The American journal of physiology
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We studied the effects of metabolic and respiratory acidosis (pH 7.20) and alkalosis (pH 7.60) on pulmonary vascular tone in 32 pentobarbital-anesthetized dogs ventilated with hyperoxia (inspired oxygen fraction, FIO2 0.40) and with hypoxia (FIO2 0.10). Ventilation, pulmonary capillary wedge pressure (Ppw), and cardiac output (3 l.min-1.m-2) were maintained constant to prevent passive changes in pulmonary arterial pressure (Ppa). Metabolic acidosis and alkalosis were induced with HCl (2 mmol.kg-1.h-1) and NaHCO3-Na2CO3 (5 mmol.kg-1.h-1) infusions, respectively, and respiratory acidosis and alkalosis by modifying the inspiratory CO2 fraction. ⋯ Linear relationships were found between pH and Ppa-Ppw gradients. These data indicate that in intact anesthetized dogs, metabolic acidosis and alkalosis, respectively, enhance and reverse hypoxic pulmonary vasoconstriction (HPV). Respiratory acidosis did not affect HPV and respiratory alkalosis blunted HPV, which suggests an pH-independent vasodilating effect of CO2.
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At 37 degrees C, pH 7.4, carbonic anhydrase activity (kenz) of disrupted rat renal proximal tubules and cortical mitochondria was 2.5 +/- 0.8 (n = 3) and 0.15 +/- 0.40 (n = 3) ml.mg-1.s-1, respectively. Turnover number for renal mitochondrial carbonic anhydrase (CA V) was 24,000 s-1. CA V activity of intact mitochondria was completely inhibited by 0.15 microM ethoxzolamide (EZ). ⋯ At no pyruvate concentration was there a change in the rate of glucose production when tubules were incubated in 50 mM HCO3- buffer with 1.6 microM EZ. These data also support the hypothesis that CA V provides the HCO3- substrate for pyruvate carboxylation when there is a high rate of intracellular CO2 production and external CO2 is low. It is further concluded that the cytosolic carbonic anhydrase (CA II) and the membrane-bound carbonic anhydrase (CA IV) are not involved in glucose synthesis from pyruvate.
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Comparative Study
Arteriovenous oximeter for O2 content difference, O2 saturations, and hemoglobin content.
We combined two spectrophotometric oximeters to measure continuously and simultaneously arteriovenous O2 content difference (AVOD) as well as arterial and venous oxyhemoglobin saturations (SaO2, SvO2) and total hemoglobin concentration (Hb). AVOD of the flowing arterial and venous whole blood was determined by the method of Guyton et al. (J. Appl. ⋯ AVOD, SaO2, SvO2, and Hb were compared with the data of the arterial and venous blood sampled near the oximeter cuvettes and measured with an IL282 CO oximeter. In one dog experiment and one in vitro blood experiment, AVOD data of the same arterial and venous blood were compared by connecting the present oximeter in series with an A-VOX Systems oximeter developed by Shepherd and Burgar. The results showed that the new arteriovenous oximeter can continuously measure AVOD, SaO2, SvO2, and Hb over wide ranges with reasonable accuracy.
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Body temperature, plasma responses, and subjective ratings of thirst and hotness were studied in 5 older men (OM, 61-67 yr) and 6 younger men (YM, 21-29 yr) during 180-min thermal dehydration and subsequent 60-min rehydration (45 degrees C, 25% relative humidity). Rectal temperature (Tre) increased more rapidly and to a greater magnitude in OM, while average total body sweat rates and chest sweat rates were not significantly different. During dehydration, both OM and YM lost similar body weight (1.52 +/- 0.11 vs. 1.55 +/- 0.22%, mean +/- SE). ⋯ Within 30 min of drinking, YM had restored Pv and Posm, whereas OM showed slower responses, restoring Posm after 60 min and Pv only after a subsequent 30 min at 25 degrees C. Despite a higher Tre and greater change in Pv and Posm, OM rated themselves less thirsty and not significantly hotter than YM. These findings suggest that aging results in decreased ability to maintain Tre during heat stress and that the mechanisms comprise a combination of alterations in body fluid distribution and perception.
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The effect of verapamil (VER) resuscitation from shock on cardiac function, regional blood flow, as well as skeletal muscle transmembrane potential (TMP) and electrolyte redistribution were studied. Two hours of hypotensive shock in the dog significantly impaired cardiac function and coronary perfusion; TMP fell from 89.9 +/- 0.9 to 75.1 +/- 1.2 mV. Skeletal muscle (SMS) extracellular water decreased 40 +/- 2%, whereas intracellular sodium and chloride increased and intracellular potassium fell. ⋯ SMS calcium was lower in VER dogs (148 +/- 4 micrograms/g) compared with dogs treated with fluid alone (322 +/- 24 micrograms/g, P = 0.01). Myocardial calcium fell in all dogs after volume replacement regardless of calcium-channel blockade (VER: 148 +/- 8, Ringer: 165 +/- 17 micrograms/g; P greater than 0.05). Our data indicate a potential role for calcium-entry blockade in the treatment of hemorrhagic shock.