The Japanese journal of physiology
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The effects of electrical stimulation of cervical sympathetic trunks for 1-min duration at supramaximal intensity with various stimulus frequencies on local cortical cerebral blood flow were investigated in urethane-anesthetized rats. Electrical stimulation with low frequency (1-2 Hz) produced a significant increase in local cortical cerebral blood flow during the stimulation. ⋯ High-frequency stimulation (20-30 Hz) produced the short-term increase during the stimulation, which was followed by the dominant and long-lasting decrease, and the local cortical CBF reached 87% (at 30 Hz) of the resting value after the end of stimulation. The response of increase in flow was abolished by intravenous administration of beta adrenergic blocking agent (propranolol, 1.3 mg/kg i.v.), while the response of decrease in flow was abolished by alpha adrenergic blocking agent (phenoxybenzamine, 0.5 mg/kg i.v.).
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To estimate the influence of ventilatory conditions on the CO2 equilibration between the alveolar gas and arterial blood during steady state hypercapnia, we measured arterial and end-tidal PCO2 (PaCO2, PETCO2) of the anesthetized rat under the following three conditions: spontaneously breathing with CO2 inhalation, artificial respiration with gas mixture containing CO2, and artificial respiration with reduced ventilatory volume (hypoventilation). In each ventilatory condition, PaCO2 correlated linearly with PETCO2. However, in spontaneously breathing animals, the PaCO2-PETCO2 difference which was positive in a control condition (without CO2 inhalation) became negative during CO2 inhalation. ⋯ These observations suggest that for a given increase in PCO2 by administration of exogenous CO2, the extent to which PaCO2 increases is smaller than that of PETCO2. This peculiar relationship together with changes in breathing pattern during CO2 inhalation likely results in "negative" PaCO2-PETCO2 difference in the spontaneously breathing animal. We conclude that the PaCO2-PETCO2 difference, either as positive or negative values, depends upon both the level of PCO2 and the ventilatory condition to increase PCO2.
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The Haldane effect coefficient in vivo and arterial-venous O2 content difference [a-v)Co2) are, more or less, influenced by the contact time (tc), PO2 and PCO2 differences between venous blood and alveolar air. To increase the accuracy of the (a-v)CO2 and the cardiac output measured by means of the rebreathing technique, factors to correct the Haldane effect (F(H] and (a-v)CO2 (F(avCO2] were obtained theoretically from the numerical solutions of simultaneous O2 and CO2 diffusions in the red blood cell. Both the factors were complicated functions of tc, the difference in PCO2 between venous blood and alveolar air, as well as (a-V)CO2. ⋯ The (a-v)CO2 was calculated by dividing the product of F(H) and the slope of the CO2 dissociation curve by that of a gas exchange ratio against the PCO2 in rebreathing air. The F(avCO2) was given by a ratio of (a-v)CO2 at any alveolar PCO2 to the standard one, in which arterial blood has the same intracellular pH as that in venous blood. It was a linear function of the difference in PCO2 between venous blood and alveolar air, whose slope was inversely related to the (a-v)CO2 itself.
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Serial measurements of extracellular fluid (ECF), and plasma volumes were evaluated in dogs before and during general anaesthesia with sodium pentobarbitone and under controlled conditions of arterial pH, pO2, pCO2, and blood pressure. Sodium pentobarbitone anaesthesia caused an early, significant rise in ECF volume with a fall in haematocrit, plasma protein, and plasma potassium concentrations. Plasma osmolality and sodium concentrations were unchanged. ⋯ It is unlikely that intracellular sodium stores contribute to a significant extent in these changes. During prolonged anaesthesia plasma volume progressively increased while total ECF volume returned towards control values. This work clarifies previous observations and suggests that major fluid movements occur during sodium pentobarbitone anaesthesia primarily associated with altered cell membrane properties and generalised haemodynamic changes.
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When mixed venous blood is oxygenated in alveolar air with higher PCO2, the PCO2 within the red cell is though to exceed the alveolar PCO2 due to the Haldane effect and to block the inward CO2 diffusion. If the direction of the CO2 diffusion is not reversed during the contact time, the HCO2-gain in the plasma will not exceed the amount estimated from venoalveolar PCO2 difference by using a CO2 dissociation curve of separated plasma. In order to clarify the validity of the above thought, the venoarterial CO2 content difference was measured by using a van Slyke apparatus and a PCO2 electrode at various alveolar PCO2 levels in rebreathing dogs. ⋯ The reduction, however, was slightly stronger in normoxia than in hyperoxia with alveolar PO2 of 300 to 420 mmHg. These data seem to support the following explanation: When venous blood was oxygenated in normoxic air with PCO2 higher than true venous, the inward CO2 diffusion was inhibited by the Haldane effect and the reversed diffusion after the oxygenation could also be disregarded during the contact time. Because the oxygenation was accelerated in hyperoxia and the direction of the CO2 diffusion was reversed earlier than in normoxia, the plasma CO2 content became higher in hyperoxia than in normoxia.