PubMed · 4194724
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M Carruthers, P Taggart, W Somerville. 1970-08-22. Plasma-catecholamine estimations.. https://doi.org/10.1016/s0140-6736(70)90034-6
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It has been suggested that hyperventilation and the disproportionate increase in VCO2 versus VO2 above the ventilatory threshold (V(TH)) in ramp exercise are due to the production of nonmetabolic CO2 in muscle because of lactic acid buffering by plasma bicarbonate entering the cell in exchange with lactate [Wasserman, K., 1982. Dyspnea on exertion. Is it the heart or the lungs? JAMA 248, 2039-2043]. According to this model, plasma standard bicarbonate concentration decreases in a approximately 1:1 ratio with the increase in plasma lactate concentration, 1 mmol of CO2 is generated above that produced by aerobic metabolism for each mmol of lactic acid buffered, and nonmetabolic CO2 produced in the muscle is partly responsible for hyperventilation because of the resulting increase in the CO2 flow to the lungs. The present report shows that this model is not consistent with experimental data: (1) bicarbonate is not the main buffer in the muscle; (2) the decrease in standard bicarbonate concentration is not the mirror image of the increase in lactate concentration; (3) buffering by bicarbonate does not increase CO2 production in muscle (no nonmetabolic CO2 is produced in tissues); (4) the CO2 flow to the lungs, which should not be confused with VCO2 at the mouth, does not increase at a faster rate above than below V(TH). The disproportionate increase in VCO2 at the mouth above V(TH) is due to hyperventilation (not the reverse) and to the low plasma pH which both reduce the pool of bicarbonate readily available in the body.
The coordination chemistry of Zn in an N(3)ArOH environment has been explored. The ligands are based on calix[6]arenes that present two imidazole arms and an amino phenol moiety at the narrow rim. Three different types of complexes have been characterized. One is dicationic with Zn(2+) coordinated to the three nitrogen atoms and to the oxygen of the phenol group of the calix[6]ligand. This complex is very sensitive to exogenous coordinating molecules and exists as a 5-coordinate species due to the endo-complexation of a guest. The second species is a monocationic complex for which the phenol group has been deprotonated. The resulting N(3)ArOZn complex can also bind a guest ligand albeit with a lower affinity than the dicationic complex. The third species is neutral. It can be obtained upon reaction with a base to yield a hydroxo complex or with an anion such as a chloride that coordinates the metal center from the outside of the calixarene cavity. The simultaneous binding of two anionic donors decreases the Zn Lewis acidity, allowing an impressive conformational reorganization of the system. One imidazole arm is released by the metal center. The other one undergoes self-inclusion into the pi-basic calixarene cavity because the low affinity of the metal center for neutral ligand does not allow the endo-coordination of an exogenous guest. Hence, the calix[6]N(3)ArOH-based Zn complexes act as an acid-base switch for guest binding. Several aspects of this system appear reminiscent of Zn-peptidases of the astacin and serralisin families.
For many years it has been apparent from estimates of the anion gap and the strong ion gap that anions of unknown identity can be generated in sepsis and shock states. Evidence is emerging that at least some of these are intermediates of the citric acid cycle. The exact source of this disturbance remains unclear, because a great many metabolic blocks and bottlenecks can disturb the anaplerotic and cataplerotic pathways that enter and leave the cycle. These mechanisms require clarification with the use of tools such as gas chromatography-mass spectrometry.