[Developmental trends in legislature on the field of emission prevention (proceedings)].
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Biomedical subjects
Publications and source records attributed to R Elsner.
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Stimulation of the carotid-body chemo-receptors by asphyxia during an apnoeic episode may contribute to the vagally mediated cardiac arrest and sudden death that sometimes occurs in man. Apnoeic asphyxia may be induced centrally or reflexly by stimulation of upper airways receptors. Conditions associated with apnoeic asphyxia and in which the risk is likely to be greatest include intubation, laryngoscopy and bronchoscopy; accidents involving underwater swimming; inhalation of sympathomimetic amines in aerosols by asthmatic patients; and chronic hypoventilation syndromes. These reflexes may be responsible for some victims of sudden infant death syndrome. Stimulation of the carotid bodies normally produces hyperventilation and bradycardia. When apnoea occurs centrally or reflexly, carotid chemoreceptor excitation resulting from asphyxia now causes a much enhanced bradycardia and even cardiac arrest, but paradoxically does not usually affect respiration. These reflexes and their interactions normally serve protective and purposeful functions, but may under certain circumstances become exaggerated and put the patient's life at risk.
Several hundred thousand northern fur seals (C. ursinus) are born each summer during July at St. Paul Island in the Bering Sea. The weather in the area is usually cold, wet, and windy during the breeding season. At birth the pups are small (5--6 kg) and insulated only by a partly wettable pelt and a 2- to 4-mm layer of blubber. In air, the pups' lower critical temperature appears to be below the 6 degrees C 50-yr record low July temperature for the islands. During rainy weather much of the insulative value of the pelt is lost, and the pups, which already have a high resting metabolic rate of 3.5 W.kg-1, must increase heat production by shivering and/or nonshivering thermogenesis to maintain deep body temperature. The high level of metabolism (up to 18 W.kg-1) is supported by a very rich milk. The pups will, nevertheless, become hypothermic if their insulation is not improved through peripheral vasoconstriction and shedding of water from the pelt by periodic shudder. Even with these protections the newborn and very young pups are brought close to their limit of tolerance during rainy and windy days. Unfit pups are likely to succumb under such circumstances.
Studies have been carried out on human erythrocytes in vitro to clarify the deficit of pyruvate formation under conditions when 2,3 DPG is degraded. The results lead to the conclusion that there exist a cross connection between the glycolytic and the oxidative pentose phosphate pathway which is mediated by the NADP/NADPH couple. NADPH serves as additional reducing equivalent in the reaction of the LDH. In the absence of glucose the pool of the metabolites of the pentose phosphate pathway is able to supply glucose-6-phosphate for the production of NADPH by recombination. The reaction of NADPH at the LDH is probably of significance under in vivo conditions.
Ouabain exerts only a minor effect on ATP breakdown at 37 degrees C and practically none at 4 degrees C. The effect is less at higher pH values. At 4 degrees C the rates of breakdown at ATP, AMP and of 2,3 P2G are nearly two orders of magnitude less than at 37 degrees C.
1) The rate of 2,3-bisphosphoglycerate breakdown is independent of pH value. 2) The adenine nucleotide pattern at alkaline pH values with its characteristic lowering of ATP and the accompanying accumulation of fructose-1,6-bisphosphate is caused by a relative excess of the activity of the hexokinase-phosphofructokinase system as compared wity pyruvate kinase. 3) The breakdown of adenine nucleotides proceeds via AMP mainly through phosphatase and not via AMP deaminase. 4) The constancy of the sum of nucleotides as long as glucose is present is postulated to be due to resynthesis via adenosine kinase which competes successfully with adenosine deaminase. 5) A procedure is given to calculate ATPase activity of glucose-depleted red cells. The results indicate that the ATPase activity is less at lower pH values and declines with time. An ATPase with a high Km for ATP is postulated. 6) During glucose depletion ATP production is mostly derived from the breakdown of 2,3-bisphosphoglycerate and the supply from the pentose phosphate pool both of which proceed at a constant rate. The contribution of pentose phosphate from the breakdown of adenine nucleotides amounts to 40% of the lactate formed at pH 6.8 and is about twice the lactate at pH 8.1.
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A systematic study of the pH-dependent changes in the range 6.6--7.4 of 2,3-bisphosphoglycerate and the adenine nucleotides was performed in the presence and absence of glucose during transitional and steady states. 1. The results indicatethat 2,3-gisphosphoglycerate phosphatase breaks down 2,3-bisphosphoglycerate nearly independent of pH at a rate of 480 mumol 2,3-bisphosphoglycerate x1 cells-1xh-1.2,3-Bisphosphoglycerate mutase is practically completely inhibited below pH value increases in long-term experiments with lower 2,3-bisphosphoglycerate levels. The formation of pyruvate corresponds to the breakdown of 2,3-bisphosphoglycerate afterconsumption of an unknown reducing substance.
A systematic study of the pH dependent changes in the range 6.6--7.4 of 2,3 bisphosphoglycerate (2,3-DPG) was performed in the presence and absence of glucose during transitional and steady states. The results indicate that 2,3-DPGase breaks down 2,3-DPG nealy independent of pH at a rate of 480 mu moles 2,3-DPG/1 cells.h. The 2,3-DPG mutase is practically completely inhibited below pH 6.9. The 2,3-DPG level in the presence of glucose reaches a pH dependent steady state after about 18 h. The share of the 2,3-DPG bypass in the steady state decreases from 24% at pH 7.4 to 12% at pH 7.0. The formation of pyruvate corresponds to the beadkdown of 2,3-DPG after consumption of an unknown reducing substance.
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The time course of the rate of the glycolysis of human erythrocytes and of some metabolites were determined before and after rapid deoxygenation at constant intracellular pH. For this purpose stripped deoxygenated haemoglobin was used as a rapid oxygen acceptor. Deoxygenation causes an increase of the glycolytic rate by 26%. Glucose 6-phosphate is decreased while the adenine nucleotides and 2,3-bisphosphoglycerate remain constant. Fructose 1,6-bisphosphate and the triose phosphates decrease transiently before rising. The data can be explained by increased binding of phosphocompounds to deoxygenated as compared with oxygenated haemoglobin. Thereby the control enzymes hexokinase and phosphofructokinase are influenced. It is concluded that under physiological conditions changes in the oxygenation state of haemoglobin per se alter the glycolytic rate.