Land atmosphere feedbacks and their role in the water resources of the Ganges basin.

The northern Indian subcontinent has frequently been identified as a hotspot for land atmosphere interactions. It is also a region with the highest concentration of irrigated land and highest (and increasing) population density in the world. The available water in the region with which to grow food depends on the Asian monsoon, groundwater and melt from Himalayan snows. Any changes or disruptions to these sources of water could threaten the food supply. It is therefore essential to understand how the land surface, and in particular irrigated land, interacts with the atmosphere. It is anticipated that the interactions will occur on many scales. To an extent the magnitude and form of these will depend on the depth of the atmosphere which is affected. Thus at the local, or micro, scale it is the surface layer (some 10 s m deep) which is cooled and moistened by the evaporation of irrigated water, at the meso-scale the Planetary boundary layer (up to 1 or 2 km) will be modified - with possible atmospheric moistening, increased cloud and rain formation and at very large scales the whole dynamics of the south Asian Monsoon will be affected. This illustrates a strong interaction between the Asian monsoon and the regional topography. Of considerable significance is the finding in this paper that up to 60% of the evaporation from irrigated areas in the summer months is ultimately recycled to Himalayan rainfall and so feedbacks to river flows in the Ganges.

Protection against cellular damage in the rat heart by iodoacetate.

In this comparative study, rat hearts were perfused at 37 degrees C with three clearly defined protocols: the Ca2+ paradox, the O2 paradox, and with 20 mM caffeine. Each protocol involved an initial priming (Ca2+o depletion or anoxia; stage 1) and subsequent full activation (Ca2+o repletion, caffeine or reoxygenation; stage 2) of the damage system of the sarcolemma. Iodoacetate (1 mM) provided complete protection in the O2 paradox and over 80% protection in the Ca2+ paradox and caffeine protocols against creatine kinase release when present throughout the experiment (P < 0.001). Almost identical protection was found when iodoacetate was present only in stage 2 (P < 0.001). However, it was concluded that iodoacetate had limited protective effects when present only in stage 1 in any of the three protocols and that its action is to inhibit the activity of the transsarcolemma damage system in stage 2 when it has been activated in stage 1. It is suggested that iodoacetate interacts with thiol groups on the damage system of the sarcolemma.

Protection against cellular damage in the rat heart by hyperosmotic solutions.

In this comparative study, rat hearts were perfused at 37 degrees C with three clearly defined protocols: the Ca2+ paradox, the O(2) paradox, and with 20 mM caffeine. Each protocol involved an initial priming (Ca(2+)(0) depletion or anoxia; stage 1) and subsequent full activation (Ca(2+)(0) repletion, caffeine or reoxygenation; stage 2) of the damage system of the sarcolemma. Creatine kinase release in stage 2 was completely inhibited (P < 0.001) in all three protocols when 420 mOsm was added to the perfusion medium throughout the experiments, or only during stage 1, or only during stage 2. Increasing the perfusion pressure in the Ca2+ paradox significantly (P < 0.001) exacerbated creatine kinase release, although this was still completely inhibited at 28 degrees C. Amiloride (1 mM) inhibited creatine kinase release completely at 40 cm of water pressure but only some 50% at 80 cm of water pressure. It is suggested that the transmembrane damage system needs to be uncoupled or deactivated by modifying its relationship with the cytosol or with the underlying cytoskeleton by hyperosmotic cell shrinkage for only one of the stages in all three protocols to block the damage pathway. Increased perfusion pressure has the opposite effect and exacerbates damage.

Protection against cellular damage in the perfused rat heart by lowered pH.

In this comparative study, rat hearts were perfused at 37 degrees C with three clearly defined protocols: the Ca2+ paradox, the O2 paradox and with 20 mM caffeine. Each protocol involved an initial priming (Ca2+(o) depletion or anoxia; stage 1) and subsequent full activation (Ca2+(o) repletion or reoxygenation; stage 2) of the damage system of the sarcolemma. Creatine kinase release in stage 2 was completely inhibited (P < 0.001) in all three protocols when pH was reduced to 6.5 throughout the experiments, or only during stage 1, or only during stage 2. The inhibitor of the Na+/H+ antiporter, amiloride (1 mM), completely prevented creatine kinase release in the Ca2+ paradox (P < 0.001) and markedly reduced damage in the caffeine protocol. Amiloride had no significant effect on creatine kinase release in the O2 paradox. The possible role of Na+(i) was studied in the caffeine protocol: ouabain (5 x 10(-6) M) had little effect whereas substitution of choline for Na+ in the perfusion medium reduced creatine kinase release by about 50%. It is suggested that the same damage system is activated in stage 1 in all three protocols and that a key event is the intracellular production of H+ which are exported via Na+(o)/H(i) exchange. Prevention of H+ efflux by lowered pH(o), even during stage 2, protected against creatine kinase release. The possible role of Na+ movements in the genesis of sarcolemma damage is discussed.

Extracellular K+ and protection against cellular damage in the rat heart.

Rat hearts were perfused at 37 degrees C with three clearly-defined protocols: the Ca2+ paradox, the O2 paradox and with 20 mM caffeine. Each protocol involved an initial priming (stage 1) and a subsequent full activation (stage 2) of the damage system of the sarcolemma. Raising [K+]o from 5.4 to 6.5 mM in the Ca2+ paradox had no significant effect, but creatine kinase release was significantly inhibited (P < 0.001) at 7.5, 10.8 or 16.2 mM. Raising [K+]o to 16.2 mM only during stage 1 or only during stage 2 also inhibited creatine kinase release (P < 0.001); protection was greater than when 16.2 mM [K+]o was present throughout. [K+]o at 10.8 mM exacerbated creatine kinase release in the O2 paradox (P < 0.001) and also when present only during stage 1. However, significant protection was provided when [K+]o was raised only during stage 2 (P < 0.001). Creatine kinase release in the caffeine protocol was significantly inhibited (P < 0.001) at 10.8 mM [K+]o and when [K+]o was raised only during stage 1 or stage 2. It is concluded that raised [K+]o has two opposing effects: prevention of the activation of the membrane damage system and an exacerbation of damage via an increased Ca2+ influx.

Protective effect of lidocaine on cell damage in the perfused rat heart.

The effect of lidocaine (2 mM) on cell damage in the perfused rat heart is compared in three experimental protocols: the Ca(2+)-paradox, the O2-paradox and perfusion with caffeine. Lidocaine protected against creatine kinase (CK) release when perfused throughout or only during the priming stage in all three protocols. Lidocaine also protects against CK release in the Ca(2+)-paradox when present only during Ca(2+)-reperfusion. Lidocaine protects against myofilament damage in the Ca(2+)-paradox but not in the O2-paradox and caffeine protocols, even though CK release is inhibited. Analysis of these different effects of lidocaine on the priming and full activation stages in the three protocols suggests the sequence of the underlying biochemical events of the two separate damage pathways associated with the release of cytosolic proteins and the degradation of the myofilament apparatus.

The protective effect of lowered temperature on the oxygen paradox in the rat heart.

The isolated rat heart was completely protected against creatine kinase (CK) release in the standard Ca2+ or O2 paradoxes when perfused at 28 degrees C instead of 37 degrees C, as previously reported. Hearts subjected to the O2 paradox at 28 degrees C recovered normal contractile activity, and electron microscopy revealed normal, undamaged ultrastructure. The mitochondria remained contracted and showed no signs of Ca2+ uptake following a rise in Ca2+ concentration in the cytosol that would be expected following the prolonged period of anoxia. It is concluded that the rise in [Ca2+]i that results from a perturbation of Ca2+ homeostasis during anoxic perfusion in the O2 paradox is not sufficient to cause either CK release or myofilament degradation which follow only on reoxygenation in the second phase of the paradox. Since both the Ca2+ and O2 paradoxes are completely protected when the first stage is carried out at 28 degrees C, it is concluded that the initial activation of the sequence of damage events is prevented at this temperature.