The American journal of physiology
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A hypothesis for the operation and control of nasal heat exchange in reindeer is presented that originated from studies of the nasal vascular anatomy and has been supported by physiological measurements as well as test experiments on a physical prototype model of the reindeer nose. A central theme of our hypothesis is that the nasal mucosa possesses arterial and venous retia that communicate by way of capillaries and arteriovenous anastomoses. ⋯ During heat dissipation, however, the retia are perfused unidirectionally in the anterior direction, whereby the temperature gradient along the nasal mucosa is reduced and heat loss facilitated. In this situation cooled venous blood, routed by way of the dorsal nasal vein, may be distributed either to the caval veins directly, for general body cooling, or, by way of the cavernous sinus that encases the carotid rete, for selective cooling of the brain.
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Mathematical modeling and simulation techniques were used to analyze the role of medullary collecting duct NaCl transport in the urinary concentrating process. The mathematical model incorporated experimentally determined epithelial transport parameters and anatomical parameters obtained chiefly from experiments in rabbit kidneys. ⋯ However, despite optimal choice of collecting duct transport parameters and the use of experimentally determined permeability coefficients, only modest total solute gradients could be generated axially in the inner medullary interstitium, and passive luminal dilution did not occur in the thin ascending limb. We conclude: 1) Axial heterogeneity of transport properties along the inner medullary collecting duct must be assumed to explain in vivo findings from micropuncture and microcatheterization studies. 2) Active NaCl transport from the inner medullary collecting ducts is important chiefly for efficient conservation of NaCl rather than for concentration of solutes in the renal inner medulla. 3) Important inconsistencies exist between several previously reported experimental observations and the theoretical requirements for passive luminal dilution in the thin ascending limb of Henle's loop.
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The metabolic effects of NaHCO3 therapy in hypoxic lactic acidosis were evaluated in the anesthetized dog. Hypoxic lactic acidosis was induced by ventilating the dogs with a hypoxic gas mixture of 8% O2/92%N2, resulting in arterial PO2 of less than 30 mmHg, pH below 7.20, bicarbonate less than 12 mM, and lactate more than 7 mM. In this situation lactate accumulates because of overproduction of lactate by gut and carcass in the presence of a diminished capacity of the liver to extract lactate. ⋯ Concomitantly NaHCO3-treated animals showed a decrement in liver and gut blood flow that did not occur with NaCl treatment. Only NaHCO3 therapy was associated with a further decrease of liver intracellular pH, which could be attributed to both an increase in the CO2 load to the liver and increased tissue lactate levels, which were not observed with NaCl or no therapy. Additionally, liver lactate extraction was not improved by administration of NaHCO3 or NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
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Pulmonary arterial occlusion pressure (Ppao) may not accurately reflect left ventricular filling pressure (LVFP) during ventilation with positive end-expiratory pressure (PEEP) because increases in pleural pressure (Ppl) increase measured intrathoracic vascular and cardiac chamber pressures relative to atmospheric while decreasing LVFP by decreasing venous return. Steady-state values of Ppao off PEEP are not useful in understanding the hemodynamics on PEEP because of changes in blood volume distribution and ventricular afterload associated with the removal of PEEP. ⋯ For all conditions at low LVFP (less than 9 Torr), nadir Ppao reflects Platm better than on-PEEP Ppao, while at higher LVFP (greater than 9 Torr), on-PEEP Ppao better reflects Platm than nadir Ppao (P less than 0.05). Accurate predictions of on-PEEP Platm can be made using both on-PEEP and nadir Ppao values in a multiple regression equation.
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This study examined the relative roles of the right vs. left vagi in mediating the inhibitory influence of vagal sensory input on sympathetic outflow to the cardiovascular system. This objective was pursued through examination of responses to 1) interruption of tonic vagal input and 2) intracoronary administration of veratridine (Bezold-Jarisch effect). Bilateral vagal cold block (BVB) (n = 16) increased arterial pressure 25 +/- 3 mmHg and heart rate 66 +/- 7 beat/min, whereas right vagal cold block (RVB) and left vagal cold block (LVB) increased arterial pressure 13 +/- 2 and 4 +/- 2 mmHg, respectively. ⋯ During RVB the depressor effect of veratridine was reduced to -18 +/- 5 mmHg, and changes in heart rate or LV (dP/dt)max were abolished. Veratridine administration during LVB decreased arterial pressure (-39 +/- 6 mmHg), heart rate (-22 +/- 6 beat/min), and LV (dP/dt)max (-250 +/- 60 mmHg). We conclude that in the conscious dog the tonic inhibitory influence of vagal afferent nerves on vasomotor outflow is predominantly associated with the right vagus as in Bezold-Jarisch effect.