Predominantly, Hoplias malabaricus inhabits stagnant 0, poor environments, whereas Hoplias lacrrdae occurs in well-aerated streams. The present study evaluates the influence of mode of life on 0, uptake and gill ventilation in equally-sized (300 g) specimens of this genus at 25-C. Comparing the species, H . lacerdae was characterized by the highest 0, uptake and gill ventilation combined with a relatively higher cost of breathing and a lower 0, extraction. Both species substantially increased ventilation in response to hypoxia with the difference that H. malaharicus exclusively augmented tidal volume, whereas H. lacerdae also increased breathing frequency.

In light of the relationship of lungfish to the origin of tetrapods, information on the respiratory biology of lungfish can give insight into the functional morphological and physiological prerequisites for the conquest of land by the first tetrapods. Stereological methods were employed in order to determine the respiratory surface area and thickness of the water-blood barrier or air-blood of the gills, lungs, and skin, respectively, of the South American lungfish Lepidosiren paradoxa. The morphometric diffusing capacity was then determined by multiplying by the appropriate Krogh diffusion constants (K). Our results indicate a total diffusing capacity of all respiratory organs of 0.11 mL min(-1) mmHg(-1) kg(-1), which is more than twice the value of the physiological diffusion capacity (approximately 0.04 mL min(-1) mmHg(-1) kg(-1)). Of this, 99.15% lies in the lungs, 0.85% in the skin, and only 0.0013% in the gills. Since K for CO(2) is 20-25 times greater than for O(2), diffusing capacity of CO(2) through the skin is potentially important. That of the gills, however, is negligible, raising the question as to their function. Our results indicate that the morphological prerequisites for terrestrial survival with regard to supporting aerobic metabolism already existed in the lungfish.

Previous studies showed that leptin-deficient (ob/ob) mice develop obesity and impaired ventilatory responses to CO2 (trueV.normalE − CO2). In this study, we examined if leptin replacement improves chemorespiratory responses to hypercapnia (7 % CO2) in ob/ob mice and if these effects were due to changes in body weight or to the direct effects of leptin in the central nervous system (CNS). trueV.normalE−CO2 was measured via plethysmography in obese leptin-deficient- (ob/ob) and wild-type-(WT) mice before and after leptin (10 μg/2 μl day) or vehicle (phosphate buffer solution) were microinjected into the fourth ventricle for four consecutive days. Although baseline trueV.normalE was similar between groups, obese ob/ob mice exhibited attenuated trueV.normalE−CO2 compared to WT mice (134±9 versus 196±10 ml min−1). Fourth ventricle leptin treatment in obese ob/ob mice significantly improved trueV.normalE−CO2 (from 131 ± 15 to 197 ± 10 ml min−1) by increasing tidal volume (from 0.38±0.03 to 0.55±0.02 ml, vehicle and leptin, respectively). Subcutaneous leptin administration at the same dose administered centrally did not change trueV.normalE−CO2 in ob/ob mice. Central leptin treatment in WThad no effect on trueV.normalE−CO2. Since the fourth ventricle leptin treatment decreased body weight in ob/ob mice, we also examined trueV.normalE−CO2 in lean pair-weighted ob/ob mice and found it to be impaired compared to WT mice. Thus, leptin deficiency, rather than obesity, is the main cause of impaired trueV.normalE−CO2 in ob/ob mice and leptin appears to play an important role in regulating chemorespiratory response by its direct actions on the CNS.

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