Hb and PaO2 as independent variables on mPAP and PVR as dependent variables. Results: Significant correlations were found between PaO2 and mPAP (or PVR), or Hb and mPAP (or PVR), indicating that both Hb and PaO2 are contributory to mPAP and PVR. The F test demonstrated that Hb and PaO2 could directly affect the level of either mPAP or PVR. Conclusions: It was concluded that Hb had a direct effect on mPAP and PVR, independently of hypoxia in patients with chronic emphysema.
> This can be caused by erythrocytosis / polycythaemia > On Jul 4, 4:59 pm, "Andrew B. Chung, MD/PhD" <lov...@thetruth.com> > wrote:The enlargement of the right-ventricle occurs to compensate for > its weakening from the chronic pressure overload of pulmonary > hypertension. <<
> "Chronic pressure overload of pulmonary hypertension"
> This can be caused by erythrocytosis / polycythaemia .. which .. > coincidentally .. HAPPENS .. in this incidence.
> Therefore in theory erythrocytosis / increased red blood cell > production could BE THE **cause** OF pulmonary hypertension down here > amongst those normally residing at sea level.
> Spoor.
> Increased red blood cells happens only in a few ways.
> > This is in accord with Starling's law. > > Marcus Aurelius wrote: > > > Pulmonary hypertension may lead to "cor pulmonale". In this disorder, > > > the right ventricle, which pumps blood to the lungs, > > > becomes enlarged,eventually resulting in right sided heart failure.
> > The enlargement of the right-ventricle occurs to compensate for its > > weakening from the chronic pressure overload of pulmonary > > hypertension.
> > This is in accord with Starling's law.
> > May you and other dear neighbors, friends, and brethren have a > > blessedly wonderful 2008th year since the birth of our LORD Jesus > > Christ as our Messiah, the Son of Man ...
On Jul 4, 6:38 pm, ironjustice <ironjust...@cashette.com> wrote:On Jul 4, 6:38 pm, ironjustice <ironjust...@cashette.com> wrote::"Chronic pressure overload of pulmonary hypertension" This can be caused by erythrocytosis / polycythaemia <<
Enalapril used for hypertension is also used to lower red blood cell count. THAT must be a .. coincidence.
Enalapril is an angiotensin converting enzyme (ACE) inhibitor used in the treatment of hypertension and some types of chronic heart failure. --------------------- Titre du document / Document title Use of aminophylline and enalapril in posttransplant polycythemia Auteur(s) / Author(s) MAZZALI M. (1) ; ALVES G. FILHO (1) ; Affiliation(s) du ou des auteurs / Author(s) Affiliation(s) (1) Nephrology Unit, Internal Medicine Department, Faculty of Medical Sciences, State University of Campinas, Campinas, São Paulo, BRESIL
Résumé / Abstract Background. Posttransplant polycythemia (PTP) affects 6-30% of renal transplant recipients and can result in thromboembolic disease. The pathogenesis of PTP remains unknown and may be multifactorial. Although phlebotomy has previously been the treatment for PTP, drugs such as adenosine receptor antagonists or angiotensin-converting enzyme inhibitors can be used to control PTP. Methods. The authors performed a prospective study of two different drugs to treat PTP: aminophylline and enalapril. Twenty-seven patients with PTP lasting more than 6 months were evaluated. During phase 1, aminophylline was compared with enalapril. The patients sequentially received aminophylline and enalapril during 12-week periods, intercalated by 12- week periods of no drugs. During phase 2, enalapril was administered for 12 weeks. Results. From January 1984 to December 1993, 110 of 333 patients with PTP lasting more than 6 months (33%) developed polycythemia, and 27 patients were included in the present study. In phase 1, aminophylline had no effect on PTP. Enalapril promoted an erythropoiesis inhibition, characterized by a decrease in hematocrit and an increase in iron stores and ferritin levels. After withdrawal of enalapril, the hematocrit increased and the iron stores decreased. In phase 2, there was a progressive reduction in hematocrit after the 4th week of therapy. The lowest hematocrit was observed in the 12th week and then enalapril was stopped, leading to a subsequent rise in hematocrit. Erythropoietin levels and renal function remained constant during all periods of both phases of the study. Conclusion. The use of adenosine antagonists was ineffective to treat PTP in our series. However, treatment with enalapril promoted an erythropoiesis inhibition, demonstrated by a reduction in hematocrit, hemoglobin, red blood cell count, and reticulocyte count, associated with an increase in iron stores. This response occurred independently from erythropoietin levels or hemodynamic graft changes. Revue / Journal Title Transplantation ISSN 0041-1337 CODEN TRPLAU Source / Source 1998, vol. 65, no11, pp. 1461-1464 (22 ref.) Langue / Language Anglais
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> On Jul 4, 6:19 pm, ironjustice <ironjust...@cashette.com> wrote: > "Chronic pressure overload of pulmonary hypertension" This can be > caused by erythrocytosis / polycythaemia <<
> " Hemoglobin had a direct effect on Pulmonary Arterial Pressure"
> Effects of Hemoglobin on Pulmonary Arterial Pressure and Pulmonary > Vascular Resistance in Patients with Chronic Emphysema > Akira Nakamuraa, Norio Kasamatsua, Ikko Hashizumea, Takushi Shiraia, > Suguru Hanzawab, Shigeru Momikib, Kazuyoshi Sasakib, Masao Kinoshitab, > Osamu Okadac, Koichiro Tatsumic, Takayuki Kuriyamac
> Departments of > aRespiratory Medicine and > bThoracic Surgery, Hamamatsu Medical Center, Hamamatsu, and > cDepartment of Chest Medicine, Chiba University, Chiba, Japan
> Background: > The increase in viscosity caused by secondary polycythemia is thought > to be one of the major causes of pulmonary hypertension secondary to > chronic emphysema. However, very few clinical studies considered the > relation between pulmonary hypertension and polycythemia in the case > of chronic obstructive pulmonary disease. > Objective: > The purpose of this study is to elucidate the relative contribution of > an increase in hemoglobin level (Hb) to mean pulmonary arterial > pressure (mPAP) and pulmonary vascular resistance (PVR). > Methods: > We retrospectively investigated 41 patients with chronic emphysema who > had undergone a right heart catheterization. Multiple-regression > analysis and F test were performed to investigate both direct effects > of Hb and PaO2 as independent variables on mPAP and PVR as dependent > variables. > Results: > Significant correlations were found between PaO2 and mPAP (or PVR), or > Hb and mPAP (or PVR), indicating that both Hb and PaO2 are > contributory to mPAP and PVR. The F test demonstrated that Hb and PaO2 > could directly affect the level of either mPAP or PVR. > Conclusions: > It was concluded that Hb had a direct effect on mPAP and PVR, > independently of hypoxia in patients with chronic emphysema.
> > This can be caused by erythrocytosis / polycythaemia > > On Jul 4, 4:59 pm, "Andrew B. Chung, MD/PhD" <lov...@thetruth.com> > > wrote:The enlargement of the right-ventricle occurs to compensate for > > its weakening from the chronic pressure overload of pulmonary > > hypertension. <<
> > "Chronic pressure overload of pulmonary hypertension"
> > This can be caused by erythrocytosis / polycythaemia .. which .. > > coincidentally .. HAPPENS .. in this incidence.
> > Therefore in theory erythrocytosis / increased red blood cell > > production could BE THE **cause** OF pulmonary hypertension down here > > amongst those normally residing at sea level.
> > Spoor.
> > Increased red blood cells happens only in a few ways.
> > > This is in accord with Starling's law. > > > Marcus Aurelius wrote: > > > > Pulmonary hypertension may lead to "cor pulmonale". In this disorder, > > > > the right ventricle, which pumps blood to the lungs, > > > > becomes enlarged,eventually resulting in right sided heart failure.
> > > The enlargement of the right-ventricle occurs to compensate for its > > > weakening from the chronic pressure overload of pulmonary > > > hypertension.
> > > This is in accord with Starling's law.
> > > May you and other dear neighbors, friends, and brethren have a > > > blessedly wonderful 2008th year since the birth of our LORD Jesus > > > Christ as our Messiah, the Son of Man ...
