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This study used electrical impedance tomography (EIT) measurements of regional ventilation and perfusion to elucidate the reasons for severe gas exchange impairment reported in rhinoceroses during opioid-induced immobilization. EIT values were compared with standard monitoring parameters to establish a new monitoring tool for conservational immobilization and future treatment options. Six male white rhinoceroses were immobilized using etorphine, and EIT ventilation variables, venous admixture, and dead space were measured 30, 40, and 50 min after becoming recumbent in lateral position. Pulmonary perfusion mapping using impedance-enhanced EIT was performed at the end of the study period. The measured impedance (∆Z) by EIT was compared between pulmonary regions using mixed linear models. Measurements of regional ventilation and perfusion revealed a pronounced disproportional shift of ventilation and perfusion toward the nondependent lung. Overall, the dependent lung was minimally ventilated and perfused, but remained aerated with minimal detectable lung collapse. Perfusion was found primarily around the hilum of the nondependent lung and was minimal in the periphery of the nondependent and the entire dependent lung. These shifts can explain the high amount of venous admixture and physiological dead space found in this study. Breath holding redistributed ventilation toward dependent and ventral lung areas. The findings of this study reveal important pathophysiological insights into the changes in lung ventilation and perfusion during immobilization of white rhinoceroses. These novel insights might induce a search for better therapeutic options and is establishing EIT as a promising monitoring tool for large animals in the field. NEW & NOTEWORTHY Electrical impedance tomography measurements of regional ventilation and perfusion applied to etorphine-immobilized white rhinoceroses in lateral recumbency revealed a pronounced disproportional shift of the measured ventilation and perfusion toward the nondependent lung. The dependent lung was minimally ventilated and perfused, but still aerated. Perfusion was found primarily around the hilum of the nondependent lung. These shifts can explain the gas exchange impairments found in this study. Breath holding can redistribute ventilation.

Seven Standardbred horses were exercised on a treadmill at speeds (approximately 12 m/s) producing maximal heart rate, hypoxemia, and a mean pulmonary arterial pressure of approximately 75 mmHg. Extravascular lung water was measured by using transients in temperature and electrical impedance of the blood caused by a bolus injection of cold saline solution. Lung water was approximately 3 ml/kg body wt when standing but did not increase significantly with exertion. We conclude that any increase in fluid extravasation from the pulmonary hypertension accumulates in the lung at a level that is less than that detectable by this method. At maximal exertion, the volume of blood measured between the jugular vein and the carotid artery increased by approximately 8 ml/kg, and the actively circulating component of the systemic blood volume increased by approximately 17 ml/kg with respect to corresponding values obtained when walking before exertion. These volume increases, reflecting recruitment and dilatation of capillaries, increase the area for respiratory gas exchange and offset the reduced transit times that would otherwise be imposed by the approximately eightfold increase in cardiac output at maximal exertion.

The object of this study was to relate pulmonary capillary pressure to arterial and wedge pressures during exercise. Pulmonary vascular pressures were measured in six standardbred horses exercising at speeds equivalent to 75, 90, and 100% of maximal heart rate. Vascular pressures were measured with transducer-tip catheters and expressed relative to esophageal pressure. Pulmonary capillary pressure was estimated by the arterial-occlusion technique modified for exercise. Mean pulmonary arterial, capillary and wedge pressures increased from 30.5 +/- 6.3, 17.8 +/- 4.3, and 13.4 +/- 1.6 mmHg, respectively, at rest, to 70.5 +/- 5.2, 42.1 +/- 5.3, and 38.4 +/- 5.6 mmHg, respectively, at maximal exercise. The largest part of the increase occurred during the first level of exertion. With exercise, the pressure across the lung barely doubled at a time when the cardiac output would have increased at least fivefold. Thus the absolute resistance in both pre- and postcapillary segments must have decreased. The capillary and wedge pressures rose similarly, whereas the difference between them did not change with exertion. The fractional resistance of the precapillary segment increased with exercise. The postcapillary resistance, initially 28% of the total pulmonary vascular resistance, fell to 9% at maximal exercise. The rise (to approximately 45 mmHg) in pulmonary capillary pressure with exertion is consistent with an increase in transvascular filtration.

Pregnant rats were kept at a simulated altitude of 4,500 m (PO2 91 Torr) for the whole of gestation and returned to sea level 1 day after giving birth. During pregnancy, body weight gain and food intake were approximately 30% less than in controls at sea level. Measurements were made on the 1-day-old (HYPO) pups after a few hours at sea level. In normoxia, ventilation (VE) measured by flow plethysmography was more (+17%) and O2 consumption (VO2) measured by a manometric method was less (-19%) than in control (CONT) pups; in HYPO pups VE/VO2 was 44% greater than in CONT pups. In acute hyperoxia, VE/VO2 of HYPO and CONT pups decreased by a similar amount (15-20%), indicating some limitation in O2 availability for both groups of pups in normoxia. However, VE/VO2 of HYPO pups, even in hyperoxia, remained above (+34%) that of CONT pups. HYPO pups weighed slightly less than CONT pups, their lungs were hypoplastic, and their hearts were a larger fraction of body weight. An additional group of female rats was acclimatized (8 days) to high altitude before insemination. During pregnancy, body weight gain and food intake of these females were similar to those of pregnant rats at sea level. Measurements on the 1-day-old pups of this group were similar to those of HYPO pups. We conclude that newborn rats born after hypoxic gestation present metabolic adaptation (low VO2) and acclimatization (high VE/VO2), possibly because of hypoxemia. Maternal acclimatization before insemination substantially alters maternal growth in hypoxia but does not affect neonatal outcome.

Because chronic hypoxia in the neonatal period has long-term effects on the mechanical properties of the respiratory system (S. Okubo and J. P. Mortola, J. Appl. Physiol. 66: 1772-1778, 1989), we asked whether similar effects would occur after neonatal exposure to hypercapnia. Three groups of rats were used. The first was exposed to 7% CO2 in normoxia from day 1 to 7 after birth and then returned to normocapnia (NB-CO2). The second was exposed to the same level and duration of hypercapnia from day 36 to 42, i.e., approximately 2 wk after weaning (AD-CO2). The third was raised in normoxia and normocapnia (control). At approximately 50 days, i.e., 1-2 wk after puberty, the passive mechanical properties of the respiratory system, lung, and chest were measured during artificial ventilation in the anesthetized and paralyzed animal. No differences were observed between AD-CO2 and control. NB-CO2 had higher compliance of the lung (approximately +40%) and respiratory system (+32%) than control or AD-CO2. Average values of resistance of the total respiratory system, lung, and chest wall were consistently lower in NB-CO2 than in control and AD-CO2, although the magnitude and statistical significance of the decrease depended on the method of measurement. In a separate group of NB-CO2, lung compliance was measured during spontaneous breathing, and it averaged 34% more than in control. The exponential constant of the deflation quasi-static pressure-volume curve of the liquid-filled lungs was also significantly higher than in control.(ABSTRACT TRUNCATED AT 250 WORDS)