Decrease In Blood pH Research Articles

Acid–base and electrolyte status during early induced pregnancy toxaemia in goats

Eleven Murciano-Granadina goats in late pregnancy were separated into two groups (1) control (n=6) and (2) fasting for 72 h to induce pregnancy toxaemia (n=5). Venous blood was taken daily to determine acid-base and electrolyte parameters. Significant decreases in blood pH, bicarbonate concentration and base excess, and a significant increase in anion gap were observed after 24h of fasting. These changes were significantly correlated with non-esterified fatty acid concentration. No significant changes were observed in pCO(2), and electrolyte or lactate concentrations. Clinical signs of pregnancy toxaemia in fasted goats appeared by 72h post-fasting. These signs and the changes in acid-base balance disappeared once feed was reintroduced. Blood pH, bicarbonate concentration, base excess and anion gap could be indicators of early pregnancy toxaemia in goats.

Hematocrit and blood osmolality in developing chicken embryos (Gallus gallus): In vivo and in vitro regulation

Hematocrit (Hct) regulation is a complex process involving potentially many factors. How such regulation develops in vertebrate embryos is still poorly understood. Thus, we investigated the role of blood pH in the regulation of Hct across developmental time in chicken embryos. We hypothesized that blood pH alterations in vitro (i.e., in a test tube) would affect Hct far more than in vivo because of in vivo compensatory regulatory processes for Hct. Large changes in Hct (through mean corpuscular volume (MCV)) and blood osmolality (Osm) occur when the blood was exposed to varying ambient temperatures (T(a)'s) and P(CO2) in vitro alongside an experimentally induced blood pH change from ~7.3 to 8.2. However, homeostatic regulatory mechanisms apparently limited these alterations in vivo. Changes in blood pH in vitro were accompanied by hydration or dehydration of red blood cells depending on embryonic age, resulting in changes in Hct that also were specific to developmental stage, due likely to initial blood gas and [HCO(3)(-)](v) values. Significant linear relationships between Hct and pH (Hct/ΔpH=-21.4%/(pH unit)), Hct and [HCO(3)(-)] (ΔHct/Δ[HCO(3)(-)]=1.6%/(mEq L(-1))) and the mean buffer value (Δ[HCO(3)(-)]/ΔpH=-13.4 (mEq L(-1))/(pH unit)) demonstrate that both pH and [HCO(3)(-)] likely play a role in the regulation of Hct through MCV at least in vitro. Low T(a) (24°C) resulted in relatively large changes in pH with small changes in Hct and Osm in vitro with increased T(a) (42°C) conversely resulting in larger changes in both Hct and Osm. In vivo exposure to altered T(a) caused age-dependent changes in Hct, demonstrating a trend towards increased Hct at higher T(a). Further, exposing embryos to a gas mixture where P(CO2) = 5.1 kPa for >4 h period at T(a) of 37 or 42°C also did not elicit a change in Hct or Osm. Presumably, homeostatic mechanisms ensured that in vivo Hct was stable during a 4-6 h temperature and/or hypercapnic stress. Thus, although blood pH decreases (induced by acute T(a) increase and exposure to CO(2)) increase MCV and, consequently, Hct in vitro, homeostatic mechanisms operating in vivo are adequate to ensure that such environmental perturbations have little effect in vivo.

THERAPEUTIC EFFECT OF VITAMIN C IN ENDOTOXIN-INDUCED METABOLIC ACIDOSIS AND OXIDATIVE STRESS IN LAMBS

Endotoxemia associated with Gram-negative sepsis is an emergency clinical state that causes rapid biochemical changes and substantial mortalities in livestock. The present study aimed to investigate the therapeutic effect of vitamin C on blood gases, acid-base balance and nitric oxide in lamb model of lipopolysaccharide [LPS]- induced endotoxemia. The study was conducted on 15 lambs, 3-5 months of age. Animals were randomly grouped into 3 groups, five each as followings: Group 1 (control): received only normal saline, Group 2: received only LPS at dose 25 µg/kg B.W. and Group 3: received vitamin C at dose 20 mg/kg B.W. one hour before LPS infusion. Saline (10 ml) or LPS in saline were infused through jugular canula. The experimental fever elicited by iv injection of LPS 25 μg/kg/ B.W. was accompanied by metabolic acidosis, hypoxemia and significance increased production of nitric oxide. A significant decrease in blood pH, base excess and HCO3− was noticed during fever. Although the concentrations of HCO3− were decreasing till the end of the experiment, there was no substantial falls in PCO2 for compensation of the noticed acidosis. However, hypoxemia was evident as indicated with marked reduction in oxygen saturation and oxygen tension. Nitric oxide level increased during the period of experiment and reached peak 5 hours post LPS administration. Pretreatment with i.v. 20 mg/kg B.W. of vitamin C an hour pre LPS administration reduced the febrile response and reversed the postpyrogen changes in pH, HCO3− and nitric oxide. Possible mechanisms by which vitamin C could affect the LPS-induced disturbances of acid-base balance are being considered. Finally, it could be concluded that vitamin C pretreatment prevented LPS –induced metabolic acidosis and nitric oxide production.

Effects of sodium bicarbonate ingestion on EMG, effort sense and ventilatory response during intense exercise and subsequent active recovery

To determine whether post-exercise ventilation is related to decrease in blood pH and also whether post-exercise ventilation, associated or not with decreased blood pH, involves an increase in central motor command during exercise, we examined the effects of NaHCO(3) ingestion on the ventilatory response ([Formula: see text]E), integrated electromyogram (iEMG) and effort sense of legs (ESL) during intense exercise (IE) and subsequent active recovery. Subjects performed two IE tests (105-110% of maximal work rate, 2min) after ingestion of NaHCO(3) or CaCO(3). Subjects performed light load exercise (20W) before and after IE for 6min and 30min, respectively. Although there was a significant difference in blood pH between the two conditions during and after IE, [Formula: see text]E, iEMG and ESL were similar. iEMG returned to the pre-IE level immediately after the end of IE, while ESL showed slow recovery. [Formula: see text]E decreased rapidly until about 50s after the end of IE (fast phase) and then showed a slow recovery kinetics (slow phase). The ventilatory responses during the fast phase and during the slow phase were correlated with ESL at the end of IE and from 3min after the end of IE, respectively. Moreover, there was no significant difference in the slopes and intercepts of regression lines between [Formula: see text]E and ESL under the two conditions in both phases. These results suggest that the ventilatory response after IE is associated with effort sense indirectly-elicited by central motor command, but the effort sense-mediated response is not affected by blood pH.

Perioperative use of metformin in cardiac surgery

Metformin is an oral antidiabetic agent, used to reduce blood glucose concentration in patients with non-insulin-dependent diabetes mellitus. Metformin was approved in Europe in 1957, and it is used for the treatment of non-insulin-dependent diabetes mellitus for more than 50 years. One of the most serious complications of the treatment with this drug is metformin-induced lactic acidosis. It is a rare but dangerous metabolic complication with a mortality rate of up to 50% that can result from the accumulation of lactates. Lactic acidosis is also associated with conditions such as diabetes mellitus, significant tissue hypoperfusion, and hypoxemia caused by lactic acid overproduction or underutilization. It is characterized by an increased serum lactate level (>5mmol/L or >45 mg/dL), decreased blood pH (<7.35), and electrolyte imbalance with an increased anion gap. The rate of lactic acidosis in patients receiving metformin is not precisely known. The estimated incidence of this syndrome is 2-9 cases per 100 000 patients. However, in the majority of cases, lactic acidosis is diagnosed in patients with severe acute renal failure, which itself can cause lactic acidosis. Currently, there are no standardized guidelines for metformin administration during the perioperative period, and published data remain controversial. According to some investigators, metformin should be withdrawn before major surgery. Concerns have been raised for the use of metformin in patients with cardiovascular, renal, hepatic, and respiratory failure. The aim of the article is to overview the frequency of metformin-caused lactic acidosis and the latest recommendations for the use of metformin in the perioperative period proposed in recent years.

The importance of carbonic anhydrase II in red blood cells during exposure of chicken embryos to CO2

The importance of carbonic anhydrase (CA) during exposure of chicken embryos to CO(2) during the second half of incubation was investigated. The protein abundance and activity of CAII in erythrocytes was significantly higher in CO(2)-exposed embryos compared to normal conditions. Daily injections of acetazolamide (ATZ), an inhibitor of CA, increased blood P(CO2) and decreased blood pH in both control and CO(2)-incubated embryos. ATZ increased blood bicarbonate concentration in embryos exposed to normal atmosphere and in day-12 embryos exposed to high CO(2). The tendency of an increased blood potassium concentration in ATZ-injected embryos under standard atmospheric conditions might indicate that protons were exchanged with intracellular potassium. However, there was no evidence for such an exchange in CO(2)-incubated ATZ-treated embryos. This study shows for the first time that chicken embryos adapt to CO(2) during the second half of incubation by increasing CAII protein expression and function in red blood cells. This response may serve to "buffer" elevated CO(2) levels.

Effects Of Aerobic Fitness On Blood Buffering And Maximal Cycling Power During Variable Intensity Exercise.

Variable intensity exercise (VAR = short bouts of high-intensity exercise followed by low intensity for recovery) is typically used by aerobically-trained (AET) and untrained people (UT) to improve endurance performance. However VAR lowers blood pH which is associated with reductions in muscle force. PURPOSE: To determine if acid-base regulation during VAR differs between UT and AET and its effects on maximal cycling power. METHODS: Ten AET and ten UT (= 64 ± 6 vs 55 ± 6 mL·kg-1·min-1; P < 0.05) pedaled alternating high (1.5 min) with low (4.5 min) exercise intensity for 24 min. Exercise intensity was normalized to their ventilatory threshold (VT) resulting in 3 trials; VARLOW = 87.5-37.5% VT; VARMODERATE, 125-25% VT; and VARHIGH 162.5-12.5% VT. Total work was the same for all trials (213 ± 8 and 149 ± 23 kJ for AET and UT). Arterialized-blood samples and expired gas were obtained during exercise and maximal cycling power (PMAX) was measured prior and after exercise. RESULTS:Table 1 shows the mean ± SD for blood pH (pHblood) and bicarbonate concentration ([HCO3-]blood), ventilatory equivalent for CO2 (VE · VCO2-1) and change in PMAX at the end of each protocol. * Different from VARLOW at P < 0.05. † Different from VARMODERATE at P < 0.05. ‡ Different from AET at P < 0.05TABLECONCLUSIONS: To increase the exercise intensity during VAR produced similar decrease in blood pH and bicarbonate concentration and comparable increase in the respiratory compensation between AET and UT. This suggests that blood-respiratory buffering systems are not impaired in UT people during VAR. However, despite similar low blood pH, only UT reduced the maximal cycling power after VARHIGH. Thus, training may confer adaptations to withstand low pH without loosing neuromuscular power.

Epigalocatechin-3-gallate Advances The Onset Of The Ventilatory Threshold But Does Not Affect Maximal Oxygen Uptake

Epigalocatechin-3-gallate (EGCG), a catechin present in green tea, increases endurance performance in animals and promotes fat oxidation during prolonged cycle ergometer exercise in adult humans. Accordingly, we hypothesized that EGCG delays the onset of the ventilatory threshold (TVE) and increases maximal oxygen uptake (VO2max). PURPOSE: To compare TVE and VO2max after consumption of EGCG and placebo. METHODS: 7 EGCG capsules (135 mg/capsule) and 7 placebo capsules were administered in a randomized, double blind manner to 8 recreationally active young adults (6 males, 2 females, age: 29 ± 5 yr (mean ± SE)). One capsule was consumed every 12 hours over 48 hours, and the final capsule consumed 2-hours prior to exercise testing. On two occasions, separated by a minimum of 14 days, TVE and VO2max were determined from breath-by-breath indirect calorimetry data collected during continuous incremental stationary cycle ergometer exercise (20-25 W/min), from rest until volitional fatigue. RESULTS: Contrary to our hypothesis the VO2 corresponding to TVE was lower (P = 0.04) following consumption of EGCG (1.5 ± 0.1 L/min) compared with placebo (1.7 ± 0.2 L/min). VO2max, maximal heart rate and maximal work rate were unaffected (Placebo: 3.2 ± 0.4 L/min, 179 ± 7 beats/min, 307 ± 25 W vs. EGCG: 3.3 ± 0.4 L/min, 179 ± 7 beats/min, 297 ± 29 W; all P > 0.05). CONCLUSION: The onset of the TVE is advanced by EGCG. EGCG is thought to inhibit catechol-O-methyl transferase, an enzyme contributing to the degradation of catecholamines. Delayed degradation of catecholamines could contribute to accelerated glycolysis and decreased blood flow to lactate clearing tissues during incremental exercise. These combined actions may promote earlier lactate accumulation, decreased blood pH, and hence advanced TVE.

Inhibition of TASK1‐like channels by muscarinic receptor stimulation in rat adrenal medullary cells

The muscarinic receptor is known to be involved in the acetylcholine-induced secretion of catecholamines in the adrenal medulla (AM) cells of various mammals. The ionic mechanisms, however, have not been elucidated yet. Thus, we investigated the issue in acutely isolated rat AM cells with the perforated patch clamp method. Bath application of 30 muM muscarine induced depolarization with the consequent generation of action potentials or an inward current at negative membrane potentials. The muscarine-sensitive current instantaneously changed in amplitude upon application of command pulses without a time-dependent component, altered the polarity as a K(+)-electrode, and showed rectification of the Goldman-Hodgkin-Katz (GHK) type. The whole-cell current at -20 mV was inhibited by external H(+) ions with a concentration responsible for half inhibition of pH 7.09 and muscarine failed to induce a further inward current during exposure to a saline in which pH decreased to 6.5. A similar occlusion occurred in secretion when pH in muscarine-containing saline decreased to 6.6. RT-PCR, immunoblotting, and immunocytochemistry suggested that rat AM cells mainly express the TASK1 channel. This TASK channel in AM cells may directly sense a decrease in blood pH, which occurs during exercise. The muscarine action was mimicked by oxotremorine-methiodide, but not by oxotremorine. The present results indicate that activation of muscarinic receptors or a decrease in external pH in the rat AM cell induces secretion through the inhibition of TASK1-like channels.

BREATHE IN...

Northern elephant seals (Mirounga angustirostris) are most at home in the water, plumbing the depths during their extensive dives and holding their breath for an hour or more, tolerating conditions that would damage humans irreversibly. The seals only emerge onto land for 2-4 months of the year to breed and moult. When asleep on land they show long natural breath-holds called apneas, which last up to 25 min. These apneas probably occur to conserve energy and water since the seals fast while they are on land, and studying them might give scientists clues as to how seals manage their oxygen stores when they hold their breath. To find out more, Torre Stockard, Paul Ponganis and colleagues monitored nine juvenile elephant seals as they slept (p. 2607).To measure oxygen levels in the blood, the team inserted catheters into the arteries and veins supplying the major internal organs and took blood samples during normal breathing and at regular intervals during apnea. To find out how much of a blood oxygen store the seals had available before apnea, they measured the percentage of the blood that is made up of red blood cells, blood volume, haemoglobin content and its saturation with oxygen. They found that the seals could store around 52 ml O2 in their blood per kilo of body mass, whereas humans can only hold around 10 ml O2 per kilo in their blood, showing that large oxygen stores contribute to seals' diving prowess.When the seals nodded off and started showing apneas, which lasted between 3 and 11 min, they used up oxygen at a rate of 2-2.3 ml oxygen per 100 ml blood each minute, which is a similar rate to normal conditions. By the end of 7-9 min apneas, the seals had significantly depleted their blood O2store from around 26 ml per 100 ml blood, to around 7 ml per 100 ml blood, a very low level that humans couldn't tolerate.To find out how much oxygen can be transferred from blood to tissue during apnea, the team measured oxygen partial pressure, which is the pressure exerted by an individual gas in a gas mixture, or in solution. The lower the partial pressure gradient, the slower the transfer to tissues. Although the oxygen partial pressure varied greatly during normal breathing, between 34 and 108 mmHg, partial pressure dropped in all the seals during apnea, and the lowest recorded arterial value was 18 mmHg. Humans black out at an oxygen partial pressure of around 25-30 mmHg, showing that the seals are able to squeeze the most out of their oxygen store to get the gas to the tissues that need it, and tolerate very low oxygen levels without any ill-effects.The seals used up around 56% of their oxygen stores during a typical 7 min apnea, but one animal pushed the limit and used up nearly 88% of its store during an 11 min apnea. Despite the oxygen stores getting very low in some cases, none of the seals showed evidence of anaerobic metabolism, since there wasn't a build up of anaerobic by-product lactate in the blood. A small decrease in blood pH was accounted for by carbon dioxide accumulating in the blood. `Their breath-holding is very efficient', says Stockard. `Diving is the norm for these seals, so next we're going to find out what's really happening in diving animals'.

The effects of inhalation anaesthetics on common clinical pathology parameters in laboratory rats

Effects of common anaesthetics such as ether, methoxyflurane, isoflurane, carbon dioxide (at 100%, 80% or 60% admixed with O 2) on toxicity and clinical pathology parameters in rats were investigated. Ether, methoxyflurane and 100% CO 2 induced toxicity in some animals. Erythrocyte, haemoglobin and haematocrit were reduced in females by 100% CO 2, methoxyflurane and isoflurane. Glucose was increased by 60% CO 2, 80% CO 2, ether, isoflurane and methoxyflurane in males. Chloride was reduced by isoflurane and all CO 2 concentrations in females. Serum proteins were reduced by isoflurane and methoxyflurane. Sodium, inorganic phosphate, calcium and magnesium were reduced by methoxyflurane and isoflurane, but increased by all CO 2 concentrations. Potassium was reduced by ether, methoxyflurane or isoflurane. Triiodothyronine and thyroxine were reduced by all anaesthetics. Prolactin was reduced by methoxyflurane, but raised by ether and isoflurane. Erythrocyte cholinesterase (E-ChE) activity is markedly reduced (20–40%) after anaesthesia with all CO 2 concentrations in both sexes. E-ChE was unaffected by ether, methoxyflurane, or isoflurane. Serum and brain cholinesterase activities were not affected. E-ChE inhibition correlated with decreased blood pH, suggesting that this was caused by acidosis. This is of practical relevance in the risk assessment of cholinesterase inhibitors. Conclusions: Clinical pathology data were affected by all anaesthetics. CO 2/O 2 (80%/20%) and isoflurane are the most suitable anaesthetics. If E-ChE activity is to be determined, isoflurane is the anaesthetic of choice.

Effects of Long-term Heat Exposure on Adaptive Mechanism of Blood Acid-base in Buffalo Calves

In order to investigate the mechanism of adaptation to long-term heat stress, six female buffalo calves of about 7 to 8 months age, were exposed to the cool-comfort environment (THI 65) for 21 days to obtain normal values of blood acid-base. An adaptive response of acid-base regulation was determined to long term (21 days) exposure of buffalo calves to hot-dry (THI 80) and hot-humid (THI 84) conditions. Higher rectal temperature and respiratory rate was recorded under hot-humid exposure compared to hot-dry. Significant reduction in the rectal temperature and respiratory rate on day 21 of hot-dry exposure indicated early thermal adaptation compared to hot-humid. Decreasing rectal temperature and respiratory rate from day 1 to 21 was associated with concurrent decrease in blood pH and pCO 2 . Increased plasma chloride concentration with low base excess in blood and in extracellular fluid suggested compensatory response to respiratory alkalosis. Reduced fractional excretion of sodium with increased fractional excretion of potassium and urine flow rate indicated renal adaptive response to heat stress.

Point:Counterpoint: Lactic acid accumulation is an advantage/disadvantage during muscle activity

Point:Counterpoint: Lactic acid accumulation is an advantage/disadvantage during muscle activity

Effect of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exercise

The present study examined the effects of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exhaustive exercise. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) breathing air = MAX (maximal exercise), or (2) under hypercapnia (HC: 21% O(2), 6% CO(2)) that had been maintained from 60 min before to 30 min after exercise = HC; and (3) exercise of the same intensity as HC in air = SUB (submaximal exercise). Arterialized blood was drawn from a superficial vein. Blood pH in HC was significantly lower than in MAX or SUB at rest, at the end of exercise and throughout recovery (P<0.05). Plasma lactate and ammonia concentration in HC was significantly lower than in MAX (P<0.05), and similar to that in SUB at the end of exercise and throughout recovery. Respiratory acidosis resulting from hypercapnia shifted the linear lactate to blood pH relationship during exhaustive exercise below that at normocapnia (P<0.001). The reduced slope of linear blood pH to ammonia relationship under hypercapnia (P<0.001) is attributed to lactic acidosis that is less, due to the lesser work intensity at the end of exhaustion, than that of normocapnia. From these results we conclude that (1) hypercapnia-induced respiratory acidosis promoted the decrease in blood pH due to lactate production throughout recovery; (2) plasma lactate concentration at maximal exercise was lowered under hypercapnia; (3) plasma ammonia concentration at maximal exercise was reduced, probably due to a less intense lactic acidosis.

Evidence from renal proximal tubules that \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\setlength{\oddsidemargin}{-69pt}\begin{document}\begin{equation*}{\mathrm{HCO}}_{3}^{-}\end{equation*}\end{document} and solute reabsorption are acutely regulated not by pH but by basolateral \documentclass[12pt]{minimal}\usepackage{amsmath}\usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy}\usepackage{mathrsfs}\setlength{\oddsidemargin}{-69pt}\begin{document}\begin{equation*}{\mathrm{HCO}}_{3}^{-}\end{equation*}\end{document} and CO2

Respiratory acidosis, a decrease in blood pH caused by a rise in [CO(2)], rapidly triggers a compensatory response in which the kidney markedly increases its secretion of H(+) from blood to urine. However, in this and other acid-base disturbances, the equilibrium CO(2) + H(2)O HCO(3)(-) + H(+) makes it impossible to determine whether the critical parameter is [CO(2)], [HCO(3)(-)], and/or pH. Here, we used out-of-equilibrium CO(2)/HCO(3)(-) solutions to alter basolateral (BL) [HCO(3)(-)], [CO(2)], or pH, systematically and one at a time, on isolated perfused S2 rabbit proximal tubules. We found that increasing [HCO(3)(-)](BL) from 0 to 44 mM, at a fixed [CO(2)](BL) of 5% and a fixed pH(BL) of 7.40, caused HCO(3)(-) reabsorption (J(HCO(3))) to fall by half but did not significantly affect volume reabsorption (J(V)). Increasing [CO(2)](BL) from 0% to 20%, at a fixed [HCO(3)(-)](BL) of 22 mM and pH(BL) of 7.40, caused J(HCO(3)) to rise 2.5-fold but did not significantly affect J(V). Finally, increasing pH(BL) from 6.80 to 8.00, at a fixed [HCO(3)(-)](BL) of 22 mM and [CO(2)](BL) of 5%, did not affect either J(HCO(3)) or J(V). Analysis of the J(HCO(3)) and J(V) data implies that, as the tubule alters J(HCO(3)), it compensates the reabsorption of other solutes to keep J(V) approximately constant. Because the cells cannot respond acutely to pH changes, we propose that the responses of J(HCO(3)) and the reabsorption of other solutes to changes in [HCO(3)(-)](BL) or [CO(2)](BL) involve sensors for basolateral HCO(3)(-) and CO(2).

Effects of dietary supplementation with L-carnitine and fat on blood acid–base responses to handling in slaughter weight pigs1

Blood acid-base responses to handling were evaluated in slaughter weight pigs fed diets supplemented with l-carnitine and fat. The study was carried out as a randomized block design with a 2 x 2 factorial arrangement of treatments: 1) dietary L-carnitine supplementation (0 vs. 150 ppm, as-fed basis); and 2) dietary fat supplementation (0 vs. 5%, as-fed basis). Sixty pigs (91.1 +/- 5.14 kg BW) were housed in mixed-gender groups of five and had ad libitum access to test diets (0.68% true ileal digestible lysine, 3,340 kcal of ME/kg, as-fed basis) for 3 wk. At the end of the feeding period (110.3 +/- 7.52 kg BW), pigs were subjected to a standard handling procedure, which consisted of moving individual animals through a facility (12.2 m long x 0.91 m wide) for eight laps (up and down the facility), using electric prods (two times per lap). There was no interaction between dietary L-carnitine and fat supplementation for any measurement. Pigs fed 150 ppm of supplemental L-carnitine had lower baseline blood glucose (P < 0.05) and higher baseline blood lactate (P < 0.05) concentrations than the nonsupplemented pigs. After handling, pigs fed L-carnitine-supplemented diets had a higher (P < 0.05) blood pH and showed a smaller (P < 0.05) decrease in blood pH and base excess than those fed the nonsupplemental diets. Baseline plasma FFA concentrations were higher (P < 0.01) in pigs fed the 5% fat diet. After the handling procedure, blood glucose, lactate, and plasma FFA were higher (P < 0.05) in pigs fed the 5 vs. 0% fat diets, but blood pH, bicarbonate, and base excess were not affected by dietary fat. The handling procedure decreased (P < 0.01) blood pH, bicarbonate, base excess, and total carbon dioxide and increased (P < 0.01) blood lactate, partial pressure of oxygen, and glucose, and also increased (P < 0.01) rectal temperature. Free fatty acid concentrations were increased by handling in pigs fed both 0 and 5% fat and 150 ppm L-carnitine. In conclusion, dietary L-carnitine supplementation at the level and for the feeding period evaluated in the current study had a relatively small but positive effect on decreasing blood pH changes in finishing pigs submitted to handling stress; however, dietary fat supplementation had little effect on blood acid-base balance.

Hydroxyethyl starch produces attenuation of circulatory shock and cerebral ischemia during heatstroke.

We hypothesized that hydroxyethyl starch (HES), which maintains colloid osmotic pressure and potentially "seals" capillary leaks, would ameliorate circulatory shock and cerebral ischemia during heatstroke in a rat model. Animals under urethane anesthesia were exposed to high ambient temperature (Ta) of 42 degrees C until mean arterial pressure and local cerebral blood flow in the striatum began to decrease from peak level, which was arbitrarily defined as the onset of heatstroke. Control rats were exposed to 24 degrees C. In rats treated with 1 mL/kg, 11 mL/kg, or 22 mL/kg of normal saline (NS) immediately after the onset of heatstroke, the values for survival time (interval between the initiation of heatstroke and animal death) were found to be 21 +/- 2, 36 +/- 9, or 92 +/- 7 min, respectively. Intravenous administration of 11 mL/kg of HES (about 5 times the volume-expanding effect of 11 mL/kg of NS), but not 2 mL/kg of HES (about the same volume-expanding effect as 11 mL/kg NS), significantly increased the survival time from the control values of 36 +/- 9 min to new values of 181 +/- 13 min. In NS (11 mL/kg)-treated or HES (2 mL/kg)-treated rats after heatstroke onset, the values for mean arterial pressure, stroke volume, total peripheral resistance, cerebral blood flow, blood pH, Paco2, Pao2, and brain Po2 were significantly lower than those of rats kept at Ta 24 degrees C. In contrast, the values for colonic temperature and the extracellular concentrations of glutamate, glycerol, and lactate/pyruvate ratio obtained in striatum were significantly higher than those of controls. The heatstroke-induced arterial hypotension, decreased stroke volume and total peripheral resistance, decreased blood pH and Pao2, decreased brain Po2, and increased levels of striatal glutamate, glycerol, and lactate/pyruvate ratio in NS-treated rats were all attenuated significantly by increasing the volume expansion with 11 mL/kg of HES administered immediately at the onset of heatstroke. Our data suggest that HES therapy seems superior to NS treatment during heatstroke. The benefit of HES therapy during heatstroke might have something to do with volume expansion rather than capillary permeability.

Effect of Blood pH on VO2 Kinetics During High-Intensity Exercise

1590 Several investigators have reported faster Phase II (i.e., rapid component) VO2 kinetics for exercise that was preceded by exercise above the lactate threshold. The initial exercise bout decreased blood pH for the start of the subsequent bout, and investigators theorized that this enhanced circulation and increased oxygen delivery to working muscle for the subsequent bout. However, the initial exercise bout may have also caused a metabolic disturbance that contributed to the faster VO2 kinetics. PURPOSE: To investigate the effects of blood pH on VO2 kinetics by altering pH without prior exercise. METHODS: Nine active subjects (29 ± 9 y; 80.1 ± 12.0 kg) completed two 6-min cycling bouts (214 ± 42 W) at 25 W above their ventilatory threshold on separate days. One h prior to exercise, each subject ingested 0.3 g·kg−1 of sodium bicarbonate with ∼1 L of water or water alone. VO2 was measured breath-by-breath and interpolated to 1-s values; 5-s averages were used to examine the VO2 kinetics using a three-component mono-exponential model. RESULTS: Prior to exercise, blood pH was 7.421 ± 0.023 and 7.505 ± 0.031 for the control and bicarbonate trials, respectively. The Phase II VO2 time constant (τ2) was slower for the bicarbonate trial (P = 0.020), but the overall mean response time (MRT) was unaffected. Moreover, blood pH did not affect the amplitude (A3) for Phase III (i.e., slow component) or the difference in VO2 between minutes 3 and 6 (VO2 diff63). The increased blood pH during the bicarbonate trial is thought to have caused a leftward shift of the oxygenhemoglobin disassociation curve and to have diminished vasodilation in working muscle. This would have decreased oxygen delivery to working muscle and slowed VO2 kinetics. CONCLUSION: Our results suggested that oxygen delivery is a limiting factor during exercise above the lactate threshold for only the rapid, but not slow, component of VO2 kinetics.Table

Metabolic findings after colocystoplasty in children

ObjectivesTo investigate whether colocystoplasty has resulted in metabolic changes in the growing child during long-term follow-up according to whether cecum with ascending or sigmoid colon was used. MethodsTwenty-eight patients (mean age at surgery 11 years) were included in the study and divided into two groups: group 1, cystoplasty with cecum and ascending colon (12 patients) and group 2, sigmoid cystoplasty (16 patients). Patients' linear growth, body mass index, and the following parameters were estimated before surgery and at 3, 6, and 12 months, and then yearly after surgery: blood and urine electrolytes (sodium, potassium, chloride, calcium, phosphorus, magnesium), creatinine, urea, blood gases, blood pH, urine pH, and blood alkaline phosphatase (ALP). All the data were statistically analyzed. ResultsIn group 1, the blood ALP increased significantly (P = 0.026) during follow-up. Severe metabolic acidosis with or without hyperchloremia was found in 7 patients. In group 2, the serum sodium and serum calcium levels decreased significantly (P = 0.014 and P = 0.003, respectively); however, the blood ALP, urine sodium, and urine phosphorus levels increased significantly (P = 0.033, P = 0.027, and P = 0.026, respectively) during follow-up. A statistically significant decrease in blood pH (P = 0.022) was found after surgery. Severe metabolic acidosis with or without hyperchloremia was detected in 5 patients. The average linear growth decreased significantly (P = 0.001 and P = 0.016, respectively) 1 and 2 years postoperatively. ConclusionsThe statistically significant increase in blood ALP and decrease in serum calcium indicate bone demineralization after colocystoplasty. Our investigations in children suggest that bone demineralization is more frequent after sigmoid cystoplasty than after the use of cecum and ascending colon.

Swimming Performance and Physiological Responses to Exhaustive Exercise in Radio-Tagged and Untagged Pacific Lampreys

Abstract Populations of Pacific lamprey Lampetra tridentata have declined in the Columbia River basin. One factor that may have contributed to this reduction in population size is an excessive use of energy by adult lampreys as they negotiate fishways at dams during spawning migrations. To gain an understanding of the performance capacity of Pacific lampreys, we estimated the critical swimming speed (U crit) and documented physiological responses of radio-tagged and untagged adult lampreys exercised to exhaustion. The mean (±SD) U crit of untagged lampreys was 86.2 ± 7.5 cm/s at 15°C, whereas the U crit for radio-tagged lampreys was 81.5 ± 7.0 cm/s, a speed that was significantly lower than that of untagged fish. The physiological responses of tagged and untagged lampreys subjected to exhaustive exercise included decreases in blood pH of 0.3–0.5 units, a 40% decrease in muscle glycogen levels, a 22% increase in hematocrit for untagged fish only, and a 4- to 5-fold increase in muscle and a 40- to 100-fold ...