Respiratory Sensitivity to Acute Hypoxia in Goat Kids Born at High Altitude

1969 ◽  
Vol 77 (4) ◽  
pp. 439-441
Author(s):  
Allan H. Mines ◽  
Søren C. Sørensen
2020 ◽  
Vol 120 (12) ◽  
pp. 2693-2704
Author(s):  
Erika Schagatay ◽  
Alexander Lunde ◽  
Simon Nilsson ◽  
Oscar Palm ◽  
Angelica Lodin-Sundström

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.


2017 ◽  
Vol 123 (6) ◽  
pp. 1443-1450 ◽  
Author(s):  
William Ottestad ◽  
Tor Are Hansen ◽  
Gaurav Pradhan ◽  
Jan Stepanek ◽  
Lars Øivind Høiseth ◽  
...  

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.


2022 ◽  
Vol 12 ◽  
Author(s):  
Sebastián Castillo-Galán ◽  
Daniela Parrau ◽  
Ismael Hernández ◽  
Sebastián Quezada ◽  
Marcela Díaz ◽  
...  

Calcium signaling is key for the contraction, differentiation, and proliferation of pulmonary arterial smooth muscle cells. Furthermore, calcium influx through store-operated channels (SOCs) is particularly important in the vasoconstrictor response to hypoxia. Previously, we found a decrease in pulmonary hypertension and remodeling in normoxic newborn lambs partially gestated under chronic hypoxia, when treated with 2-aminoethyldiphenyl borinate (2-APB), a non-specific SOC blocker. However, the effects of 2-APB are unknown in neonates completely gestated, born, and raised under environmental hypoxia. Accordingly, we studied the effects of 2-APB-treatment on the cardiopulmonary variables in lambs under chronic hypobaric hypoxia. Experiments were done in nine newborn lambs gestated, born, and raised in high altitude (3,600 m): five animals were treated with 2-APB [intravenous (i.v.) 10 mg kg–1] for 10 days, while other four animals received vehicle. During the treatment, cardiopulmonary variables were measured daily, and these were also evaluated during an acute episode of superimposed hypoxia, 1 day after the end of the treatment. Furthermore, pulmonary vascular remodeling was assessed by histological analysis 2 days after the end of the treatment. Basal cardiac output and mean systemic arterial pressure (SAP) and resistance from 2-APB- and vehicle-treated lambs did not differ along with the treatment. Mean pulmonary arterial pressure (mPAP) decreased after the first day of 2-APB treatment and remained lower than the vehicle-treated group until the third day, and during the fifth, sixth, and ninth day of treatment. The net mPAP increase in response to acute hypoxia did not change, but the pressure area under the curve (AUC) during hypoxia was slightly lower in 2-APB-treated lambs than in vehicle-treated lambs. Moreover, the 2-APB treatment decreased the pulmonary arterial wall thickness and the α-actin immunoreactivity and increased the luminal area with no changes in the vascular density. Our findings show that 2-APB treatment partially reduced the contractile hypoxic response and reverted the pulmonary vascular remodeling, but this is not enough to normalize the pulmonary hemodynamics in chronically hypoxic newborn lambs.


2015 ◽  
Vol 118 (5) ◽  
pp. 509-519 ◽  
Author(s):  
Andrew M. Luks

With the growing interest in adventure travel and the increasing ease and affordability of air, rail, and road-based transportation, increasing numbers of individuals are traveling to high altitude. The decline in barometric pressure and ambient oxygen tensions in this environment trigger a series of physiologic responses across organ systems and over a varying time frame that help the individual acclimatize to the low oxygen conditions but occasionally lead to maladaptive responses and one or several forms of acute altitude illness. The goal of this Physiology in Medicine article is to provide information that providers can use when counseling patients who present to primary care or travel medicine clinics seeking advice about how to prevent these problems. After discussing the primary physiologic responses to acute hypoxia from the organ to the molecular level in normal individuals, the review describes the main forms of acute altitude illness—acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema—and the basic approaches to their prevention and treatment of these problems, with an emphasis throughout on the physiologic basis for the development of these illnesses and their management.


Author(s):  
Cory W Dugan ◽  
Shane K Maloney ◽  
Kristina J Abramoff ◽  
Sohan S Panag ◽  
Elizabeth A Davis ◽  
...  

Abstract Context Current exercise guidelines for individuals with type 1 diabetes (T1D) do not consider the impact that high altitude may have on blood glucose levels (BGL) during exercise. Objective To investigate the effect of acute hypoxia (simulated high altitude) on BGL and carbohydrate oxidation rates during moderate intensity exercise in individuals with T1D. Methods Using a counterbalanced, repeated measures study design, 7 individuals with T1D completed two exercise sessions; normoxia and hypoxia (~4,200m simulated altitude). Participants cycled for 60min on an ergometer at 45% of their sea-level V̇O2peak, and then recovered for 60min. Before, during and after exercise, blood samples were taken to measure glucose, lactate and insulin levels. Respiratory gases were collected to measure carbohydrate oxidation rates. Results Early during exercise (&lt;30min), there was no fall in BGL in either condition. After one hour of exercise and during recovery, BGL were significantly lower under the hypoxic condition compared to both pre-exercise levels (p=0.008) and the normoxic condition (p=0.027). Exercise in both conditions resulted in a significant rise in carbohydrate oxidation rates, which returned to baseline levels post-exercise. Before, during and after exercise, carbohydrate oxidation rates were higher under the hypoxic compared with the normoxic condition (p&lt;0.001). Conclusions The greater decline in BGL during and after exercise performed under acute hypoxia suggests that exercise during acute exposure to high altitude may increase the risk of hypoglycemia in individuals with T1D. Future guidelines may have to consider the impact altitude has on exercise-mediated hypoglycemia.


2013 ◽  
Vol 690-693 ◽  
pp. 1305-1309
Author(s):  
Wen Hua Li

Objective observation of Tibetan medicine rhodiola on high altitude Pulmonary edema in rats and HIF-1a expression changes. Method Will 50 only male SD rats randomly divided into 5 group , are often oxygen control group (Xi'an , altitude 5m ), acute hypoxia control group (Xi'an , altitude 5m ), acute hypoxia Group (naqu , elevation 4500m ), rhodiola acclimatization control group ( Xi'an , altitude 5m ), rhodiola altitude acclimatization group (naqu, elevation 4500m ) , light and electron microscopic observation of lung tissue samples , immunohistochemical detection of various groups of lung tissue HIF-la expression, RT-PCR method detection altitude hypoxia group animal lungs HIF-la mRNA expression changes. Results Acute hypoxia group lung tissue microstructure and Ultrastructure of a discernible high altitude pulmonary edema, and after the Tibetan medicine rhodiola after high altitude pulmonary edema is significantly reduced, ( as in Figure 123456). Lung tissue within the immunohistochemical detection not see HIF-la protein expression, RT-PCR detection SD big rat intraperitoneal injection of rhodiola extract 40g BGE/kg, 2h open back began to rise 4h, peak, after declining 24h, basically back to their normal control group , level rhodiola medicine acclimatization group HIF a 1 am RNA expression are clearly higher than the atmospheric oxygen control group and acute hypoxia group (p < 0.01). Conclusions Tibetan medicine rhodiola on lung tissue HIF-lamRNA expression of conducive to reduce hypoxic rats high altitude pulmonary edema.


1995 ◽  
Vol 89 (2) ◽  
pp. 201-204 ◽  
Author(s):  
A. D. Wright ◽  
C. H. E. Imray ◽  
M. S. C. Morrissey ◽  
R. J. Marchbanks ◽  
A. R. Bradwell

1. Raised intracranial pressure has been noted in severe forms of acute mountain sickness and high-altitude cerebral oedema, but the role of intracranial pressure in the pathogenesis of mild to moderate acute mountain sickness is unknown. 2. Serial measurements of intracranial pressure were made indirectly by assessing changes in tympanic membrane displacement in 24 healthy subjects on rapid ascent to 5200 m. 3. Acute hypoxia at 3440 m was associated with a rise in intracranial pressure, but no difference was found in pressure changes at 4120 or 5200 m in subjects with or without symptoms of acute mountain sickness. 4. Raised intracranial pressure, though temporarily associated with acute hypoxia, is not a feature of acute mountain sickness with mild or moderate symptoms.


2008 ◽  
Vol 104 (2) ◽  
pp. 490-498 ◽  
Author(s):  
Philip N. Ainslie ◽  
Shigehiko Ogoh ◽  
Katie Burgess ◽  
Leo Celi ◽  
Ken McGrattan ◽  
...  

We hypothesized that 1) acute severe hypoxia, but not hyperoxia, at sea level would impair dynamic cerebral autoregulation (CA); 2) impairment in CA at high altitude (HA) would be partly restored with hyperoxia; and 3) hyperoxia at HA and would have more influence on blood pressure (BP) and less influence on middle cerebral artery blood flow velocity (MCAv). In healthy volunteers, BP and MCAv were measured continuously during normoxia and in acute hypoxia (inspired O2 fraction = 0.12 and 0.10, respectively; n = 10) or hyperoxia (inspired O2 fraction, 1.0; n = 12). Dynamic CA was assessed using transfer-function gain, phase, and coherence between mean BP and MCAv. Arterial blood gases were also obtained. In matched volunteers, the same variables were measured during air breathing and hyperoxia at low altitude (LA; 1,400 m) and after 1–2 days after arrival at HA (∼5,400 m, n = 10). In acute hypoxia and hyperoxia, BP was unchanged whereas it was decreased during hyperoxia at HA (−11 ± 4%; P < 0.05 vs. LA). MCAv was unchanged during acute hypoxia and at HA; however, acute hyperoxia caused MCAv to fall to a greater extent than at HA (−12 ± 3 vs. −5 ± 4%, respectively; P < 0.05). Whereas CA was unchanged in hyperoxia, gain in the low-frequency range was reduced during acute hypoxia, indicating improvement in CA. In contrast, HA was associated with elevations in transfer-function gain in the very low- and low-frequency range, indicating CA impairment; hyperoxia lowered these elevations by ∼50% ( P < 0.05). Findings indicate that hyperoxia at HA can partially improve CA and lower BP, with little effect on MCAv.


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