• The Korean Journal of Pharmacology
• /
• v.10 no.1 s.15
• /
• pp.55-59
• /
• 1974

Further elucidation of the mechanism of halothane's negative inotropic action has resulted from a study of the effect of various substrates on halothane-depressed rat atria. Approximately 6 mg% halothane was required to maintain a 50% depression of the contractility of rat atria suspended in a modified Krebs-Ringer bicarbonate glucose medium, pH 7.4, $30^{\circ}C$ for 2hr. Both lactate and acetate were found to restore partially the contractility of halothane-depressed atria. The maximally effective concentration of lactate was 5 mM; for acetate it was 2.5mM. Neither 5 nor 20 mM of additional glucose was effective in restoring the force of contraction of halothane-depressed atria. The results are consistent with the hypothesis that halothane exerts at least a part of its negative inotropic effect on rat atria by inhibiting either the uptake or utilization of glucose by the myocardium. The site of blockade must be prior to the conversion of pyruvate to acetyl CoA. In our previous report dealing with the mechanism of cardiac depressant action of inhalation anesthetic halothane, it has been demonstrated that: 1) approximately 6 mg/100 ml halothane is required to maintain 50% depression of the force of contraction of isolated rat atria in Krebs-Ringer bicarbonate glucose medium; 2) pyruvate partially restores the contractility of halothane-depressed atria, but has no effect on normal atria; the partial recovery of depressed atria by the addition of sodium pyruvate is due to the effect of the pyruvate ion itself, not to the sodium ion; 4) addition of pyruvate, to atria depressed with hypertonic medium, produced only further depression. From these findings we concluded that the cardiac depressant action of halothane on rat atria is a manifestation of inhibition of glucose uptake or utilization. The present studies were undertaken to observe the effect of other substrates on halothane-depressed atria in order to substantiate our conclusion. As with the case of pyruvate, lactate and acetate also partially restored the force of contraction of halothane-depressed atria. These data are consistent with the hypothesis that halothane inhibits glucose uptake or utilization in the glycolytic cycle of the myocardium.

• Journal of Chest Surgery
• /
• v.20 no.1
• /
• pp.1-12
• /
• 1987

Respiratory care with oxygen inhalation is often a necessity to maintain life, and it is one of the important therapeutic adjuncts in respiratory disease and in intensive care after surgery. However, it has been reported that oxygen toxicity occurs after prolonged exposure to 100% 0, [Smith, 1899; Kistler et al. 1967; Schaffner et al. 1967; Rowland and Newman, 1969. Subjective symptoms of oxygen toxicity include tracheal irritation, frequent cough, some burning sensation in the trachea, tachypnea, severe dyspnea, etc. [Welch, 1963; Fisher et al, 1968; Milier et al, 1970; Clark and Lambertsen, 1971; Sackner, 1975]. Pathologic findings are atelectasis, injuries to the pulmonary capillaries and hemorrhage in the alveoli in gross specimens. There can be inflammation, proliferation of fibrin, thickening of alveolar membranes, degeneration of collagen fibers and interstitial edema in the microscopic findings. [Penrod, 1956; Cedergren, 1959; Bean, 1965; Schaffner, 1967]. Dubois and colleagues [1961] found that the amount of pulmonary surfactant was decreased in oxygen toxicity and atelectasis followed by the decreased pulmonary surfactant. Many authors reported that vital capacity, inspiratory force, pulmonary compliance, pulmonary capillary blood flow and pulmonary elasticity were deceased and arteriovenous shunting increased. [Comroe et al, 1945; Fuson et al, 1965; Kistler et al, 1966; Knowles and Blenner-hassett, 1967; Barber et al, 1978]. Many human volunteers were examined after prolonged exposure in a high oxygenated chamber and there were a few reports on animals with oxygen toxicity, subjects including rabbits. Gas partial pressures of alveoli and arteries were measured in rabbits exposed to 100% $O_2$ and the alveolar-arterial gas gradients were analyzed, which is the basis for the study of oxygen toxicity. These rabbits were divided into two groups; rabbits under natural respiration, and second group under artificial respiration with a respirator. The alveolar $PO_2$ [$P]AO_2$] and $PCO_2$ [$PACO_2$], and the arterial $PO_2$ [$PaO_2$] were measured under varying $O_2$ pressures; 15% $O_2$, 21% $O_2$ and 100% $O_2$.

• Journal of the Korean Applied Science and Technology
• /
• v.31 no.4
• /
• pp.688-693
• /
• 2014

This study is to increase the utilization of the ozonated water generator to make it easier to take advantage of the ozone water in the world today, there will be to develop a system that operates in one motion. Furthermore, olive oil and ozone is reacted with the wish to apply to the manufacturing technology. In the case of many existing products ozone generator driven mostly non-ozone system. In the case of ozone, but handwriting is implied general way pressure ozone gas leakage risks of suction force to the pump, it is the case of the challenge by using the injector, and limit the generation of ozone and ozone inhalation according to whether the water inlet leakage of existing products risk due to minimized. Despite the disadvantages of the injector system was found the effectiveness of the ozonated water production unit injector system used in this study to maintain the microbiological disinfection performance.