Hematological alterations and response to acute hypobaric stress

1975 ◽  
Vol 39 (6) ◽  
pp. 1034-1037 ◽  
Author(s):  
D. Penney ◽  
M. Thomas
Keyword(s):  
Ventilation Rate ◽  
Response Patterns ◽  
Large Decrease ◽  
Simulated Altitude ◽  
Altitude Exposure ◽  
Two Parameters ◽  
Hematological Alterations ◽  
Sodium Cyanate ◽  
2,3 Dpg ◽  
Nembutal Anesthesia

Exposure of rats to simulated altitude (15,000 ft) for 1 day and 3 and 9 wk produced progressive polycythemia, elevated 2,3-diphosphoglycerate levels and raised P50 values; the latter two parameters decreased toward control values after 9 wk. Carbon monoxide (38–43% HbCO) exposure produced polycythemia after 3- and 9-wk exposure, no change in 2,3-DPG and a fall in P50 value. Ten days' treatment with sodium cyanate produced a large decrease in 2,3-DPG and P50. Survival during 90 min of acute hypobaria (0.3 atm) under Nembutal anesthesia was highest with NaOCN (75%), intermediate with 3- and 9-wk exposure to altitude and CO (56–58%) lower in 1-day altitude exposure (44%) and lowest in controls (5%). Heart and ventilation rate was monitored during this hypobaric test and response patterns established for each exposure/treatment. In states of extreme oxygen deprivation the results suggest, in order of importance, the survival value of 1) increased oxygen-hemoglobin affinity, and 2) polycythemia.

Altitude-induced erythrocytic 2,3-DPG and hemoglobin changes in rats of various ages

1975 ◽  
Vol 39 (2) ◽  
pp. 258-261 ◽  
Author(s):  
L. G. Martin ◽  
J. M. Connors ◽  
J. J. McGrath ◽  
J. Freeman
Keyword(s):  
High Altitude ◽  
Sea Level ◽  
Age Groups ◽  
Altitude Exposure ◽  
Simulated High Altitude ◽  
Erythropoietic Response ◽  
2,3 Dpg

Rats of various ages (2, 12, 24, and 40 mo of age) were exposed for 4 wk to either a simulated high altitude of 23,000 ft or to a Peoria, Ill., altitude of 650 ft above sea level. Hematocrit ratios, hemoglobin, and erythrocytic 2,3-diphospho-glycerate (2,3-DPG) concentrations were measured. Hematocrit and hemoglobin determinations revealed a decrease in erythrocytic content with increasing age, and the augmented erythropoietic response was seen in all age groups of animals as a result of altitude exposure. The maximal erythrocytic content of hemoglobin in the 40-mo-old animals was significantly lower than that of all other age groups. Erythrocytic 2,3-DPG levels were significantly changed by aging alone. In the 40-mo-old group there was a 35% increase over the next highest sea-level value. However, while erythrocytic 2,3-DPG content increased significantly in all other age groups following altitude exposure, it decreased 46% in the 40-mo-old group.

Effect of Acute Simulated Altitude Exposure on Excess Postexercise Oxygen Consumption

2017 ◽  
Vol 49 (5S) ◽  
pp. 246
Author(s):  
James W. Navalta ◽  
Elizabeth A. Tanner ◽  
Debra K. Tacad ◽  
Nathaniel G. Bodell
Keyword(s):  
Oxygen Consumption ◽  
Simulated Altitude ◽  
Altitude Exposure ◽  
Excess Postexercise Oxygen Consumption

scholarly journals Simulated altitude exposure assessment by hyperspectral imaging

2017 ◽  
Vol 22 (5) ◽  
pp. 056012 ◽  
Author(s):  
Mihaela Antonina Calin ◽  
Adrian Macovei ◽  
Sorin Miclos ◽  
Sorin Viorel Parasca ◽  
Roxana Savastru ◽  
...  
Keyword(s):  
Exposure Assessment ◽  
Hyperspectral Imaging ◽  
Simulated Altitude ◽  
Altitude Exposure

scholarly journals Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia

1996 ◽  
Vol 81 (5) ◽  
pp. 1908-1910 ◽  
Author(s):  
Robert C. Roach ◽  
Jack A. Loeppky ◽  
Milton V. Icenogle
Keyword(s):  
Significant Contribution ◽  
Acute Mountain Sickness ◽  
Barometric Pressure ◽  
Normal Pressure ◽  
Normobaric Hypoxia ◽  
Simulated Altitude ◽  
Healthy Men ◽  
Altitude Exposure ◽  
Symptom Scores ◽  
Mountain Sickness

Roach, Robert C., Jack A. Loeppky, and Milton V. Icenogle.Acute mountain sickness: increased severity during simulated altitude compared with normobaric hypoxia. J. Appl. Physiol. 81(5): 1908–1910, 1996.—Acute mountain sickness (AMS) strikes those in the mountains who go too high too fast. Although AMS has been long assumed to be due solely to the hypoxia of high altitude, recent evidence suggests that hypobaria may also make a significant contribution to the pathophysiology of AMS. We studied nine healthy men exposed to simulated altitude, normobaric hypoxia, and normoxic hypobaria in an environmental chamber for 9 h on separate occasions. To simulate altitude, the barometric pressure was lowered to 432 ± 2 (SE) mmHg (simulated terrestrial altitude 4,564 m). Normobaric hypoxia resulted from adding nitrogen to the chamber (maintained near normobaric conditions) to match the inspired[Formula: see text] of the altitude exposure. By lowering the barometric pressure and adding oxygen, we achieved normoxic hypobaria with the same inspired[Formula: see text] as in our laboratory at normal pressure. AMS symptom scores (average scores from 6 and 9 h of exposure) were higher during simulated altitude (3.7 ± 0.8) compared with either normobaric hypoxia (2.0 ± 0.8; P < 0.01) or normoxic hypobaria (0.4 ± 0.2; P < 0.01). In conclusion, simulated altitude induces AMS to a greater extent than does either normobaric hypoxia or normoxic hypobaria, although normobaric hypoxia induced some AMS.

A comparison of the physiological response to simulated altitude exposure and r-HuEpo administration

2001 ◽  
Vol 19 (11) ◽  
pp. 831-837 ◽  
Author(s):  
Michael J. Ashenden ◽  
Allan G. Hahn ◽  
David T. Martin ◽  
Peter Logan ◽  
Robin Parisotto ◽  
...  
Keyword(s):  
Physiological Response ◽  
Simulated Altitude ◽  
Altitude Exposure

Splenic erythropoiesis in polycythemic response of the rat to high-altitude exposure

1980 ◽  
Vol 48 (5) ◽  
pp. 857-861 ◽  
Author(s):  
L. C. Ou ◽  
D. Kim ◽  
W. M. Layton ◽  
R. P. Smith
Keyword(s):  
Bone Marrow ◽  
Body Weight ◽  
Blood Cells ◽  
Sharp Increase ◽  
Inhibitory Influence ◽  
Red Cell ◽  
Simulated Altitude ◽  
Altitude Exposure ◽  
Cell Counts ◽  
Intact Rats

Intact rats exposed for 30 days to various levels of simulated altitude from 12,000 (3,658 m) to 20,000 ft (6,096 m) showed a sharp increase in circulating red blood cells in reticulocytes, and in spleen-to-body weight ratios above 15,000 ft (4.572 m). Nucleated erythrocytes in splenic section increased significantly at 18,000 ft (5,486 m), but not at 12,000 ft. Acute splenectomy 1 day before killing sharply reduced the reticulocyte counts at 18,000 and 20,000 ft, but the red cell counts were not reduced at any altitude by the operation. Indeed, at 18,000 ft the splenectomy significantly increased the degree of polycythemia. With altitude exposure the spleen but not the liver or the bone marrow showed an increased 59Fe uptake that was related to the degree of hypoxia. These results suggest that the rat spleen of the present strain carries the full load of the erythropoietic effort in response to a hypoxic stimulus, and that it may exert an inhibitory influence on any extraerythropoietic effort by the bone marrow. In intact rats returned from 18,000 ft to sea level, the reticulocytosis is reversed much more slowly than it is in splenectomized rats, suggesting the presence of a persistent stimulus initiated by hypoxia or a committed pool of reticulocyte precursors.

scholarly journals Blood Destruction in the Polycythemia Induced by Hypoxia

Blood ◽  
1952 ◽  
Vol 7 (3) ◽  
pp. 337-349 ◽  
Author(s):  
KURT R. REISSMANN ◽  
WILLIAM L. BURKHARDT ◽  
BERNARD HOELSCHER
Keyword(s):  
Normal Cell ◽  
Ground Level ◽  
Blood Levels ◽  
Bile Pigment ◽  
Red Cell ◽  
Simulated Altitude ◽  
Cell Destruction ◽  
Altitude Exposure ◽  
Active Mechanism ◽  
Bile Fistula

Abstract The hemoglobin catabolism during the development and during the disappearance of polycythemia induced by hypoxia was studied by measuring the total circulating hemoglobin and the daily bile pigment excretion in bile-fistula dogs before, during, and after prolonged periods of exposure to 20,000 feet simulated altitude. 1. The inscreased erythropoiesis during the first weeks of altitude exposure was accompanied by a signiflcant increase in bile pigment output. The possible sources of this pigment excretion are discussed. 2. The life spans of the red cells during altitude exposure was found to be about 115 days. No differences were observed in the longevity of the cells in animals at ground level and at altitude. 3. The normalization of the polycythemic blood levels took place within six to eight weeks after returns to ground level, and was achieved by the combined effect of a depressed erythropoiesis and of an increased blood destruction. The increase in red cell destruction observed under these conditions demonstrates the existence of an "active" mechanism of blood destrunction by which the organism is able to destroy normal blood cells before their life span is exhausted. This increased red cell destruction, however, accounted for only 21 to 39 per cent of the hemoglobin which disappeared from circulation after return to ground level. The major part of the normalization of altitude polycythemia was brought about by a temporary depression of erythropoiesis which was estimated to amount to 30 or 40 per cent of the normal cell production in the six weeks after the discontinuation of the altitude exposure.

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