Susceptibility to high-altitude pulmonary edema in Madison and Hilltop rats. I. Ventilation and fluid balance

1995 ◽  
Vol 78 (6) ◽  
pp. 2279-2285
Author(s):  
G. L. Colice ◽  
Y. J. Lee ◽  
J. Chen ◽  
H. K. Du ◽  
G. Ramirez ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Minute Ventilation ◽  
Plasma Renin ◽  
Barometric Pressure ◽  
Simulated Altitude ◽  
Sprague Dawley ◽  
Lung Water ◽  
Fluid Handling ◽  
High Altitude Pulmonary Edema

The pathogenesis of high-altitude pulmonary edema (HAPE) is not well understood. Ventilation and fluid-handling abnormalities at high altitude (HA) may play a role in HAPE. Because ventilatory and cardiopulmonary responses to chronic HA exposure in the Hilltop (H) strain of Sprague-Dawley rat are different from those in the Madison (M) strain, it was hypothesized that these strains would have different susceptibilities to developing HAPE. M and H rats were studied at sea level (SL) and in a hypobaric chamber after 9 and 12 h at a simulated altitude of 24,000 ft (barometric pressure = 295 mmHg) and 1, 12, and 24 h at a simulated altitude of 18,000 ft (barometric pressure = 380 mmHg). Both strains developed HAPE, but the M rat was more susceptible to HAPE, as demonstrated by a higher mortality rate from hemorrhagic pulmonary edema after 9 h at 24,000 ft and an earlier increase in lung water after exposure to 18,000 ft. Minute ventilation was similar in both strains at HA, but arterial PO2 was significantly higher in the M rat. Both strains had a significant decrease in fluid intake and negative sensible water balance at HA. No changes in plasma renin activity, aldosterone concentrations, antidiuretic hormone levels, and atrial natriuretic peptide levels were found at HA. The increased susceptibility of the M rat to HAPE is therefore not explained by ventilation or fluid-handling abnormalities.

Viral respiratory infection increases susceptibility of young rats to hypoxia-induced pulmonary edema

1998 ◽  
Vol 84 (3) ◽  
pp. 1048-1054 ◽  
Author(s):  
Todd C. Carpenter ◽  
John T. Reeves ◽  
Anthony G. Durmowicz
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Respiratory Infection ◽  
Sendai Virus ◽  
Lung Water ◽  
Young Rats ◽  
Cell Counts ◽  
High Altitude Pulmonary Edema ◽  
Viral Respiratory Infection ◽  
Viral Respiratory

Recent clinical observations of a high incidence of preexisting respiratory infections in pediatric cases of high-altitude pulmonary edema prompted us to ask whether such infections would increase the susceptibility to hypoxia-induced pulmonary edema in young rats. We infected weanling rats with Sendai virus, thus causing a mild respiratory infection. Within 7 days of infection, Sendai virus was essentially undetectable by using viral culture and immunohistochemical techniques. Animals at day 7 of Sendai virus infection were then exposed to normobaric hypoxia (fraction of inspired O2= 0.1) for 24 h and examined for increases in gravimetric lung water and in vascular permeability, as well as for histological evidence of increased lung water. Bronchoalveolar lavage was performed on a separate series of animals. Compared with control groups, infected hypoxic animals showed significant increases in perivascular cuffing, gravimetric lung water, and lung protein leak. In addition, infected hypoxic animals had increases in lavage fluid cell counts and protein content compared with controls. We conclude that young rats, exposed to moderate hypoxia while recovering from a mild viral respiratory infection, may demonstrate evidence of early pulmonary edema formation, a finding of potential relevance to human high-altitude pulmonary edema.

Abnormal control of ventilation in high-altitude pulmonary edema

1988 ◽  
Vol 64 (3) ◽  
pp. 1268-1272 ◽  
Author(s):  
P. H. Hackett ◽  
R. C. Roach ◽  
R. B. Schoene ◽  
G. L. Harrison ◽  
W. J. Mills
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
High Frequency ◽  
Minute Ventilation ◽  
Causative Role ◽  
Hypoxic Ventilatory Response ◽  
Ventilatory Responses ◽  
High Altitude Pulmonary Edema ◽  
Arterial O2 Saturation

We wished to determine the role of hypoxic chemosensitivity in high-altitude pulmonary edema (HAPE) by studying persons when ill and upon recovery. We studied seven males with HAPE and seventeen controls at 4,400 m on Mt. McKinley. We measured ventilatory responses to both O2 breathing and progressive poikilocapnic hypoxia. Hypoxic ventilatory response (HVR) was described by the slope relating minute ventilation to percent arterial O2 saturation (delta VE/delta SaO2%). HAPE subjects were quite hypoxemic (SaO2% 59 ± 6 vs. 85 ± 1, P less than 0.01) and showed a high-frequency, low-tidal-volume pattern of breathing. O2 decreased ventilation in controls (-20%, P less than 0.01) but not in HAPE subjects. The HAPE group had low HVR values (0.15 ± 0.07 vs. 0.54 ± 0.08, P less than 0.01), although six controls had values in the same range. The three HAPE subjects with the lowest HVR values were the most hypoxemic and had a paradoxical increase in ventilation when breathing O2. We conclude that a low HVR plays a permissive rather than causative role in the pathogenesis of HAPE and that the combination of extreme hypoxemia and low HVR may result in hypoxic depression of ventilation.

scholarly journals Exercise Responses to Metabolic Function on High Altitude Pulmonary Edema Susceptible Individuals

2018 ◽  
Vol 3 (3) ◽  
pp. 224
Author(s):  
Kaushik Halder ◽  
RK Gupta ◽  
Anjana Pathak ◽  
Montu Saha
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Sea Level ◽  
Past History ◽  
Minute Ventilation ◽  
Metabolic Responses ◽  
Prior History ◽  
High Altitude Pulmonary Edema ◽  
History Of ◽  
Exercise Induced

<p>The study was aimed to evaluate and compare resting and exercise induced metabolic responses between acclimatized high altitude pulmonary edema (HAPE) susceptible (HAPE-s) and HAPE resistance (HAPE-r) volunteers at sea level. A group of 14 Indian soldiers volunteered for this study, divided into two groups, (i) HAPE-s, with past history of HAPE [n<sub>1</sub> = 7; age = 33.3 ± 4.5 (M ± SD)] and (ii) HAPE-r, with prior history of repeated exposure to high altitude and without suffering HAPE [n<sub>2</sub> = 7; age = 31.9 ± 4.2 (M ± SD)]. Respiratory frequency (f<sub>R</sub>), tidal volume (<sub>T</sub>), minute ventilation (<sub>E</sub>), oxygen consumption (O<sub>2</sub>), carbon dioxide output (CO<sub>2</sub>), heart rate (HR) and respiratory quotient (RQ) were recorded on all the volunteers during resting and exercise conditions. Ventilatory equivalent for oxygen (EqO<sub>2</sub>) and oxygen pulse (O<sub>2</sub>P) were calculated. Significant differences were observed between HAPE-s and HAPE-r volunteers in f<sub>Rrest </sub>(25.3% higher), O<sub>2</sub>P<sub>rest </sub>(23.7% lower), <sub>Emax</sub> (50.9% lower) (all P&lt;0.05), f<sub>Rmax </sub>(55.7% lower), O<sub>2max </sub>(55.5% lower), O<sub>2</sub>P<sub>max </sub>(34.2% lower) (all P&lt;0.01) and CO<sub>2max</sub> (42.1% lower, P&lt;0.001). Rest of the parameters did not show any significant differences between the study groups. The study revealed that resting and exercise induced metabolic responses of HAPE-r volunteers was better as compared to acclimatized HAPE-s volunteers at sea level.</p>

scholarly journals The Oxygen Transport Triad in High-Altitude Pulmonary Edema: A Perspective from the High Andes

2021 ◽  
Vol 18 (14) ◽  
pp. 7619
Author(s):  
Gustavo Zubieta-Calleja ◽  
Natalia Zubieta-DeUrioste
Keyword(s):  
Pulmonary Edema ◽  
High Altitude ◽  
Oxygen Transport ◽  
Acute Mountain Sickness ◽  
Breath Holding ◽  
Acid Base Balance ◽  
Initial Exposure ◽  
High Altitude Pulmonary Edema ◽  
Tolerance To Hypoxia ◽  
Dynamic Pump

Acute high-altitude illnesses are of great concern for physicians and people traveling to high altitude. Our recent article “Acute Mountain Sickness, High-Altitude Pulmonary Edema and High-Altitude Cerebral Edema, a View from the High Andes” was questioned by some sea-level high-altitude experts. As a result of this, we answer some observations and further explain our opinion on these diseases. High-Altitude Pulmonary Edema (HAPE) can be better understood through the Oxygen Transport Triad, which involves the pneumo-dynamic pump (ventilation), the hemo-dynamic pump (heart and circulation), and hemoglobin. The two pumps are the first physiologic response upon initial exposure to hypobaric hypoxia. Hemoglobin is the balancing energy-saving time-evolving equilibrating factor. The acid-base balance must be adequately interpreted using the high-altitude Van Slyke correction factors. Pulse-oximetry measurements during breath-holding at high altitude allow for the evaluation of high altitude diseases. The Tolerance to Hypoxia Formula shows that, paradoxically, the higher the altitude, the more tolerance to hypoxia. In order to survive, all organisms adapt physiologically and optimally to the high-altitude environment, and there cannot be any “loss of adaptation”. A favorable evolution in HAPE and pulmonary hypertension can result from the oxygen treatment along with other measures.

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