PubMed · 8753554
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K Matsuzaki. 1995. [Base excess and buffer base].. https://pubmed.ncbi.nlm.nih.gov/8753554/
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In the present paper we tried to test the hypothesis that nonspecific flunitrazepam-membrane interactions are consistent with drug molecules accommodated between lipid molecules, becoming an integral part of the bilayer. We developed a spectrophotometric method to determine FNTZH+ equilibrium dissociation constant and applied it to the study of the acid-base equilibria of this drug in homogeneous media of different polarity. In these conditions, pK decreased with the decrement in the dielectric constant (D) of the media. These results, analyzed under the light of the theory developed by Fernandez and Fromherz (1977; J. Phys. Chem. 81, 1755-1761) let us infer that flunitrazepam is localized a region with D = 60. This D value is lower that Dwater = 78 and higher than D of hydrocarbon chains zone (D = 2-5) and would correspond to D of the region of polar groups. This result is compatible with the hypothesis.
Larval Ambystoma tigrinum were cannulated nonocclusively in the truncus arteriosus and allowed to recover for 20-24 hr. In one group of animals a peritoneal cannula was inserted in order to induce acidosis through the injection of lactic acid (2 micromol/g). Immediately following a control blood sample (hr 0), lactic acid was injected, and blood samples were collected at 1, 4, 8, and 24 hr and analyzed for pH, PCO2, PO2, [HCO3-], and aldosterone. These animals exhibited a significant metabolic acidosis, which was accompanied by a significant increase in plasma aldosterone, and recovered in approximately 24 hr. Additional groups of animals were subjected to the same acidosis and also received either saralasin (0.01 or 1 microg/g at 0, 1, and 4 hr) or captopril (0.01-0.1 or 1 microg/g at 0, 1, and 4 hr). The groups of animals whose renin-angiotensin system was blocked by saralasin or captopril did not show a significant change in their ability to recover from the metabolic acidosis. Furthermore, saralasin and captopril were ineffective in inhibiting the normal rise in circulating aldosterone in response to acidosis. In another group of animals, synthetic human angiotensin II (1 microg/g; Ang II) was infused immediately following the control blood sample (hr 0) and blood samples were collected at 2, 4, 6, and 8 hr and assayed for aldosterone. Plasma aldosterone levels increased significantly from 133 +/- 91 pg/ml at hr 0 to a maximum of 3288 +/- 519 pg/ml at hr 4. Sham-treated animals did not increase circulating aldosterone. When Ang II (1 microg/g) and saralasin (1 microg/g) were given simultaneously, however, the rise in plasma aldosterone was only about 35% that of animals which received Ang II alone. We conclude that administration of Ang II leads, either directly or indirectly, to synthesis and release of aldosterone from the interrenal tissues of larval Ambystoma tigrinum and that this rise can be significantly attenuated by saralasin. We furthermore conclude that although the renin-angiotensin system may be indirectly involved in recovery from an acid challenge, it does not appear to be the stimulus for the observed increase in plasma aldosterone in response to acidosis in these animals.
In early infancy, complex disorders of acid base metabolism are more frequent than in any other age group, with a predisposition to metabolic acidosis due to an age-related low renal capacity for acid excretion and an unphysiologically high actual renal acid load in nutrition with common formulas. Recently in preterm and small-for-gestational-age infants, persistent maximum renal net acid excretion (NAE) with subnormal or normal blood acid base status, impaired weight gain, and adaptive hormonal reactions have been observed. Incipient late metabolic acidosis is one example of a mixed disorder of acid base metabolism with maximum renal NAE in early infancy. Alkali therapy is highly effective and can be realized both on an individual basis, using urine pH screening as a diagnostic criterium for maximum renal acid stimulation, or on a general preventive level using modified standard formula with a reduced actual renal NAE similar to that seen on alimentation with human milk. From an integrated point of view, the low glomerular filtration rate and renal capacity for acid excretion beyond the developmental age of more than 44 weeks, may well be interpreted as the result of a specific adaptation to breast feeding sparing energy, and thus an evolutionary advantage for the survival of mother and child.