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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 344 (1973), S. 275-286 
    ISSN: 1432-2013
    Keywords: Acute Hypoxia ; Acute Hyperoxia ; Chronic Hypoxia ; High Altitude ; Pulmonary Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hemodynamic studies were done in nine male Holstein calves, born at sea level, at 250 m (P B 740 mm Hg) and in eight of these calves after 2 and 4 weeks at 3400 m altitude (P B 510 mm Hg). Cardiac index (CI) decreased significantly as compared to sea level after 2 weeks at altitude and it was further decreased after 4 weeks. This reduction in CI resulted from decreased stroke index (SI) with unchanged heart rate (HR). Mean pulmonary arterial pressure (PAM) rose from 26 mm Hg at sea level to 63 and 74 mm Hg after 2 and 4 weeks at 3400 m, respectively. Both pulmonary arterial systolic and diastolic pressures were substantially increased at altitude, the diastolic relatively more than the systolic pressure (4.5 fold increase vs. 2.5 fold). Aortic blood pressures (systolic, diastolic and mean) did not change significantly at 3400 m. Right ventricular (systolic) and atrial (mean) pressures increased at altitude. During acute severe hypoxia (P IO 2 55 mm Hg) at sea level CI remained essentially unchanged, while SI and HR, respectively, decreased and rose significantly; PAM was double the normoxic value. Acute hypoxia after 4 weeks at 3400 m did not elicit significant changes in blood gases and pH, CI, SI and HR while PAM increased by 25 mm Hg. There were slight reductions in CI, SI, HR and PAM during acute hyperoxia at sea level. Hyperoxia after 4 weeks at altitude did not change CI, while SI rose significantly; PAM decreased by 30 mm Hg. Apparently, the Holstein calf has a highly reactive pulmonary vascular bed to acute and chronic hypoxia which could make this cattle breed more susceptible to right heart failure during exposure to chronic hypoxia at high altitude.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Pflügers Archiv 340 (1973), S. 89-99 
    ISSN: 1432-2013
    Keywords: Panting ; Hypoxic Response ; Control of Respiration ; Thermoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ventilatory response to isocapnic hypoxia was studied in anesthetized dogs during normothermia and thermally induced panting. In the normothermic dog, minute ventilation (E), tidal volume (V T) and respiratory frequency (f) did not vary significantly with changes ofPaO2 above 80–90 mm Hg. Below this value, these three parameters increased substantially with progressively decreasingPaO2. During panting the ventilatory response was triphasic: 1. withPaO2 values above 90 mm Hg ventilation remained unaffected; 2. whenPaO2 progressively decreased from 90 to 45 mm Hg, ventilation increased significantly over the levels of ventilation reached in response to heat alone; 3. withPaO2 under 45 mm Hg ventilation abruptly decreased as compared to the second phase of the response.V T increased significantly during the second and third segments as compared to the first. Respiratory frequency progressively decreased whenPaO2 was under 60 mm Hg Isocapnic hypoxia suppressed thermally induced panting (tachypnea) but led to reduction of evaporative heat loss only at the lowest values ofPaO2. Apparently, in the panting animal chemical control of respiration is set aside by the thermoregulatory control. However, chemical regulation of respiration may set aside the normal respiratory pattern of thermal polypnea in response to acute chemical stimuli, such as arterial hypoxia.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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