Isotherms for adsorption of organic solutes are divided into four main classes, according to the nature of slope of the initial portion of the curve, and thereafter into sub-groups.The main classes are: (i) S Curves, indicative of vertical orientation of adsorbed molecules a t the surface. (ii) L Curves, the normal or " Langmuir " isotherms, usually indicative of molecules adsorbed flat on the surface, or, sometimes, of vertically oriented adsorbed ions with particularly strong intermolecular attraction. (iii) H Curves ( ' I high affinity ") (commencing a t a positive value on the " concentration in solid " axis) , often given by solutes adsorbed as ionic micelles, and by high-affinity ions exchanging with lowaffinity ions. (iv) C Curves (" constant partition "), linear curves, given by solutes which penetrate into the solid more readily than does the solvent.The sub-groups of these classes are arranged according to the shape of the parts of the curves farther from the origin, and the significance of plateaux and changes of slope are described. Thus, if the adsorbed solute molecules in the monolayer are so oriented that the new surface they present to the solution has low attraction for more solute molecules, the curve has a long plateau ; if they are oriented so that the new surface has high attraction for more solute, the curve rises steadily and has no plateau.The choice of solutes for reliable measurement of specific surface areas is very restricted. It is suggested that p-nitrophenol may be one of the best compounds for this purpose.The significance of their features is discussed.* Part I, J., 1954, 4360; previous papers in this series were divided into two series, for inorganic and organic substrates respectively. Parts I-V, organic series, are considered as Parts VI-X in the present series. Thus, Part X is J . SOC. Dyers Colourists, 1958, 74, 846 (ref. 12a).

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The kidney is faced with unique challenges for oxygen regulation, both because its function requires that perfusion greatly exceeds that required to meet metabolic demand and because vascular control in the kidney is dominated by mechanisms that regulate glomerular filtration and tubular reabsorption. Because tubular sodium reabsorption accounts for most oxygen consumption (Vo2) in the kidney, renal Vo2 varies with glomerular filtration rate. This provides an intrinsic mechanism to match changes in oxygen delivery due to changes in renal blood flow (RBF) with changes in oxygen demand. Renal Vo2 is low relative to supply of oxygen, but diffusional arterial-to-venous (AV) oxygen shunting provides a mechanism by which oxygen superfluous to metabolic demand can bypass the renal microcirculation. This mechanism prevents development of tissue hyperoxia and subsequent tissue oxidation that would otherwise result from the mismatch between renal Vo2 and RBF. Recent evidence suggests that RBF-dependent changes in AV oxygen shunting may also help maintain stable tissue oxygen tension when RBF changes within the physiological range. However, AV oxygen shunting also renders the kidney susceptible to hypoxia. Given that tissue hypoxia is a hallmark of both acute renal injury and chronic renal disease, understanding the causes of tissue hypoxia is of great clinical importance. The simplistic paradigm of oxygenation depending only on the balance between local perfusion and Vo2 is inadequate to achieve this goal. To fully understand the control of renal oxygenation, we must consider a triad of factors that regulate intrarenal oxygenation: local perfusion, local Vo2, and AV oxygen shunting.

SUMMARY1. Renal blood flow, local tissue perfusion and blood oxygen content are the major determinants of oxygen delivery to kidney tissue. Arterial pressure and segmental vascular resistance influence kidney oxygen consumption through effects on glomerular filtration rate and sodium reabsorption.2. Diffusive shunting of oxygen from arteries to veins in the cortex and from descending to ascending vasa recta in the medulla limits oxygen delivery to renal tissue. Oxygen shunting depends on the vascular network, renal haemodynamics and kidney oxygen consumption. Consequently, the impact of changes in renal haemodynamics on tissue oxygenation cannot necessarily be predicted intuitively and, instead, requires the integrative approach offered by computational modelling and multiple measuring modalities.3. Tissue hypoxia is a hallmark of acute kidney injury (AKI) arising from multiple initiating insults, including ischaemia-reperfusion injury, radiocontrast administration, cardiopulmonary bypass surgery, shock and sepsis. Its pathophysiology is defined by inflammation and/or ischaemia resulting in alterations in renal tissue oxygenation, nitric oxide bioavailability and oxygen radical homeostasis. This sequence of events appears to cause renal microcirculatory dysfunction, which may then be exacerbated by the inappropriate use of therapies common in peri-operative medicine, such as fluid resuscitation.4. The development of new ways to prevent and treat AKI requires an integrative approach that considers not just the molecular mechanisms underlying failure of filtration and tissue damage, but also the contribution of haemodynamic factors that determine kidney oxygenation. The development of bedside monitors allowing continuous surveillance of renal haemodynamics, oxygenation and function should facilitate better prevention, detection and treatment of AKI.