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PubMed1999

Microvascular responses to hemodilution with Hb vesicles as red blood cell substitutes: influence of O2 affinity.

Phospholipid vesicles encapsulating purified hemoglobin (HbV) were developed to provide O2-carrying capacity to plasma expanders. Microvascular perfusion was determined for HbV with different O2 affinity (P50 = 9, 16, and 30 mmHg) prepared by coencapsulating pyridoxal 5'-phosphate (PLP) at the molar ratios of [PLP]/[Hb] = 0, 0.5, and 3, respectively (cf. hamster blood, P50: 28 mmHg), and suspended in 8 g/dl human serum albumin (HSA). Eighty percent of the red blood cell (RBC) mass of conscious Syrian golden hamsters fitted with dorsal skinfold windows was substituted with either of the HbV-HSA suspensions, washed hamster RBC suspended in HSA (RBC-HSA), and HSA alone. All three HbV-HSA groups and RBC-HSA groups showed stable blood pressure and heart rate, which could not be sustained with HSA alone. Only the HbV (P50 = 9)-HSA group showed an increase in arterial O2 tension (89.8 +/- 14.7 mmHg, baseline 58.4 +/- 4.0 mmHg) because of hyperventilation, and microvascular perfusion was decreased, indicating that facilitated O2 unloading of HbV by decreasing the O2 affinity (increasing P50) with PLP as an allosteric effector is important. Microvascular perfusion and microvascular and interstitial O2 tensions in the HbV (P50 = 16 and 30)-HSA groups were significantly higher than those in the HSA group. The O2 release rate from the HbV was 18-32 s-1 vs. 4.4 s-1 for RBC. Functional capillary density was improved from 17 to 41% on average by decreasing P50 from 30 to 16 mmHg, which appears to be an optimal value for the P50 in this system.

Animals↗
PubMed1999

Plasma volume expansion with solutions of hemoglobin, albumin, and Ringer lactate in sheep.

We have measured plasma volume expansion (Evans blue and hematocrit changes) and hemodynamic responses in conscious hemorrhaged and normovolemic splenectomized sheep after a 30-min infusion of either 20 ml/kg of diaspirin cross-linked hemoglobin (DCLHb), 20 ml/kg of human albumin (Alb), or 60 ml/kg of a solution of Ringer lactate (RL). All regimens expanded blood volume and increased blood pressure and cardiac output after hemorrhage. However, only 15 +/- 3% of the infused volume of RL was evident as intravascular expansion 10-min postinfusion, compared with 67 +/- 16% and 139 +/- 139% for Alb and DCLHb, respectively. DCLHb infusions were associated with higher blood pressures and lower cardiac outputs compared with RL and Alb infusions, but the increased oxygen content of blood with DCLHb resulted in systemic delivery of oxygen similar to that of the other infusions. These differences in hemodynamics and vascular volume continued for 6 h, and at 24 h vascular volume and all hemodynamics were similar in all three groups. The better volume expansion with DCLHb may be due to greater mobilization of endogenous interstitial protein or reduced transcapillary loss as total intravascular endogenous plasma protein increased after infusion of DCLHb, whereas there was an apparent loss of endogenous intravascular protein after infusions of Alb and RL. Vasoconstriction by DCLHb is one mechanism that could lower blood-to-tissue transport of fluid and protein. In addition to its oxygen-carrying capacity and vasoactivity, DCLHb is associated with volume expansion properties out of proportion to its colloid osmotic pressure.

Animals↗
PubMed2002

Influence of hypoxia and of hypoxemia on the development of cardiac activity in zebrafish larvae.

Cardiac activity and anaerobic metabolism were analyzed in zebrafish larvae raised under normoxia (PO(2) = 20 kPa) and under chronic hypoxia (PO(2) = 10 kPa) at three different temperatures (25, 28, and 31 degrees C). Heart rate increased with development and with temperature. Under normoxia, cardiac output increased significantly at high temperature (31 degrees C), but not at 28 or at 25 degrees C. Under chronic hypoxia, however, heart rate as well as cardiac output increased at all temperatures in larvae at about hatching time or shortly thereafter. Cardiac activity of larvae raised for 2 wk after fertilization with a reduced hemoglobin oxygen-carrying capacity in their blood (hypoxemia; due to the presence of CO or of phenylhydrazine in the incubation water) was not different from control animals. Whole body lactate content of these animals did not increase. Thus there was no indication of a stimulated anaerobic energy metabolism. The increase in cardiac activity observed during hypoxia suggests that at about hatching time receptors are present that sense hypoxic conditions, and this information can be used to induce a stimulation of convective oxygen transport to compensate for a reduction in bulk oxygen diffusion in the face of a reduced oxygen gradient between environmental water and tissues. Under normoxia, however, the PO(2) gradient between environmental water and tissues and diffusional oxygen transport assure sufficient oxygen supply even if hemoglobin oxygen transport in the blood is severely impaired. Thus, under normoxic conditions and with a normal metabolic rate of the tissues, convective oxygen transport is not required until approximately 2 wk after fertilization.

Anaerobiosis↗
PubMed1984

High-altitude adaptation and maximum work performance.

The treadmill work performance of rats at sea level with normal or elevated hematocrits was compared with that of rats conditioned in a hypobaric chamber at 450 Torr for 3 wk with similar hematocrit adjustments. A mean increase in hematocrit to 62 significantly improved the work performance of rats at sea level and at ambient O2 tensions of 100, 75, and 35 Torr. By contrast, rats conditioned in a hypobaric chamber with mean hematocrits of 40 and 58 performed similarly at all O2 tensions compared with sea-level rats with hematocrits of 43. Thus, although an increase in O2-carrying capacity of the blood of sea-level animals increased work capacity, altitude adaptation did not appear to result in any positive effect on work capacity, and indeed, seemed to interfere with the beneficial effect of polycythemia on maximum work performance.

Adaptation, Physiological↗
PubMed1985

Temperature regulation in lizards: effects of hypoxia.

Temperature regulation during external (lowered lung PO2) and internal hypoxia (anemia) was examined in four species of lizards. Exposure to a hypoxic gas mixture in a thermogradient resulted in the animals lowering their selected (preferred) body temperature. A 50% reduction in the O2 carrying capacity of the blood also reduced the selected body temperature. Lizards "shuttle" when forced to select a temperature either above or below their normal selected temperature. Exposure to hypoxia decreases the upper and lower exit temperatures during shuttling. Furthermore, a decrease in the inspired O2 causes the rate of heating to no longer exceed the rate of cooling as is normal. The behavioral reduction of body temperature and the altered neural and physiological aspects of temperature regulation appear to be generalized responses to impaired O2 transport and not PO2 per se. The reduced body temperature, by lowering metabolic demand, provides an effective, even life-saving, adaptation to hypoxia.

Anemia↗
PubMed1985

Isolated perfused head of rainbow trout. I. Gas transfer, acid-base balance, and hemodynamics.

Branchial gas transfer, acid-base balance, and hemodynamics were critically evaluated and compared in Ringer-perfused and blood-perfused heads of rainbow trout. Blood perfusion stimulated O2 uptake and CO2 excretion across the gills to values more representative of intact fish. The stimulatory effect of blood on gas transfer was due to increased O2 carrying capacity (O2 uptake) and the presence of erythrocytic carbonic anhydrase (CO2 excretion). Adding carbonic anhydrase to Ringer enhanced CO2 excretion in a manner similar to blood. During Ringer perfusion, arteriovenous pH gradients were abnormal (arterial pH less than venous pH). Perfusion with blood or addition of carbonic anhydrase to Ringer reversed the pH gradients to typical in vivo levels. Branchial vascular resistance to flow was abnormally high in both Ringer- and blood-perfused preparations, primarily as a result of low dorsal aortic pressure. Input pressure increased during blood perfusion and was similar to ventral aortic pressure in vivo. Perfusion with Ringer may have caused irreversible deterioration of gill function as indicated by decreased arterial Po2 and O2 extraction effectiveness after a rapid switch from Ringer to blood perfusion. The results are discussed with reference to the suitability of perfused trout head preparations for studying gill gas transfer, acid-base balance, and hemodynamics. Comparisons are made between the perfused head preparation and intact fish as well as with other types of perfused gill preparations.

Acid-Base Equilibrium↗
PubMed1985

Blood respiratory properties in pigeons at high altitudes: effects of acclimation.

Many birds thrive at high altitudes where environmental temperatures are low. Previous studies have shown that tolerance of and acclimation to hypoxia involve cardiopulmonary and hematological adaptations. We investigated blood respiratory properties during exposure to simulated high altitude (hypobaric hypoxia) and low temperature in unanesthetized resting pigeons (Columbia livia, mean mass 0.38 kg). A control group (C) and a group acclimated to 7 km above sea level (ASL) in a hypobaric chamber at 25 degrees C (HA group) were used. All were acutely exposed to altitudes through 9 km ASL at 5 or 25 degrees C. Arterial and mixed venous blood gas tensions and O2 and CO2 content during steady state decreased with increased altitude, whereas blood lactate increased in both groups at both temperatures. Acute high-altitude exposure did not affect hematocrit, hemoglobin concentrations, or O2 carrying capacity, but at any altitude these were all greater in HA than in C birds. At 5 degrees C blood pH increased with altitude in controls but remained unchanged in HA birds. At 25 degrees C in both groups mean intracellular pH did not change, averaging 6.97, whereas extracellular (venous) pH increased with altitude. At the highest altitudes tissue O2 extraction was virtually complete in both groups. Acclimation changed blood O2 and CO2 combining properties in ways likely to improve gas transport at high altitudes. The previously unreported shifts in blood respiratory and acid-base properties with acclimation indicate that innate extrapulmonary adaptations contribute to avian hypoxia tolerance.

Acid-Base Equilibrium↗
PubMed1987

Substrate and O2 fluxes during rest and exercise in a high-altitude-adapted animal, the llama.

Llamas were trained to exercise on a treadmill at graded speeds. O2 uptake values at rest, at modest exercise (ME, 0.58 m/s), and at heavy exercise (HE, 1.84 m/s) were 0.069, 0.297, and 0.594 ml O2 X kg-1 X s-1. Corresponding values for cardiac output were 1.64, 4.39, and 6.85 ml X kg-1 X s-1. Palmitate, glucose, and lactate replacement rates (Ra values) were determined at these varying work rates using a single-bolus injection of 14C- or 3H-labeled metabolites, two at a time. Ra values for palmitate, glucose, and lactate at rest were 6.2, 61.4, and 36.1 mumol X kg-1 X min-1, respectively. During ME, the Ra values for glucose and palmitate increased about twofold but showed no further increase when exercise intensity was increased about twofold. In contrast to these results, Ra values for lactate increased much more with increasing work rate. A combination of increased perfusion (increased cardiac output) and increased lactate availability (increased plasma concentration) could account for the lactate Ra data. During prolonged ME, the Ra for lactate decreased because lactate availability decreased; concurrently, both the plasma free fatty acid availability and the Ra values for palmitate greatly increased. Because O2 carrying capacity is low in the llama (as in all high-altitude-adapted mammals), a given level of exercise required exaggerated increases in cardiac output (and hence in perfusion rates of working muscles). As a result, the flux rates of palmitate, glucose, and lactate through the plasma compartment could readily account for O2 flux rates even at relatively high sustainable rates of exercise.

Acclimatization↗
PubMed1993

Mechanisms of acute hemoconcentration in bullfrogs in response to hypoxemia.

Three general mechanisms have been proposed to explain rapid increases in red blood cell concentration in vertebrates in response to hypoxia: spleen emptying, red blood cell swelling, and decreases in plasma volume. We have experimentally tested these potential mechanisms for the hemoconcentration of red blood cells associated with hypoxemia in cold (10 degrees C), submerged bullfrogs. The mean increase of hematocrit was approximately 1.4-fold (the increase was highly variable between individual frogs) when arterial oxygen saturation was reduced from 80% to 8% by lowering ambient O2 partial pressure (PO2). The largest response was seen when arterial oxygen saturation was below 33% (a saturation that is not unusual in submerged amphibians). There was no difference between hematocrit increases during hypoxemia in spleen-ligated compared with sham-operated frogs submerged in hyperoxic, normoxic, and hypoxic water, suggesting that spleen emptying is not the primary mechanism. Increased hematocrit was not due to red blood cell swelling: mean corpuscular hemoglobin concentration increased slightly as hematocrit increased, indicating that red blood cells shrank slightly rather than swelling. Plasma volume, measured in a separate group of animals by dilution of 51Cr-labeled autologous red blood cells, decreased almost 50% during hypoxemia, closely correlated with a mean increase of 1.76-fold of hematocrit. We thus conclude that the hematocrit increase seen during hypoxemia in bullfrogs is caused by a loss of plasma volume. This has important implications for cardiovascular function, since blood viscosity, oxygen carrying capacity, and cardiac output are all affected by changes in plasma volume.

Animals↗
PubMed2001

Brain stem PO(2) and pH of the working heart-brain stem preparation during vascular perfusion with aqueous medium.

The rat working heart-brain stem preparation (WHBP) is an in situ preparation having many of the advantages associated with in vitro preparations while retaining cardiovascular response functionality and an eupnoeic respiratory motor pattern. The preparation is perfused arterially with an aqueous medium having a much lower oxygen-carrying capacity than blood. To evaluate the efficacy of the artificial perfusion in providing adequate gas exchange within the brain stem, we used polarographic PO(2) and pH microelectrodes to determine the tissue PO(2) and pH of the medulla oblongata at various depths. When the perfusate was equilibrated with 5% CO(2) and 95% O(2), average tissue PO(2) was 294 Torr and no hypoxic areas were encountered. Tissue pH was remarkably uniform throughout the tissue, and on average was only 0.04 +/- 0.02 pH units more acidic than that of the perfusate. Increasing the PCO(2) of the perfusate increased tissue PO(2) and decreased arterial resistance. Decreasing perfusate PCO(2) (while keeping pH constant) decreased tissue PO(2) and reduced the respiratory activity. These results suggest that arterial PCO(2), independent of arterial pH, is an essential variable in determining both respiratory drive and cerebrovascular perfusion. We conclude that the medulla of the WHBP is oxygenated and within a physiological pH, which accounts for the eupneic pattern of respiratory motor activity it generates. Furthermore, this preparation may be a useful model for exploring mechanisms of central chemoreception as well as the dynamics of the cerebral vasculature responses following changes in blood gases.

Animals↗
PubMed1990

Decline of erythropoietin formation at continuous hypoxia is not due to feedback inhibition.

Serum erythropoietin (EPO) levels in response to hypoxia are known to decline before an increase in blood oxygen carrying capacity. To define the possible mechanisms underlying this phenomenon, we have investigated 1) how renal EPO mRNA content and EPO production rate underlying the early kinetics of serum EPO levels change under different degrees of normobaric hypoxia, and 2) if a feedback inhibition of either EPO formation or EPO survival in the circulation exists by the hormone itself. We found that serum immunoreactive EPO levels in rats peaked after 12-h exposure to 7.5 or 9% oxygen (2,949 +/- 600 and 756 +/- 108 mU/ml, respectively, mean +/- SE) and declined to 29 and 64% of peak levels, respectively, after 36 h of hypoxia. EPO levels in response to 11.5% oxygen showed no consistent change between 12 (122 +/- 21 mU/ml, mean +/- SE) and 36 h (182 +/- 35 mU/ml) of hypoxia. The decline in EPO levels under severe hypoxia (7.5% O2) was paralleled by a marked reduction in renal EPO mRNA content, indicating that it was primarily a result of diminished hormone production. The observed reductions in serum EPO after 36 h corresponded to preceding declines of calculated EPO production rates from 163- to 62-fold (7.5% O2) and 36- to 25-fold (9% O2) basal values. Application of 50 IU recombinant human EPO to rats 12 h, 6 h, or immediately before hypoxic exposure to mimic the early increase in EPO levels did not affect endogenous EPO formation during a subsequent hypoxic exposure of 12 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

Effects of acute prolonged hypoxia on cardiovascular dynamics in dogs.

Intact anesthetized dogs were exposed for 75 min to either 5.75, 9.0, or 12.0% oxygen in nitrogen. Although pulmonary artery pressures were significantly elevated in all hypoxic exposures, systemic hypertension occurred only at the onset of severe hypoxia(5.75% O2). Coronary blood flow increased from an average of 130 during normoxia to a peak of 400 ml/100 g per min during inhalation of 5.75% O2, and coronary sinus oxygen tensions of 8 Torr and oxygen contents of 1.1 ml/100 ml were sustained for 75 min without biochemical, functional, or electrophysiological evidence of myocardial ischemia. Cardiac index (CI) increased significantly only during severe hypoxia (5.75% O2) with the greatest elevation after 30 min. Subsequently, CI decreased concomitantly with a 27% elevation in arterial hemoglobin concentration and oxygen-carrying capacity. It is concluded that the hypoxic threshold for significant elevations of cardiac output is between 6.0 and 9.0% O2.

Animals↗
PubMed1980

Cerebral blood flow during normocapnic hyperoxia in the unanesthetized pony.

The effect of hyperoxia on cerebral blood flow (CBF) was examined in 12 unanesthetized ponies. CBF was determined using radioactive microspheres, 15 micrometer in diam, durijng inspriation of the following gases: 1) room air (control); 2) 40% I2 in N2; and 3) approximately 100% O2 with 2.2-4.5% CO2 added to maintain isocapnia. CBF did not change from control values during either level of hyperoxia. However, cerebrospinal fluid (CSF) carbon dioxide tension (PCO2) increased during 40% O2 (delta 1.0 Torr) and approximately 100% O2 (delta 2.9 Torr). This rise in CSF PCO2, not due to a change in CBF, may have resulted from a decrease in the CO2 carrying capacity of cerebral venous blood during hyperoxia (Haldane effect). Although respiration did not change during 40% O2, expired minute volume increased 25% during approximately 100% O2 due to an increase in tidal volume. This rise in respiration was not associated with changes in any of the conventional stimuli to breathing (arterial pH, O2 tension, or PCO2 or CSF pH). One possible explanation was that cerebral extracellular fluid pH, in the vicinity of the central chemoreceptors, or cerebral intracellular fluid pH changed in a direction unlike CSF pH. An alternate explanation was that the CO2 in the inspired gas activated CO2-sensitive receptors in the lungs.

Acid-Base Equilibrium↗
PubMed1981

Cardiorespiratory and metabolic responses to treadmill exercise in the horse.

The purpose of this study was to measure cardiovascular, respiratory, and metabolic responses to graded treadmill exercise in the horse. A five-stage treadmill test up to 90% of predicted maximal heart rate was administered to five sedentary horses. The highest measured level of exercise produced a sixfold increase in cardiac output and a 41% elevation of stroke volume over standing values. Left ventricular, arterial, and right atrial pressures as well as the maximal time derivative of left ventricular pressure were all elevated during exercise. Under the same two conditions hematocrit (Hct) increased from 33 +/- 2 to 47 +/- 1%, oxygen uptake (VO2) from 1.1 +/- 0.1 to 32.7 +/0 2.1 1.min-1, and respiratory exchange ratio (RQ) increased from 0.83 +/- 0.02 to 0.96 +/- 0.01. In addition, three of the horses were willing to trot at a sixth stage (14 km.h-1, 11.5% grade), which elicited a VO2 of 39.8 +/- 0.31.min-1 and an RQ of 0.98 +/- 0.01. In response to the sympathetic stimulation of exercise, the horse is able to elevate Hct, hemoglobin, and oxygen-carrying capacity by emptying the spleen, thus increasing total circulating red blood cells by as much as 50%. This enabled three of the five horses used in the present study to increase aerobic metabolism almost 40-fold above resting or twice that seen in humans. Therefore, in the horse "blood-boosting" is an efficient mechanism for increasing aerobic metabolism. This finding lends further support to the view that the oxygen transport system limits maximal aerobic capacity in humans.

Animals↗
PubMed1986

Respiratory adaptation to chronic hypoxia in newborn rats.

Newborn rats were maintained in an hypoxic chamber (10% O2 in N2) from the day of birth up to 2 wk of postnatal life. Body weight (BW) and nose-tail length were less in the hypoxic exposed (H) rats than in control (C) animals growing in air. Hematocrit rose from about 37% to about 51%. Oxygen consumption (VO2), measured with a manometric method, was lower in H than in C rats; the difference remained at 5-7 days even after normalization by BW. At 5-7 days ventilation, measured with an airflow plethysmograph, was much more elevated in H rats (whether breathing 10% O2 or air) than in C rats, with an increase in both tidal volume and frequency. This indicates that the biphasic ventilatory response, characterized by an initial rise and then a fall of ventilation toward normoxic values, commonly observed in newborns during acute hypoxic challenge is an immediate but only transient response. The dry lung weight-to-BW ratio and alveolar size were larger in H than in C rats. Lung volumes at 20 cmH2O were similar, despite the smaller BW of the H rats. Hence, in the rat, chronic hypoxia in the immediate postnatal period increases O2-carrying capacity, decreases metabolic demands, increases alveolar O2 availability, and promotes structural changes in the lung that protect the gas exchange area and optimize the structure-function relationship of the lung. These results may also suggest that the lung structural alterations with chronic hypoxia should not be attributed to changes in VO2 but, eventually, to the ventilatory action of the organ.

Acclimatization↗
PubMed1987

Supramaximal exercise after training-induced hypervolemia. II. Blood/muscle substrates and metabolites.

Blood and muscle substrates and metabolites were investigated in six healthy males (ranging in age from 19 to 23 yr) during three consecutive days of supramaximal exercise training. Muscle biopsies from the vastus lateralis and arterialized blood samples from a hand vein were extracted before the exercise and at selected times during the intermittent (1 min work to 4 min rest) cycling. The results indicated that blood glucose concentration was significantly depressed (P less than 0.05) on both days 2 and 3 of the training, whereas plasma free fatty acids and blood glycerol, pyruvate, alanine, and lactate were unaffected. At the muscle level, glucose and lactate concentrations were depressed on days 2 and 3, whereas ATP and glycogen were reduced only on the final day of training. No training-induced alterations were noted for muscle glucose 6-phosphate or muscle ADP. These results indicate that the approximate 10-11% reduction in O2-carrying capacity accompanying the short-term training does not directly and negatively influence muscle energy metabolism during the exercise. Rather, the explanation for the altered muscle and blood constituents must be sought from other effects of the training such as impaired carbohydrate repletion.

Adenosine Triphosphate↗
PubMed1991

Cerebral regional capillary perfusion and blood flow after carbon monoxide exposure.

Alterations in regional cerebral blood flow (rCBF) and percent perfused capillaries (indicative of functional intercapillary distance) were determined in conscious male Long-Evans rats after reducing their blood O2-carrying capacity by exposing them to 1% CO for 12 min. rCBF was determined by the iodoantipyrine method. rCBF increased from a mean of 106 +/- 8 (SE) ml.min-1.100 g-1 before CO exposure to 173 +/- 14 ml.min-1.100 g-1 after CO exposure. There was a greater flow increase (126%) in the cerebral cortex than in the lower brain stem [pons (45%), medulla (39%)]. Presence of fluorescein isothiocyanate-labeled dextran identified the perfused capillaries before and after CO exposure. The volume fraction (Vv) and number/mm2 (Na) of all capillaries (perfused and nonperfused) in a given area of brain were determined after staining for alkaline phosphatase. The percent Vv and percent Na of perfused capillaries increased uniformly (from approximately 50% to approximately 80%) in all parts of the brain after CO exposure. In the presence of tissue hypoxia with undiminished plasma PO2, the brain vasculature allowed greater flow of blood while the microvasculature adjusted to reduce the diffusion distance for O2.

Alkaline Phosphatase↗
PubMed1992

Ventilatory and hematopoietic responses to chronic hypoxia in two rat strains.

Hilltop (H) and Madison (M) strains of Sprague-Dawley rats exhibit strikingly different susceptibilities to the effects of chronic altitude exposure. The H rats develop greater polycythemia, hypoxemia, and pulmonary hypertension. We studied ventilation, pulmonary gas exchange, tissue oxygenation, and hematologic adaptations in the two rat strains during a 50-day exposure to a simulated altitude (HA) of 5,500 m (18,000 ft). There were no strain differences among the variables we studied under sea level (SL) conditions. Within the first 14 days of hypoxic exposure, the only significant strain differences were that erythropoietin (EPO) rose much higher and erythroid activity was greater in the H rats, even though arterial Po2 and PCo2 (Pao2 and PaCo2, respectively), renal venous PO2 (Prvo2), and ventilation (VE) were equivalent in the two strains during this time. By day 14 at HA, the H rats had significantly higher erythroid activity, hematocrit (Hct), and EPO levels, significantly lower PaO2 and PrvO2, but equivalent VE and PaCO2. These changes persisted for the remainder of the exposure, except that the Hct continued to rise and the increase was greater in H rats. Despite the greater O2-carrying capacity of H rats in the later stages of hypoxic exposure, PaO2 and PrvO2 were significantly lower in H rats. There were no strain differences at either SL or HA in ventilatory responses to hypercapnia or hypoxia, in blood O2 affinity or 2,3-diphosphoglycerate, in extrarenal production of EPO, or in EPO clearance. We conclude that early in the hypoxic exposure the H rats produce more EPO at apparently equivalent levels of hypoxia, and this is the first step in the pathogenesis of the maladaptation to HA manifest by H rats. We find no consistent evidence that differences in VE contribute to the variable susceptibility to hypoxia in the two rat strains.

Altitude Sickness↗