scholarly journals Spleen contraction elevates hemoglobin concentration at high altitude during rest and exercise

2020 ◽  
Vol 120 (12) ◽  
pp. 2693-2704
Author(s):  
Erika Schagatay ◽  
Alexander Lunde ◽  
Simon Nilsson ◽  
Oscar Palm ◽  
Angelica Lodin-Sundström
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Hemoglobin Concentration ◽  
Step Test ◽  
Arterial Oxygen ◽  
Spleen Volume ◽  
Spleen Contraction ◽  
Response To Exercise ◽  
Rest And Exercise

Abstract Purpose Hypoxia and exercise are known to separately trigger spleen contraction, leading to release of stored erythrocytes. We studied spleen volume and hemoglobin concentration (Hb) during rest and exercise at three altitudes. Methods Eleven healthy lowlanders did a 5-min modified Harvard step test at 1370, 3700 and 4200 m altitude. Spleen volume was measured via ultrasonic imaging and capillary Hb with Hemocue during rest and after the step test, and arterial oxygen saturation (SaO2), heart rate (HR), expiratory CO2 (ETCO2) and respiratory rate (RR) across the test. Results Resting spleen volume was reduced with increasing altitude and further reduced with exercise at all altitudes. Mean (SE) baseline spleen volume at 1370 m was 252 (20) mL and after exercise, it was 199 (15) mL (P < 0.01). At 3700 m, baseline spleen volume was 231 (22) mL and after exercise 166 (12) mL (P < 0.05). At 4200 m baseline volume was 210 (23) mL and after exercise 172 (20) mL (P < 0.05). After 10 min, spleen volume increased to baseline at all altitudes (NS). Baseline Hb increased with altitude from 138.9 (6.1) g/L at 1370 m, to 141.2 (4.1) at 3700 m and 152.4 (4.0) at 4200 m (P < 0.01). At all altitudes Hb increased from baseline during exercise to 146.8 (5.7) g/L at 1370 m, 150.4 (3.8) g/L at 3700 m and 157.3 (3.8) g/L at 4200 m (all P < 0.05 from baseline). Hb had returned to baseline after 10 min rest at all altitudes (NS). The spleen-derived Hb elevation during exercise was smaller at 4200 m compared to 3700 m (P < 0.05). Cardiorespiratory variables were also affected by altitude during both rest and exercise. Conclusions The spleen contracts and mobilizes stored red blood cells during rest at high altitude and contracts further during exercise, to increase oxygen delivery to tissues during acute hypoxia. The attenuated Hb response to exercise at the highest altitude is likely due to the greater recruitment of the spleen reserve during rest, and that maximal spleen contraction is reached with exercise.

scholarly journals Spleen Contraction During Sudden Eupneic Hypoxia Elevates Hemoglobin Concentration

2021 ◽  
Vol 12 ◽  
Author(s):  
Frank Pernett ◽  
Felix Schagatay ◽  
Caroline Vildevi ◽  
Erika Schagatay
Keyword(s):  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Hemoglobin Concentration ◽  
Normobaric Hypoxia ◽  
Short Exposure ◽  
Arterial Oxygen ◽  
Spleen Volume ◽  
Hypoxia Exposure ◽  
Arterial Blood ◽  
Spleen Contraction

The spleen contracts progressively during moderate normobaric hypoxia exposure of 20 min, which elevates hemoglobin concentration (Hb). However, acute hypoxia exposure could be shorter and more severe when oxygen systems fail during, e.g., high-altitude sky diving, aircraft cabin pressure drop, balloon flights, extreme altitude climbing, and in some maladies. We aimed to evaluate the speed and magnitude of spleen contraction during short exposure to extreme eupneic hypoxia and its subsequent recovery on oxygen. Eight female and seven male volunteers were exposed to normobaric hypoxia (10% oxygen) for 10 min during sitting rest, followed by 10 min on 100% oxygen. Heart rate (HR), arterial oxygen saturation (SpO2), and mean arterial blood pressure (MAP) were measured continuously. The spleen was measured via ultrasonic imaging every minute for volume calculations, and venous blood samples were drawn before and after exposure for hemoglobin concentration (Hb). Mean (SD) spleen volume was 279 (115) mL before exposure, 219 (75) mL (21% reduction; P = 0.005) at 3 min of exposure, and 201 (93) mL after 10 min exposure to hypoxia (28% reduction; P &lt; 0.001). Hb was 138.8 (7.6) g·L−1 before and 142.9 (8.1) g·L−1 after 10 min of exposure (2.9% increase; P &lt; 0.001). SpO2 was 96.4 (1.7)% before exposure and 74.7 (8.4)% during the last minute of exposure (22.5% reduction; P &lt; 0.001). HR increased from 80 (14) to 90 (17) bpm during exposure (12% increase, P &lt; 0.05). MAP remained unchanged. After 10 min recovery on oxygen, values had been restored for spleen volume and Hb, while SpO2 was higher and HR lower compared with before hypoxia exposure. We concluded that acute normobaric hypoxia of only 10 min caused significant spleen volume contraction with Hb increase. This rapid spleen response, evident already after 3 min of exposure, could have a protective effect during sudden exposure to severe hypoxia.

Control of breathing in Sherpas at low and high altitude

1980 ◽  
Vol 49 (3) ◽  
pp. 374-379 ◽  
Author(s):  
P. H. Hackett ◽  
J. T. Reeves ◽  
C. D. Reeves ◽  
R. F. Grover ◽  
D. Rennie
Keyword(s):  
High Altitude ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Carbon Dioxide Tension ◽  
Arterial Oxygen ◽  
Hypoxic Ventilatory Response ◽  
Oxygen Administration ◽  
End Tidal

Sherpas are well known for their physical performance at extreme altitudes, yet they are reported to have blunted ventilatory responses to acute hypoxia and relative hypoventilation in chronic hypoxia. To examine this paradox, we studied ventilatory control in Sherpas in comparison to that in Westerners at both low and high altitude. At low altitude, 25 Sherpas had higher minute ventilation, higher respiratory frequency, and lower end-tidal carbon dioxide tension than 25 Westerners. The hypoxic ventilatory response of Sherpas was found to be similar to that in Westerners, even though long altitude exposure had blunted the responses of some Sherpas. At high altitude, Sherpas again had higher minute ventilation and a tendency toward higher arterial oxygen saturation than Westerners. Oxygen administration increased ventilation further in Sherpas but decreased ventilation in Westerners. We conclude that Sherpas differ from other high-altitude natives; their hypoxic ventilatory response is not blunted, and they exhibit relative hyperventilation.

Intermittent hypoxia increases ventilation and SaO2 during hypoxic exercise and hypoxic chemosensitivity

2001 ◽  
Vol 90 (4) ◽  
pp. 1431-1440 ◽  
Author(s):  
Keisho Katayama ◽  
Yasutake Sato ◽  
Yoshifumi Morotome ◽  
Norihiro Shima ◽  
Koji Ishida ◽  
...  
Keyword(s):  
Intermittent Hypoxia ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Submaximal Exercise ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Equivalent ◽  
Hypoxic Exercise

The purpose of this study was 1) to test the hypothesis that ventilation and arterial oxygen saturation (SaO2 ) during acute hypoxia may increase during intermittent hypoxia and remain elevated for a week without hypoxic exposure and 2) to clarify whether the changes in ventilation and SaO2 during hypoxic exercise are correlated with the change in hypoxic chemosensitivity. Six subjects were exposed to a simulated altitude of 4,500 m altitude for 7 days (1 h/day). Oxygen uptake (V˙o 2), expired minute ventilation (V˙e), and SaO2 were measured during maximal and submaximal exercise at 432 Torr before (Pre), after intermittent hypoxia (Post), and again after a week at sea level (De). Hypoxic ventilatory response (HVR) was also determined. At both Post and De, significant increases from Pre were found in HVR at rest and in ventilatory equivalent for O2(V˙e/V˙o 2) and SaO2 during submaximal exercise. There were significant correlations among the changes in HVR at rest and inV˙e/V˙o 2 and SaO2 during hypoxic exercise during intermittent hypoxia. We conclude that 1 wk of daily exposure to 1 h of hypoxia significantly improved oxygenation in exercise during subsequent acute hypoxic exposures up to 1 wk after the conditioning, presumably caused by the enhanced hypoxic ventilatory chemosensitivity.

Acute hypoxia in a simulated high-altitude airdrop scenario due to oxygen system failure

2017 ◽  
Vol 123 (6) ◽  
pp. 1443-1450 ◽  
Author(s):  
William Ottestad ◽  
Tor Are Hansen ◽  
Gaurav Pradhan ◽  
Jan Stepanek ◽  
Lars Øivind Høiseth ◽  
...  
Keyword(s):  
High Altitude ◽  
Acute Hypoxia ◽  
Supplemental Oxygen ◽  
Cerebral Oximetry ◽  
Arterial Oxygen ◽  
Hypoxic Exposure ◽  
System Failure ◽  
Oxygen System ◽  
Simulated High Altitude ◽  
Oxygen Tensions

High-Altitude High Opening (HAHO) is a military operational procedure in which parachute jumps are performed at high altitude requiring supplemental oxygen, putting personnel at risk of acute hypoxia in the event of oxygen equipment failure. This study was initiated by the Norwegian Army to evaluate potential outcomes during failure of oxygen supply, and to explore physiology during acute severe hypobaric hypoxia. A simulated HAHO without supplemental oxygen was carried out in a hypobaric chamber with decompression to 30,000 ft (9,144 m) and then recompression to ground level with a descent rate of 1,000 ft/min (305 m/min). Nine subjects were studied. Repeated arterial blood gas samples were drawn throughout the entire hypoxic exposure. Additionally, pulse oximetry, cerebral oximetry, and hemodynamic variables were monitored. Desaturation evolved rapidly and the arterial oxygen tensions are among the lowest ever reported in volunteers during acute hypoxia. PaO2 decreased from baseline 18.4 (17.3–19.1) kPa, 138.0 (133.5–143.3) mmHg, to a minimum value of 3.3 (2.9–3.7) kPa, 24.8 (21.6–27.8) mmHg, after 180 (60–210) s, [median (range)], N = 9. Hyperventilation with ensuing hypocapnia was associated with both increased arterial oxygen saturation and cerebral oximetry values, and potentially improved tolerance to severe hypoxia. One subject had a sharp drop in heart rate and cardiac index and lost consciousness 4 min into the hypoxic exposure. A simulated high-altitude airdrop scenario without supplemental oxygen results in extreme hypoxemia and may result in loss of consciousness in some individuals. NEW & NOTEWORTHY This is the first study to investigate physiology and clinical outcome of oxygen system failure in a simulated HAHO scenario. The acquired knowledge is of great value to make valid risk-benefit analyses during HAHO training or operations. The arterial oxygen tensions reported in this hypobaric chamber study are among the lowest ever reported during acute hypoxia.

Blood Volume Changes in Patients With Cystic Fibrosis

PEDIATRICS ◽  
1977 ◽  
Vol 59 (4) ◽  
pp. 588-594
Author(s):  
Amnon Rosenthal ◽  
Lawrence N. Button ◽  
Kon Taik Khaw
Keyword(s):  
Cystic Fibrosis ◽  
Blood Volume ◽  
Arterial Oxygen Saturation ◽  
Hemoglobin Concentration ◽  
Pulmonary Involvement ◽  
Progressive Increase ◽  
Cor Pulmonale ◽  
Arterial Oxygen ◽  
Mean Corpuscular Hemoglobin ◽  
Total Blood

Simultaneous red blood cell (RBC) and plasma volume determinations were obtained in 16 patients with cystic fibrosis (CF) and moderately severe pulmonary involvement. Hypervolemia with an increase in both RBC and plasma volumes was observed. Changes in blood volume were marked when values were indexed by weight but less significant when indexed by height. Decreasing systemic arterial oxygen saturation was associated with a progressive increase in RBC mass, hematocrit value, and hemoglobin level and a decrease in mean corpuscular hemoglobin concentration. RBC and total blood volumes were highest in patients with cor pulmonale and congestive heart failure. However, the compensatory polycythemic response in patients with CF was inadequate when compared with the response to hypoxemia in patients with cyanotic congenital heart disease. The insufficient oxygen-carrying capacity may compromise tissue oxygen delivery and necessitate treatment.

scholarly journals Effects of high altitude in pregnancy: an opportunity of research in KAHS

2018 ◽  
Vol 1 (3) ◽  
pp. 1-2
Author(s):  
Binod Aryal
Keyword(s):  
Birth Weight ◽  
South America ◽  
High Altitude ◽  
Work Performance ◽  
Arterial Oxygen Saturation ◽  
Functional Adaptation ◽  
European Ancestry ◽  
Arterial Oxygen ◽  
Adaptation To Hypoxia ◽  
Physiological Changes

Pregnancy is a special condition in a women’s life with unique physiological changes. There has been some research on physiological changes in human body in high altitude; however, there are many things still unknown about pregnancy at high altitude. It is an estimation that about 140 million people worldwide live in high altitude of above 2500 m, and it is believed that the hypobaric hypoxia of pregnancy at high altitude is the most common cause for maternofetal hypoxia. It has been seen that the babies born at high altitude are smaller, and the degree of smallness is inversely correlated with the number of generations of ancestors of high-altitude residence. Some studies show that women in populations with high-altitude ancestry, such as the Aymaras or Quechuas in South America and Tibetans in Asia, deliver heavier babies than women from European ancestry in South America or Han women in China living at high altitude. A study by Jensen and Moore shows that in Colorado, altitude acts as an independent factor in determining birth weight, with a reduction in birth weight of 100 g per 1000 m elevation gain. Studies have shown that low birth weight at high altitude has no association with socioeconomic status. Hence, it may reflect either hypoxia-induced intrauterine growth restriction or genetic adaptation. The latter implies a strong fetomaternal interaction involving adaptation to hypoxia on several levels. It also reflects the importance of interaction between the mother and the fetus which is stressed by the fact that better maternal ventilator response to hypoxic stress at high altitude correlates positively with birth weight. Another study shows that people living at altitudes of 4000 m and above have an arterial partial pressure of oxygen of 50 mmHg and an arterial oxygen saturation of just above 80%. There has been many studies on populations living in high-altitude regions for many generations, like Quechuas and Tibetans, which show many functional and structural adaptations in high altitude. This adaptation helps to allow for a way out for the main metabolic problem they face: maintaining an acceptably high scope for sustained aerobic metabolism despite reduced availability of oxygen in the inspired air. The functional adaptation to high altitude is measured indirectly by determining aerobic capacity, which reflects not only the maximum work performance but also the success of the individual’s biological oxygen transport system.

Regional blood flow and cardiac output during acute hypoxia in the anesthetized dog

1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Head Kidney ◽  
Arterial Oxygen ◽  
Circulatory Effects ◽  
Low Concentrations ◽  
Anesthetized Dogs

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.

P6480Asymmetric dimethylarginine (ADMA) predicts altitude-associated hypoxic pulmonary arterial hypertension

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
R H Boeger ◽  
P Siques ◽  
J Brito ◽  
E Schwedhelm ◽  
E Pena ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Logistic Regression ◽  
Oxygen Saturation ◽  
High Altitude ◽  
Sea Level ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Pulmonary Arterial

Abstract Prolonged exposure to altitude-associated chronic hypoxia (CH) may cause high altitude pulmonary hypertension (HAPH). Chronic intermittent hypobaric hypoxia (CIH) occurs in individuals who commute between sea level and high altitude. CIH is associated with repetitive acute hypoxic acclimatization and conveys the long-term risk of HAPH. As nitric oxide (NO) is an important regulator of systemic and pulmonary vascular tone and asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis that increases in hypoxia, we aimed to investigate whether ADMA predicts the incidence of HAPH among Chilean frontiers personnel exposed to six months of CIH. We performed a prospective study of 123 healthy male subjects who were subjected to CIH (5 days at appr. 3,550 m, followed by 2 days at sea level) for six months. ADMA, SDMA, L-arginine, arterial oxygen saturation, systemic arterial blood pressure, and haematocrit were measured at baseline and at months 1, 4, and 6 at high altitude. Acclimatization to high altitude was determined using the Lake Louise Score and the presence of acute mountain sickness (AMS). Echocardiography was performed after six months of CIH in a subgroup of 43 individuals with either good (n=23) or poor (n=20) aclimatization to altitude, respectively. Logistic regression was used to assess the association of biomarkers with HAPH. 100 study participants aged 18.3±1.3 years with complete data sets were included in the final analysis. Arterial oxygen saturation decreased upon the first ascent to altitude and plateaued at about 90% during the further course of the study. Haematocrit increased to about 47% after one month and remained stable thereafter. ADMA continuously increased and SDMA decreased during the study course, whilst L-arginine levels showed no distinct pattern. The incidence of AMS and the Lake Louise Score were high after the first ascent (53 and 3.1±2.4, respectively) and at one month of CIH (47 and 3.0±2.6, respectively), but decreased to 20 and 1.4±2.0 at month 6, respectively (both p<0.001 for trend). In echocardiography, 18 participants (42%) showed a mean pulmonary arterial pressure (mPAP) greater than 25 mm Hg (mean ± SD, 30.4±3.9 mm Hg), out of which 9 (21%) were classified as HAPH (mPAP ≥30 mm Hg; mean ± SD, 33.9±2.2 mm Hg). Baseline ADMA, but not SDMA, was significantly associated with mPAP at month 6 in univariate logistic regression analysis (R = 0.413; p=0.007). In ROC analysis, a cut-off for baseline ADMA of 0.665 μmol/l was determined as the optimal cut-off level to predict HAPH (mPAP >30 mm Hg) with a sensitivity of 100% and a specificity of 63.6%. ADMA concentration increases during long-term CIH. It is an independent predictive biomarker for the incidence of HAPH. SDMA concentration decreases during CIH and shows no association with HAPH. Our data support a role of impaired NO-mediated pulmonary vasodilation in the pathogenesis of high altitude pulmonary hypertension. Acknowledgement/Funding CONICYT/FONDEF/FONIS Sa 09I20007; FIC Tarapaca BIP 30477541-0; BMBF grant 01DN17046 (DECIPHER); Georg & Jürgen Rickertsen Foundation, Hamburg

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