Is there a synergistic effect between steady-state exercise and water acidification in carp?

Carp ( Cyprinus carpio ) fitted with arterial catheters were trained to swim in a swim tunnel. While constantly swimming at two body lengths per second, they were subjected to gradual water acidification (from pH 7–6 to 40 in 4 h), and monitored subsequently over 24 h. It was hypothesized that exercise would expose the gills to a larger extent and that conseq uently the effect of water acidification would be greater in exercising than in resting carp. In contrast to our earlier study with resting carp we found a constant dedine of plasma pH, and of plasma Na⁺ and Cl concentration, indicating ionoregulatory failure. While plasma catecholamincs remained at control levels, the plasma cortisol showed a three- to four-fold increase over the first 7 h. This was followed by a slow decline. We conclude that there is a synergistic effect between moderate exercise and gradual water acidification.     

施肥和增水对弃耕草地土壤酸中和容量的影响

大气氮沉降增加是草地土壤酸化的主要原因。土壤酸缓冲性能作为评估土壤酸化的重要指标,对氮输入的响应受到降水与其他限制养分含量的影响。本研究以我国北方温带弃耕草地氮、磷、水添加试验13年后的土壤为对象,利用二次多项式模型拟合酸滴定曲线,计算了土壤酸缓冲容量(ABC)以及以pH 5.0和4.0为参比的土壤酸中和容量(ANC)。结果表明: 不增水处理下,单独加氮和同时添加氮磷均显著降低土壤pH,降低以pH 5.0和4.0为参比时的酸中和容量(ANC_pH5.0和ANC_pH4.0);单独加磷对土壤pH、ANC_pH5.0和ANC_pH4.0均无显著影响。增水处理下,加氮及加氮磷显著降低土壤pH、ANC_pH5.0和ANC_pH4.0;加磷显著降低土壤pH,但增加了ANC_pH4.0,而对ANC_pH5.0无显著影响。与不增水处理相比,增水处理对土壤pH、酸中和容量均具有显著的正效应。对于初始pH值不同的土壤,采用土壤酸中和容量比酸缓冲容量能更好地指示土壤抗酸化能力。     

Cortisol and thyroid hormone responses to acid stress in the brown trout, Salmo trutta L.

Individual cannulated brown trout monitored during exposure to acidic water showed increased plasma cortisol after 3 h at pH 4.0 with low (0.05 mm) or high (2.8 mm) calcium (Ca) content, and after 2 days in acidic water with a high Ca content. Most fish did not survive for 2 days in acidic water with a low Ca content. Non-cannulated fish showed a similar increase in mean plasma cortisol after 2 days in high-Ca acidic water (pH 4.0–4.6), but not in acidic water of a low Ca content. After 7 days of exposure to acidic water, plasma cortisol appeared to recover when there was a high Ca content but increased 20-fold when Ca content was low. In cannulated fish severe acid stress resulted in a marked and rapid thyroid response. Plasma thyroxine (T₄) was elevated after 3 h exposure to acidic water of both low and high Ca content and remained elevated for 2 days of acid exposure with high Ca. In non-cannulated fish an increase in mean T₄ was apparent only after 7 days in low-Ca acidic water. Plasma triiodothyronine (T₃) levels were not significantly altered by any of the acid regimes. Plasma glucose of cannulated fish was elevated within 3 h of acid-exposure and remained elevated after 2 days in high-Ca acidic water.     

Effects of acid water exposure on plasma cortisol, ion balance, and immune functions in the "cobalt" variant of rainbow trout

This study was undertaken to examine physiological responses to acidification of environmental water in the "cobalt" variant of rainbow trout (Oncorhynchus mykiss), which exhibits malformation of the pituitary, by following changes in plasma levels of cortisol and electrolytes, blood pH, gill Na(+), K(+)-ATPase activity, and immune functions after exposure to acid water (pH 4.5). Resting levels of plasma cortisol and lysozyme were significantly lower in the cobalt variant than in the normal trout, whereas plasma ceruloplasmin was significantly higher in the cobalt variant, suggesting that some endocrine factors, lacking or deficient in the cobalt variant, are important for the regulation of its immune functions. Blood pH was slightly but significantly lower in the cobalt variant at rest. After exposure to acid water for 24 h, both the normal trout and cobalt variant showed a significant elevation in plasma cortisol, although the increased level in the cobalt variant was still lower than that in the normal trout transferred to neutral water. No differences were seen in blood pH, plasma electrolytes, and gill Na(+), K(+)-ATPase activity between the normal trout and the cobalt variant, indicating that the cobalt variant regulates ion balance when exposed to acid water, despite malformation of the pituitary. Although the normal trout showed a reduction in plasma lysozyme level after acid exposure, there was no significant change in the cobalt trout. Adverse effects of pituitary malformation on ion balance and immune functions may be compensated by extrapituitary factors in the cobalt variant when it is exposed to acid water.     

Transient increase in Ca2+ influx in Saccharomyces cerevisiae in response to glucose: effects of intracellular acidification and cAMP levels

Influx of 45Ca2+ into Saccharomyces cerevisiae was measured under experimental conditions which enabled measurements of initial rate of transport across the plasma membrane, without interference by the vacuolar Ca2+ transport system. Addition of glucose or glycerol to the cells, after pre-incubation in glucose-free medium for 5 min, caused a rapid, transient increase in 45Ca2+ influx, reaching a peak at 3-5 min after addition of substrate. Ethanol, or glycerol added with antimycin A, had no effect on 45Ca2+ influx. We have shown previously that this increase is not mediated by an effect of the substrates on intracellular ATP levels. Changes in membrane potential accounted for only a part of the glucose-stimulated 45Ca2+ influx. The roles of intracellular acidification and changes in cellular cAMP in mediating the effects of glucose on 45Ca2+ influx were examined. After a short preincubation in glucose-free medium addition of glucose caused a decrease in the intracellular pH, [pH]i, which reached a minimum value after 3 min. A transient increase in the cellular cAMP level was also observed. Addition of glycerol also caused intracellular acidification, but ethanol or glycerol added with antimycin A had no effect on [pH]i. Artificial intracellular acidification induced by exposure to isobutyric acid or to CCCP caused a transient rise in Ca2+ influx but the extent of the increase was smaller than that caused by glucose, and the time-course was different. We conclude that intracellular acidification may be responsible for part of the glucose stimulation of Ca2+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)     

The ultrastructure of chloride cells in the gills of the teleostOreochromis mossambicus during exposure to acidified water

Summary Branchial chloride cells, which actively take up ions in the gills of freshwater fish, were studied in tilapia (Oreochromis mossambicus) exposed to sublethally acidified freshwater. Structural damage of cells, resulting in cell death by necrosis, only occurred transiently, when the reduction of water pH was acute rather than gradual. The most prominent effects of water acidification were the rapid increase in the number of chloride cells and the changes in frequency of the different stages of the chloride cell cycle. In the opercular inner epithelium, a twofold increase in cells occurred 48 h after gradual acidification. Cell density stabilized after 4 weeks at a level 5 times that of control fish. Four transitory stages were distinguished in the chloride cell cycle: accessory or replacement cells, immature, mature, and degenerating (apoptotic) cells. In control fish, mature chloride cells dominated (over 50%) with immature and apoptotic cells totalling about 40%. After 4 weeks in acid water, only 13% of the cells were mature. Immature and apoptotic cells dominated, each representing about 40% of the total number of chloride cells. Mature cells apparently age rapidly under these conditions. Thus, chloride cells turn over quickly in acid water, with a minor increase in ion transport capacity of the gills. This conclusion is supported by the observation that opercular and branchial Na⁺/K⁺ ATPase activities in treated fish are only 40%–50% higher than in controls.     

The effect of secretin on pancreatic blood flow in the awake and anesthetized dog

The canine pancreatic blood flow was studied after iv secretin (resulting in a plasma level commensurate with the postcibal state), and also after larger iv doses and after duodenal acidification. We found that blood flow was unaffected by "physiological" doses of secretin, or by perfusion of duodenum at a pH as low as 2.0, but increased by bolus doses (0.5 CU/kg and above), and by acidification to pH 1.4. Anesthesia does not affect the blood flow response although the bicarbonate response appeared to be blunted under anesthesia. We conclude that increase in pancreatic blood flow is not a physiological effect of secretin.     

Tilapia are able to withstand long-term exposure to low environmental pH, judged by their energy status, ionic balance and plasma cortisol

Tilapia Oreochromis mossambicus were exposed to water at pH 4·0 for 37 days. The water was acidified slowly over 6 h enabling the animals to acclimate and preventing damage of the gill epithelium. Additional stressors, e.g. aluminium ions and handling stress, were avoided. No mortality or decreased food consumption was observed during the exposure period. No significant changes were observed between the control and acid exposed groups for the energy rich compounds and related parameters, i.e. the adenylate energy charge, the pool of total adenine nucleotides, and the IMP load of white muscle and liver, indicating maintenance of homeostasis. Moreover, there were no significant differences between control groups and acidified groups at 3, 17 and 37 days for plasma sodium, chloride, cortisol and glucose, implying that ionic balance was maintained and that there was no activation of the pituitary-interrenal axis. It is concluded that tilapia can acclimate to water at pH 4·0 when the acidification rate is slow and additional stressors are avoided.     

Catecholamine release and interrenal response of brown trout, Salmo trutta, exposed to aluminium in acidic water

Cannulated brown trout, Salmo trutta , were exposed for 36 h to synthetic water with a low calcium content of pH 5 and similar synthetic water dosed with aluminium to raise the filterable A1 from 5 to 290 μg 1⁻¹ over the 36-h period. There were no significant disturbances of plasma concentrations of glucose, cortisol or catecholamine (adrenaline and noradrenaline) in fish held in water of pH 5. The addition of aluminium to this acidic synthetic water resulted in a generalized endocrine stress response with a four-fold increase in plasma glucose concentration after 18 h and a significant increase in plasma cortisol concentration from 24 h onwards when filterable A1 exceeded 200 μg 1⁻¹. Plasma catecholamine concentration indicated an adrenergic stress response in aluminium-exposed brown trout. A transient doubling in noradrenaline after 6 h in A1 was followed by a larger increase in both plasma adrenaline and noradrenaline concentrations in fish surviving the 36-h exposure to A1.     

Skin ultrastructure in relation to prolactin and MSH function in rainbow trout (Oncorhynchus mykiss) exposed to environmental acidification

The present study describes the effects of 14 days exposure to acidified (pH 4.0) soft water in the absence of aluminium, on the ultrastructure of the skin in rainbow trout (Oncorhynchus mykiss). Compared to control fish, there was a moderate increase in the incidence of necrosis in the filament cells of the fish exposed to pH 4.0, but since the integrity of the tissue appeared to be maintained, most of the ultrastructural changes observed may be considered to be adaptive. There was an increase in epidermal thickness, a higher frequency of electrondense vesicles in filament cells, an increase in the undulation of the basal lamina, and the penetration of the epidermis by cytoplasmatic processes of melanocytes in acid-exposed specimens. An infiltration of leucocytes into the epidermis, and the appearance of serous mucous cells, was also evident. Whether these events were under the control of prolactin and/or -MSH, was also investigated, but no indication for activation or inhibition of either prolactin or -MSH producing cells was obtained. Since a previous study (Balm and Pottinger 1993) had demonstrated that plasma cortisol levels were also identical in control and low pH treated trout throughout a 14 day experimental period, it is concluded that under conditions of environmental acidification, the integument autonomically maintains the adjustments necessary for successful acclimation, presumably via paracrine regulatory circuits.     

The effect of stress and exercise on post-mortem biochemistry of Atlantic salmon and rainbow trout

Freshwater Atlantic salmon Salmo salar and rainbow trout Oncorhynchus mykiss responded similarly to increase in water flow (exercise), reduction in holding tank water level (stress), or 30 min chasing with water level reduction (stress and exercise). Stress generally resulted in elevated plasma cortisol, above the control. Fish responded to stress and exercise combined, with elevated lactate and [H⁺] which was sometimes associated with elevated plasma cortisol. These changes were combined with a depletion of the muscle adenylate pool. Post-mortem, this resulted in an increase in the rate of onset of rigor, and a higher and sometimes sustained muscle proton load. Both species produced predominantly inosine as opposed to hypoxanthine, for up to 72 h of ice storage. This study shows that the physiological disruption in Atlantic salmon and rainbow trout caused by simulated harvest conditions of stress and exercise, results in mostly transient changes in post-mortem muscle biochemistry. These changes lead to an earlier onset and resolution of rigor, and lower post-mortem muscle pH in comparison to the control.     

The effects of acid and acid/aluminum exposure on circulating plasma cortisol levels and other blood parameters in the rainbow trout, Salmo gairdneri

Softwater (Ca²⁺=50, Na⁺= 50(μequiv. l⁻¹) acclimated rainbow trout were fitted with chronic arterial catheters to allow for repetitive blood sampling. After 48 h recovery they were then exposed to either control (pH 6.5, Al = 0μg l⁻¹), acid (pH 4.8, Al = 0μg l⁻¹) or acid plus aluminum (pH 4.8, A1 = 112 μg l⁻¹) conditions for 72 h. Parameters measured included blood glucose, lactate, haemoglobin, haematocrit and plasma Na⁺, Cl⁻, protein and cortisol.
Exposure to pH 4'8 alone caused no mortality, a moderate ionoregulatory disturbance and a transient elevation in plasma cortisol. All other parameters were not significantly different from controls. Addition of aluminum to this exposure caused 100% mortality with a mean survival time of only 27.0 h. There was a marked decrease in plasma ions, hyperglycemia, lactate accumulation, haemoconcentration, red cell swelling, and a sharp rise in plasma cortisol becoming greatly increased as the fish neared death. The mechanism of toxicity of acute acid/aluminum exposure, the role for cortisol under such conditions, and the validity of cortisol and glucose as indicators of stress in fish are discussed.     

Regulation of the cAMP level in the yeast Saccharomyces cerevisiae: the glucose-induced cAMP signal is not mediated by a transient drop in the intracellular pH

Addition of glucose to derepressed cells of the yeast Saccharomyces cerevisiae is known to cause a rapid, transient increase in the cAMP level, which lasts for 1-2 min and induces a cAMP-dependent protein phosphorylation cascade. The glucose-induced cAMP signal cannot be explained solely on the basis of an increased ATP level. Transient membrane depolarization and transient intracellular acidification have been suggested as possible triggers for the cAMP peak. Addition of glucose to cells in which the plasma membrane had been depolarized still produced the increase in the cAMP level excluding membrane depolarization as the possible trigger. Using in vivo 31P NMR-spectroscopy we followed phosphate metabolism and the time course of the drop in the intracellular pH after addition of glucose with a time resolution of 15 s. Under aerobic conditions the initial pH and ATP level were high. On addition of glucose, they both showed a rapid, transient drop, which lasted for about 30 s. Under anaerobic conditions, the initial pH and ATP level were low and on addition of glucose they both increased relatively slowly compared to aerobic conditions. Several conditions were found in which the pH drop which occurs under aerobic conditions could be blocked completely without effect on the cAMP signal or without completely preventing it: addition of NH4Cl together with glucose at high extracellular pH and addition of a low concentration of glucose before a high concentration. Also, when glucose was added twice to the same cells no consistent relationship was observed between the pH drop and the cAMP peak. These results appear to exclude transient intracellular acidification as the trigger for the cAMP signal. Hence, we conclude that the effect of glucose cannot be explained on the basis of effects known to be caused by the membrane depolarizing compounds which cause increases in the cAMP level. A new, more specific kind of interaction appears to be involved.     

Effects of nutrient and non-nutrient stimuli on cytosolic pH in cultured insulinoma (HIT-T15) cells

Intracellular pH (pHi) was measured in the insulin-secreting HIT-T15 cell line using the pH-sensitive fluorescent dye, 2',7'-bis(carboxyethyl)-5'(6')-carboxyfluorescein (BCECF). It was observed that the addition of a weak acid (e.g., acetate or propionate) caused a rapid decrease in pHi, followed by a slower recovery to the resting pH value. Conversely the addition of N4Cl caused an increase in pHi followed by recovery. The addition of amiloride caused a fall in pHi; however, in this case no recovery to basal pH levels was observed. Subsequent addition of a weak acid caused a further fall in pHi with no recovery. The addition of glucose caused a transient acidification followed by alkalinization. When glucose was added to cells which had been pretreated with amiloride, the initial acidification was not followed by recovery or alkalinization. Addition of glyceraldehyde, alpha-ketoisocaproate, lactate or pyruvate to HIT cells also resulted in intracellular acidification followed by recovery. Similarly, depolarisation of HIT cells by treatment with high K+ or with Ba2+ was associated with a pronounced fall in pHi, followed by a gradual recovery. Insulin secretion from HIT cells was stimulated by glucose, glyceraldehyde, alpha-ketoisocaproate, lactate, pyruvate and KCl, whilst amiloride and weak acids exerted only modest effects in the absence of glucose, but amiloride in particular markedly potentiated glucose-induced insulin release. Thus, HIT cells appear to have an amiloride-sensitive mechanism for the extrusion of protons, probably Na+-H+ exchange. Whilst intracellular acidification appears to potentiate secretory responses to nutrient stimuli, it seems unlikely that the activation of HIT cells by these nutrients occurs as a result of intracellular acidification. The mechanisms by which various nutrient and non-nutrient stimuli might exert distinct effects on pHi are discussed.     

Development of thermotolerance and changes in intracellular pH in CHO cells heated at 45.0 degrees C at pH 6.6

Chinese hamster ovary (CHO) cells were given short heat pulses (5 to 20 min) at 45.0 degrees C and incubated at 37 degrees C for up to 20 h under either pH 7.3 or 6.6 conditions. Thermotolerance developed under both pH conditions, but at a slower rate in the pH 6.6 medium. Intracellular pH (pHi) was measured with the dye, 1,4-diacetoxy-2,3-dicyanobenzene, combined with flow cytometry. Time-dependent changes in the intracellular pH occurred under either pH condition. CHO cells incubated under normal pH conditions had a transient increase in the pHi. This pHi elevation was followed by a rapid intracellular acidification of approximately 0.15 to 0.25 pH units. The timing of both the increases and decreases in the pHi was dependent on the magnitude of the initial heat dose. With heat doses less than or equal to 10 min, the pHi returned to normal unheated levels after the acidification phase. Although cells incubated under low pH (6.6) conditions showed similar pHi alterations, differences in the kinetics were measured. The intracellular pH increased immediately after heating. In addition, when intracellular acidification occurred, the rate of acidification was significantly reduced. With heat doses longer than 5 min under the low pH conditions, the pHi did not return to normal unheated levels.     

Mechanism of control of adenylate cyclase activity in yeast by fermentable sugars and carbonyl cyanide m-chlorophenylhydrazone

The phosphorylation of fructose-1,6-bisphosphatase is preceded by a transient increase in the intracellular level of cyclic AMP which activates a cyclic AMP-dependent protein kinase (Pohlig, G., and Holzer, H. (1985) J. Biol. Chem. 260, 13818-13823). Possible mechanisms by which sugars or ionophores might activate adenylate cyclase and thereby lead to an increase in cyclic AMP concentrations were studied. Studies with permeabilized yeast cells demonstrated that neither sugar intermediates nor carbonyl cyanide m-chlorophenylhydrazone are able to increase adenylate cyclase activity. In the light of striking differences of the effects of fermentable sugars and of carbonyl cyanide m-chlorophenylhydrazone on parameters characterizing the membrane potential, it seems not reasonable that the activity of adenylate is under control of the membrane potential. Rapid quenching of 9-aminoacridine fluorescence after addition of fermentable sugars to starved yeast cells indicated an intracellular acidification. The 31P NMR technique showed a fast drop of the intracellular pH from 6.9 to 6.55 or 6.4 immediately after addition of glucose or carbonyl cyanide m-chlorophenylhydrazone. The time course of the decrease of the cytosolic pH coincides with the transient increase of cyclic AMP concentration and the 50% inactivation of fructose-1,6-bisphosphatase under the conditions of the NMR experiments. Kinetic studies of adenylate cyclase activity showed an approximately 2-fold increase of activity when the pH was decreased from 7.0 to 6.5, which is the result of a decrease in the apparent Km for ATP with no change in Vmax. These studies suggest that activation of adenylate cyclase by decrease in the cytosolic pH starts a chain of events leading to accumulation of cyclic AMP and phosphorylation of fructose-1,6-bisphosphatase.     

The Effect of Ration on Acclimation to Environmental Acidity in Rainbow Trout

Freshwater salmonids exposed to low environmental pH typically suffer a net loss of ions, primarily Na⁺ and Cl^–, across the gills, resulting in reduced plasma and tissue ion concentrations. However, in recent experiments in our laboratory, juvenile rainbow trout, Oncorhynchus mykiss, fed a ration of 1% body weight d^–1 or greater showed no ionoregulatory disturbance during chronic, sublethal acidification. This raised the possibility that these fish had acclimated to low pH in that they would be better able to withstand further, more severe acidification than fish that had no prior experience of acid conditions: previous studies had concluded that such acclimation does not occur. This hypothesis was tested by measuring unidirectional ion fluxes during a 24h acute acid challenge (pH 4.2) in juvenile rainbow trout that had previously been exposed to either ambient pH 6.2 (naive fish) or sublethal low pH 5.2 (acid pre-exposed fish) for 90 days, and fed a ration of either 1.0 or 0.25% d^–1 (wet basis). No mortalities were observed during the acute acid challenge in the fish fed the higher ration and no differences between the two groups in the response of Na⁺ fluxes were observed. Sodium influx in both groups was significantly inhibited throughout the challenge and Na⁺ net flux was significantly stimulated over the first 6h. Prior to the acute acid challenge, the fish fed the lower ration that had previously been exposed to pH 5.2 had significantly lower plasma ion concentrations than those fish previously exposed to pH 6.2. Both groups suffered mortalities; those of the naive fish (22% by 24h) being markedly lower than those of the acid pre-exposed fish (68% by 24h). However, there were no significant differences in either Na⁺ or Cl^– fluxes between the two groups of fish during the acid challenge: both showed significant inhibition of ion influxes and significantly greater net ion losses, resulting in reduced plasma ion concentrations. These results indicate that rainbow trout are unable to acclimate to environmental acidification irrespective of the availability of dietary salts.     

Heterogeneity of the changes in cytoplasmic pH upon serum stimulation of quiescent fibroblasts

Addition of mitogens to quiescent cells results in rapid ionic changes in the cytoplasm, including pH. We studied the changes in cytoplasmic pH in single Swiss 3T3 cells upon serum stimulation using fluorescence ratio imaging microscopy. Quiescence was attained using two approaches, serum deprivation of subconfluent cells and confluence. All measurements were made in the presence of bicarbonate and the absence of other organic buffers. We also used BCECF coupled to dextran to avoid several artifacts associated with using BCECF-AM, including leakage and phototoxicity. Analysis of the changes in cytoplasmic pH demonstrated a dramatic heterogeneity in the responses of single cells. There were six basic classes of responses, 1) a fast alkalinization, reaching a maximum pH in approximately 2-5 min; 2) a slow alkalinization, reaching a maximum pH in 10-20 min; 3) a very slow alkalinization, not reaching a plateau pH within the measurement time; 4) no apparent change in pH during the measurement time; 5) an early transient acidification, followed by either a fast or slow alkalinization; and 6) an acidification, followed by alkalinization and then by a decrease to some intermediate pH. Subconfluent cells exhibited greater heterogeneity in response than confluent cells, with no single dominant class of response. The dominant (55%) response for confluent cells was a gradual alkalinization of approximately 0.01 pH units/min. A larger proportion (52%) of subconfluent cells exhibited an early transient acidification compared to confluent cells (7%). A significant proportion of both types of cells (23% subconfluent, 36% confluent) exhibited no change in cytoplasmic pH upon stimulation. In general, the kinetics of changes in cytoplasmic pH were significantly different from the published results with population averaging methods.     

Effects of feeding on metabolism, gas transport, and acid-base balance in the bullfrog Rana catesbeiana

Massive feeding in ectothermic vertebrates causes changes in metabolism and acid-base and respiratory parameters. Most investigations have focused on only one aspect of these complex changes, and different species have been used, making comparison among studies difficult. The purpose of the present study was, therefore, to provide an integrative study of the multiple physiological changes taking place after feeding. Bullfrogs (Rana catesbeiana) partly submerged in water were fed meals (mice or rats) amounting to approximately (1)/(10) of their body weight. Oxygen consumption increased and peaked at a value three times the predigestive level 72-96 h after feeding. Arterial PO(2) decreased slightly during digestion, whereas hemoglobin-bound oxygen saturation was unaffected. Yet, arterial blood oxygen content was pronouncedly elevated because of a 60% increase in hematocrit, which appeared mediated via release of red blood cells from the spleen. Gastric acid secretion was associated with a 60% increase in plasma HCO3(-) concentration ([HCO3(-)]) 48 h after feeding. Arterial pH only increased from 7.86 to 7.94, because the metabolic alkalosis was countered by an increase in PCO(2) from 10.8 to 13.7 mm Hg. Feeding also induced a small intracellular alkalosis in the sartorius muscle. Arterial pH and HCO3(-) returned to control values 96-120 h after feeding. There was no sign of anaerobic energy production during digestion as plasma and tissue lactate levels remained low and intracellular ATP concentration stayed high. However, phosphocreatine was reduced in the sartorius muscle and ventricle 48 h after feeding.     

Effect of plasma [K+] on the DC potential and on ion distributions between CSF and blood.

Keeping the arterial pH at 7.4 and PaCO2 at 40 mmHg in eight anesthetized dogs, we acutely raised plasma potassium concentration from 3.4 to 8.2 meq/1, then allowed it to decay back to control levels. The cerebrospinal fluid (CSF)-blood electrical potential difference (pd) increased 13.2 mV per 10-fold increase in plasma [K+]. Again keeping arterial pH at 7.4 and PaCO2 at 40 mmHg, we elevated plasma [K+] in four dogs from 3.3 to 8.0 meq/1 and maintained this level for 6 h. We found 1) that the PD increased from a control value of +1.3 to +8.9mV, showing no tendency to decay over the 6 h; and 2) that the change in PD did not affect the distribution of Na+, K+, H+, Cl-, or HCO3- between blood and CSF over the 6 h. These results suggest that under these conditions the PD between CSF and blood may play no effective role in determining the distributions of these charged species by 6 h. These results are contrasted with recent findings which suggest that H+ and HCO3- are distributed according to passive forces between CSF and blood.