Metabolic deterioration in shock state and its modulation.
The initial cellular reaction against the deleterious effects of shock-inducing stimuli apparently elevates the energy-producing capacity so that the cell is able to sustain its normal function. Several endocrine events are fundamentally important as triggering factors for this kind of reaction. As the shock state advances, cellular metabolism deteriorates progressively and cellular energy is exhausted. Depression of intracellular cAMP may induce cellular metabolic unresponsiveness to hormonal stimuli. Consistent degradation of high-energy substances, extreme deviation of the redox state in the NAD+-NADH system, and decrease of endogenous key substances such as L-carnitine ultimately may lead to a standstill of cellular enzymatic reactions (Fig. 13). Methods intended to sustain cellular membrane and enzymatic systems may offer the best contribution to the improvement of shock therapy.
D000227:Adenine Nucleotides / Q000378:metabolism; D000493:Allopurinol / Q000627:therapeutic use; D000818:Animals; D003994:Bucladesine / Q000627:therapeutic use; D002331:Carnitine / Q000172:deficiency / Q000627:therapeutic use; D000242:Cyclic AMP / Q000378:metabolism; D003593:Cytoplasm / Q000378:metabolism; D004734:Energy Metabolism; D006801:Humans; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D010084:Oxidation-Reduction; D011817:Rabbits; D051381:Rats; D012769:Shock / Q000188:drug therapy / Q000378:metabolism*; D012771:Shock, Hemorrhagic / Q000378:metabolism
D000227:Adenine Nucleotides; D000493:Allopurinol; D003994:Bucladesine; D000242:Cyclic AMP; D002331:Carnitine