Hormonal changes in normal and polycythemic high-altitude natives

1995 ◽  
Vol 79 (3) ◽  
pp. 795-800 ◽  
Author(s):  
A. M. Antezana ◽  
J. P. Richalet ◽  
I. Noriega ◽  
M. Galarza ◽  
G. Antezana
Keyword(s):  
High Altitude ◽  
Systolic Pressure ◽  
Plasma Aldosterone ◽  
Control Group ◽  
Protective Mechanism ◽  
Hormonal Changes ◽  
Plasma Aldosterone Concentration ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Acute And Chronic Exposure

Acute and chronic exposure to high-altitude (HA) hypoxia inhibits the renin-angiotensin-aldosterone system and may modify the release of atrial natriuretic peptide (ANP) in sea-level (SL) natives. In HA natives, the release of these hormones could be influenced by changes in blood volume or pulmonary arterial pressure. Twenty-four men residing in La Paz, Bolivia, at 3,600 m were separated into two groups: one normocythemic (HAN; with hematocrit < 57%; n = 13) and the other polycythemic (HAP; with hematocrit > 57%; n = 11). A control group of 9 SL residents was studied in normoxia (SLN) as well as after 4 days spent at 4,350 m (SLH). The groups were tested for plasma active renin (PAR), plasma aldosterone concentration, ANP, and potassium and norepineprine concentrations at rest and after a maximal exercise. Pulmonary arterial systolic pressure was assessed by a Doppler technique. It was observed that PAR and plasma aldosterone concentration at rest and after exercise were lower in the SLH than in the SLN group. PAR and norepineprine concentration were higher among highlanders than in the SLN group. Renin response to exercise was normal among the HAN group and slightly decreased among the HAP group, and an exercise-induced increase in aldosterone was attenuated in both HA groups. Aldosterone response to renin was maintained among the SLH group but was attenuated in the HA groups, possibly owing to a protective mechanism against salt and water retention. Resting and exercise ANP was lower in the HA groups than in the SLN group.

Exercise-induced VA/Q inequality in subjects with prior high-altitude pulmonary edema

1996 ◽  
Vol 81 (2) ◽  
pp. 922-932 ◽  
Author(s):  
A. Podolsky ◽  
M. W. Eldridge ◽  
R. S. Richardson ◽  
D. R. Knight ◽  
E. C. Johnson ◽  
...  
Keyword(s):  
Standard Deviation ◽  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Control Group ◽  
Pulmonary Capillary ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Capillary Pressures ◽  
Exercise Induced

Ventilation-perfusion (VA/Q) mismatch has been shown to increase during exercise, especially in hypoxia. A possible explanation is subclinical interstitial edema due to high pulmonary capillary pressures. We hypothesized that this may be pathogenetically similar to high-altitude pulmonary edema (HAPE) so that HAPE-susceptible people with higher vascular pressures would develop more exercise-induced VA/Q mismatch. To examine this, seven healthy people with a history of HAPE and nine with similar altitude exposure but no HAPE history (control) were studied at rest and during exercise at 35, 65, and 85% of maximum 1) at sea level and then 2) after 2 days at altitude (3,810 m) breathing both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) gas at both locations. We measured cardiac output and respiratory and inert gas exchange. In both groups, VA/Q mismatch (assessed by log standard deviation of the perfusion distribution) increased with exercise. At sea level, log standard deviation of the perfusion distribution was slightly higher in the HAPE-susceptible group than in the control group during heavy exercise. At altitude, these differences disappeared. Because a history of HAPE was associated with greater exercise-induced VA/Q mismatch and higher pulmonary capillary pressures, our findings are consistent with the hypothesis that exercise-induced mismatch is due to a temporary extravascular fluid accumulation.

Pulmonary arterial systolic pressure and susceptibility to high altitude pulmonary edema

2011 ◽  
Vol 179 (2-3) ◽  
pp. 294-299 ◽  
Author(s):  
Rémi Mounier ◽  
Aimé Amonchot ◽  
Nicolas Caillot ◽  
Cécile Gladine ◽  
Bernard Citron ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Systolic Pressure ◽  
Arterial Systolic Pressure ◽  
Pulmonary Arterial Systolic Pressure ◽  
High Altitude Pulmonary Edema ◽  
Pulmonary Arterial

scholarly journals Bariatric Surgery Induces a Differential Effect on Plasma Aldosterone in Comparison to Dietary Advice Alone

2021 ◽  
Vol 12 ◽  
Author(s):  
Maxime Berney ◽  
Nima Vakilzadeh ◽  
Marc Maillard ◽  
Mohamed Faouzi ◽  
Eric Grouzmann ◽  
...  
Keyword(s):  
Weight Loss ◽  
Sodium Excretion ◽  
Target Organ Damage ◽  
Plasma Renin ◽  
Organ Damage ◽  
Plasma Aldosterone ◽  
Dietary Advice ◽  
Control Group ◽  
Clinical Trial Registration ◽  
Plasma Aldosterone Concentration

Background and ObjectivesThe pathophysiological mechanisms linking weight loss to blood pressure (BP) reduction are not completely understood. The objective of this study was to compare the effect of weight loss after Roux-en-Y gastric bypass (RYGB) on BP, renin-angiotensin-aldosterone system (RAAS), and urinary electrolytes excretion to those of dietary advice.MethodsThis was a case-control prospective study including obese patients referred for RYGB (cases) and obese receiving diet advice only (controls). Ambulatory BP, plasma renin activity (PRA), plasma aldosterone concentration (PAC), and urinary electrolytes were measured before (M0) and after intervention (M3: 3 months and M12: 12 months).ResultsTwenty-five patients were included in the RYGB group and twelve patients in the control group. After 12 months, weight loss (-42 ± 11.5 vs -12.3 ± 6.3 kg in the control group, p=0.001) and decrease in PAC were more pronounced in the RYGB group (-34 ± 76 vs +14 ± 45 pg/ml in the control group, p=0.002). There was no difference in PRA between both groups (-0.08 ± 1.68 vs 0.01 ± 0.37 ng/ml/h, p=0.31). Sodium excretion was more marked in the RYGB group after 3 months only (-89 ± 14.9 vs -9.9 ± 27.9 mmol/day, p=0.009). The decrease in SBP was similar between both groups (-6.9 ± 9.9 vs -7.1 ± 11.9 mmHg in the control group, p=0.96).ConclusionsBariatric-induced weight loss induces a progressive decrease in PAC independently of PRA and sodium excretion. Whether this decrease in PAC affects target organ damage in the long term remains to be determined.Clinical Trial RegistrationClinicalTrials.gov, identifier NCT02218112.

Hormonal and metabolic adjustments during exercise in hypoxia or normoxia in highland natives

1996 ◽  
Vol 80 (2) ◽  
pp. 632-637 ◽  
Author(s):  
R. Favier ◽  
D. Desplanches ◽  
H. Hoppeler ◽  
E. Caceres ◽  
A. Grunenfelder ◽  
...  
Keyword(s):  
High Altitude ◽  
Chronic Hypoxia ◽  
Incremental Exercise ◽  
Metabolic Changes ◽  
Hormonal Changes ◽  
Glucoregulatory Hormones ◽  
High Altitude Natives ◽  
Blood Lactate Accumulation ◽  
Exercise Induced ◽  
Arterial Po2

In sea-level natives, exposure to hypoxia for a few weeks is characterized by an increased dependence on blood glucose and a decreased reliance on lactate for energy metabolism during exercise. These metabolic adjustments have been attributed to behavioral changes in the sympathoadrenergic and pancreatic systems. The aim of this study was to test the hypothesis of a reduced sympathoadrenergic activation and subsequent metabolic changes when high-altitude natives are acutely exposed to normoxia. Young Andean natives performed incremental exercise to exhaustion during hypoxia (arterial PO2 55.1 +/- 1.1 Torr) or during acute normoxia (arterial PO2 78.7 +/- 1.7 Torr). As a whole, oxygen uptake was increased in normoxia compared with hypoxia during graded exercise. This finding is not related to a decrease in anaerobic metabolism but rather is interpreted as a consequence of a shift in substrate utilization during exercise (increased contribution of fat as assessed by a reduction in the respiratory exchange ratio). These metabolic changes are not accompanied by modifications of glucoregulatory hormones (catecholamines, insulin, and glucagon). In particular, the exercise-induced catecholamine secretion was similar in chronic hypoxia and acute normoxia. As a consequence, blood lactate accumulation during incremental exercise was similar in both conditions. It is concluded that high-altitude natives do not display any sign of a greater sympathoadrenergic activation during chronic hypoxia and that the exercise-induced hormonal changes remained unaffected by acute inhalation of a normoxic gas mixture.

COMPARATIVE EVALUATION OF IMMEDIATE RESULTS OF PLASTIC ATRIAL SEPTAL DEFECT IN ADULT PATIENTS, LIVING IN HIGH ALTITUDE CONDITIONS

2021 ◽  
pp. 16-21
Author(s):  
Kaldarbek Abdramanov ◽  
◽  
Emilbek Kokoev ◽  
Emir Alimbekov ◽  
Parida Arzibaeva ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Atrial Septal Defect ◽  
High Altitude ◽  
Septal Defect ◽  
Adult Patients ◽  
Control Group ◽  
Observation Data ◽  
Clinical Methods ◽  
Pulmonary Arterial ◽  
The Right

The article gives a comparative assessment of the results of surgery for atrial septal defect (ASD) surgery in patients living in low and high altitude conditions. sizes of the right ventricle were practically equal, but at the same time higher than the norm. Objective. To conduct a comparative analysis of the direct results of ASD plastic in patients living in low, medium and high mountains Material and methods. The study material included 30 patients with ASD living in highlands; the control group consisted of 30 patients living in flat areas. Using clinical methods and instrumental studies, an analysis of operated patients, ASD plastic in adult patients with complicated pulmonary hypertension, heart failure, cardiac arrhythmias and functional tricuspid insufficiency was performed. Results. The authors studied pulmonary arterial pressure (PAP) indices between the groups both in the preoperative and postoperative periods, the analysis showed significant differences. The parameters of the right ventricle (RV) in the preoperative period had significant differences, however, in the postoperative period, the sizes of the right ventricle were practically equal, but at the same time higher than the norm. Conclusion. Our observation data show a significant decrease in PAP in patients living in high altitude conditions. However, the decrease in the PAP indicators remained slightly higher than the standard indicators.

Acclimatization to high altitude increase muscle sympathetic activity both at rest and during exercise

1995 ◽  
Vol 269 (1) ◽  
pp. R201-R207 ◽  
Author(s):  
R. S. Mazzeo ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
D. A. Podolin ◽  
E. E. Wolfel ◽  
...  
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Sympathetic Activity ◽  
Chronic Exposure ◽  
Submaximal Exercise ◽  
Control Group ◽  
Beta Blockade ◽  
Plasma Norepinephrine ◽  
Altitude Exposure ◽  
Acute And Chronic Exposure

This investigation examined the relationship between alterations in plasma norepinephrine associated with 21 days of high-altitude exposure and muscle sympathetic activity both at rest and during exercise. Healthy sea level residents, divided into a control group (n = 5) receiving a placebo or a drug group (n = 6) receiving 240 mg/day of propranolol, were studied while at sea level, upon arrival (acute), and after 21 days of residence (chronic) at 4,300 m. Arterial norepinephrine levels and net leg uptake and release of norepinephrine were determine both at rest and during 45 min of submaximal exercise via samples collected from femoral arterial and venous catheters. Arterial norepinephrine levels increased significantly after chronic altitude exposure both at rest (84%) and during exercise (174%) compared with sea level and acute values. A net uptake of norepinephrine was found in resting legs at sea level (0.28 +/- 0.05 nmol/min) and with acute exposure (0.07 +/- 0.06 nmol/min); however, a significant switch to net leg norepinephrine release was observed with chronic altitude exposure (0.51 +/- 0.11 nmol/min). With exercise, a net release of norepinephrine by the leg occurred across all conditions with chronic exposure, again eliciting the greatest values (5.3 +/- 0.6, 8.0 +/- 1.7, and 14.4 +/- 3.1 nmol/min for sea level, acute, and chronic exposure, respectively). It was concluded that muscle sympathetic activity is significantly elevated both at rest and during submaximal exercise as a result of chronic high-altitude exposure, and muscle is a major contributor to the increase in plasma norepinephrine levels associated with prolonged altitude exposure. The presence of dense beta-blockade did not alter this adaptation to altitude.

scholarly journals Alterations in enzymes involved in fat metabolism after acute and chronic altitude exposure

2001 ◽  
Vol 90 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Sarah L. Kennedy ◽  
William C. Stanley ◽  
Ashish R. Panchal ◽  
Robert S. Mazzeo
Keyword(s):  
High Altitude ◽  
Citrate Synthase ◽  
Fat Metabolism ◽  
Hypoxic Exposure ◽  
Control Group ◽  
Sprague Dawley ◽  
Similar Reduction ◽  
Altitude Exposure ◽  
Cpt I ◽  
Acute And Chronic Exposure

The purpose of this study was to examine the effect of acute (24 h) and chronic (5 wk) hypobaric hypoxic exposure equivalent to a simulated altitude of 4,300 m (446 mmHg) on the enzymes of fat metabolism. Heart, liver, and skeletal muscle were taken from 32 male Sprague-Dawley rats. Altitude exposure did not affect the activity of citrate synthase in any of the tissues, suggesting that mitochondrial content was unchanged. Carnitine palmitoyltransferase-I (CPT-I) activity was significantly reduced in the heart by both acute and chronic high altitude exposure compared with controls. A similar reduction was found for CPT-I activity in extensor digitorum longus after acute and chronic exposure compared with control animals. CPT-I activity was not affected by altitude exposure in the soleus muscle or the liver. 3-Hydroxyacyl-CoA dehydrogenase (β-HAD) activity was significantly depressed in the hearts of chronically exposed animals compared with controls. No difference between acute and control animals was found in the heart for β-HAD activity. Liver β-HAD activity was also significantly decreased in the acclimatized as well as in the acute animals compared with the control group. Quadriceps β-HAD activity was reduced for the chronic animals only compared with controls. These data suggest that acclimatization to high altitude selectively decreases key enzymes in fat utilization and oxidation in the heart, liver, and select skeletal muscles.

scholarly journals Remote ischemic preconditioning for prevention of high-altitude diseases: fact or fiction?

2015 ◽  
Vol 119 (10) ◽  
pp. 1143-1151 ◽  
Author(s):  
Marc Moritz Berger ◽  
Franziska Macholz ◽  
Heimo Mairbäurl ◽  
Peter Bärtsch
Keyword(s):  
High Altitude ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Acute Mountain Sickness ◽  
Systolic Pressure ◽  
Hypoxia Tolerance ◽  
Remote Ischemic Preconditioning ◽  
High Altitude Cerebral Edema ◽  
Pulmonary Arterial ◽  
Altitude Tolerance

Preconditioning refers to exposure to brief episodes of potentially adverse stimuli and protects against injury during subsequent exposures. This was first described in the heart, where episodes of ischemia/reperfusion render the myocardium resistant to subsequent ischemic injury, which is likely caused by reactive oxygen species (ROS) and proinflammatory processes. Protection of the heart was also found when preconditioning was performed in an organ different from the target, which is called remote ischemic preconditioning (RIPC). The mechanisms causing protection seem to include stimulation of nitric oxide (NO) synthase, increase in antioxidant enzymes, and downregulation of proinflammatory cytokines. These pathways are also thought to play a role in high-altitude diseases: high-altitude pulmonary edema (HAPE) is associated with decreased bioavailability of NO and increased generation of ROS, whereas mechanisms causing acute mountain sickness (AMS) and high-altitude cerebral edema (HACE) seem to involve cytotoxic effects by ROS and inflammation. Based on these apparent similarities between ischemic damage and AMS, HACE, and HAPE, it is reasonable to assume that RIPC might be protective and improve altitude tolerance. In studies addressing high-altitude/hypoxia tolerance, RIPC has been shown to decrease pulmonary arterial systolic pressure in normobaric hypoxia (13% O2) and at high altitude (4,342 m). Our own results indicate that RIPC transiently decreases the severity of AMS at 12% O2. Thus preliminary studies show some benefit, but clearly, further experiments to establish the efficacy and potential mechanism of RIPC are needed.

Garlic prevents hypoxic pulmonary hypertension in rats

1998 ◽  
Vol 275 (2) ◽  
pp. L283-L287 ◽  
Author(s):  
Michael B. Fallon ◽  
Gary A. Abrams ◽  
Tarek T. Abdel-Razek ◽  
Jun Dai ◽  
Shi-Juan Chen ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
High Altitude ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Control Group ◽  
Nitric Oxide Synthase Inhibitor ◽  
Hypoxic Pulmonary Hypertension ◽  
Pulmonary Vasoconstriction ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor

Hypoxic pulmonary vasoconstriction underlies the development of high-altitude pulmonary edema. Anecdotal observations suggest a beneficial effect of garlic in preventing high-altitude symptoms. To determine whether garlic influences pulmonary vasoconstriction, we assessed the effect of garlic on pulmonary pressures in rats subjected to alveolar hypoxia and on vasoconstriction in isolated pulmonary arterial rings. Garlic gavage (100 mg/kg body wt) for 5 days resulted in complete inhibition of acute hypoxic pulmonary vasoconstriction compared with the control group. No difference in mean arterial pressure or heart rate response to hypoxia was seen between the groups. Garlic solution resulted in a significant dose-dependent vasorelaxation in both endothelium-intact and mechanically endothelium-disrupted pulmonary arterial rings. The administration of N G-nitro-l-arginine methyl ester (a nitric oxide synthase inhibitor) inhibited the vasodilatory effect of garlic by 80%. These studies document that garlic blocks hypoxic pulmonary hypertension in vivo and demonstrate a combination of endothelium-dependent and -independent mechanisms for the effect in pulmonary arterial rings.

scholarly journals A possible role of plasma aldosterone in hypotension secondary to iron-deficiency anaemia combined with zinc deficiency in rats

2010 ◽  
Vol 105 (4) ◽  
pp. 535-538 ◽  
Author(s):  
Aki Konomi ◽  
Katsuhiko Yokoi
Keyword(s):  
Blood Pressure ◽  
Plasma Aldosterone ◽  
Fe Deficiency ◽  
Control Group ◽  
Zn Deficiency ◽  
Sprague Dawley ◽  
Plasma Aldosterone Concentration ◽  
Deficiency Anaemia ◽  
Multiple Comparison Test ◽  
Deficient Group

Patients with Fe-deficiency anaemia are often afflicted by hypotension. However, the mechanism of secondary hypotension in Fe-deficiency anaemia is unknown. To investigate the pathogenesis of secondary hypotension in Fe-deficiency anaemia, we examined the effects of Fe deprivation on plasma aldosterone concentration and blood pressure in rats. A total of forty 4-week-old male Sprague–Dawley rats were assigned into four treatment groups of ten each for the 4-week study: Fe-deficient group (FD), Zn-deficient group (ZD), Fe/Zn-deficient group (FZD) and control group (CON). At days 26 and 27, blood pressure was measured by the tail-cuff method. Plasma aldosterone concentration was determined by ELISA. The data were analysed by Tukey's multiple comparison test. Rats in the FZD had significantly lower mean blood pressure (P < 0·01) and diastolic blood pressures (P < 0·05) and plasma aldosterone concentration (P < 0·01) compared to the CON. These results suggest that blood pressure is decreased in Fe-deficiency anaemia combined with Zn deficiency partly due to decreased circulating aldosterone concentrations in addition to decreased haematocrit.

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