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Vasoactive agents and splanchnic oxygen uptake.

Many vasoactive agents are known to alter oxygen uptake by splanchnic organs. Data from the literature indicate that, in general, vasodilators increase, whereas vasoconstrictors decrease oxygen uptake. We compare and contrast the effects of vasoactive agents on oxygen uptake observed in vivo, under constant-flow and free-flow conditions, to those observed in vitro. The discrepancies between the in vivo and in vitro data are discussed relative to the effects of vasoactive agents on blood flow, intraorgan blood flow distribution, the countercurrent exchange of oxygen, capillary exchange capacity, and oxidative metabolism. Changes in blood flow, oxidative metabolism, and capillary density appear to be the major mechanisms by which vasoactive agents alter splanchnic oxygen uptake in vivo. Experimental designs are proposed that may help minimize inconsistencies in the data in future studies.

Animals↗

Perfusion rates and the transfer of water across isolated guinea pig placenta.

The transfer of tritiated water across the isolated, artificially perfused guinea pig placenta was the subject of 21 experiments. The observed relationship between the flow rates and the relative transfer of water cannot be explained by a concurrent or pool-flow system. If the direction of the fetal flow is reversed, the rate of transfer is lowered. It may be concluded, that the decrease is a result of a change from a nonideal countercurrent flow system to a nonideal concurrent system. This conclusion, however, holds only if all other parameters that determine the exchange as well remain unaffected. In the range of flows investigated, the transfer of water is flow limited.

Animals↗

Questions and replies: renal mechanisms for urinary concentrating and diluting processes.

Mechanisms for urinary concentration or dilution depend on counterflow processes, both tubular and vascular, within the renal medulla. Recently, there have emerged differing hypotheses about the renal tubular processes responsible for maintaining a hypertonic medullary interstitium. In this Editorial Review, R.W. Berliner frames three questions germane to this issue, and J.P. Kokko and D.J. Marsh provide their responses to these queries. The major issues addressed are: 1) What are the major unresolved question(s) concerning the mechanism by which concentrated urine is formed? 2) Current evidence suggests that the urea concentration in thin ascending limbs is slightly lower in the lumen than in interstitial fluid. Is the transepithelial concentration gradient between thin ascending limb and renal medullary interstitium sufficient to permit an entirely passive mechanism for diluting tubular fluid in the thin ascending limb? 3) A simple three-compartment model for the renal medullary concentrating process would include the tubular lumen, peritubular capillary, and the interstitium. Is it possible to generate a model that, by juxtaposing medullary structures, might explain renal medullary counterflow processes more adequately than the simple three-compartment model?

Animals↗