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PubMed2006

Effect of acidosis on IL-8 and MCP-1 during hypoxia and reoxygenation in human NT2-N neurons.

Inflammation probably plays a significant role in perinatal brain injury. To study the contribution of locally produced cytokines, the effect on cell death of addition of IL-8 and MCP-1 or antibodies to these, and the impact of acidosis, human postmitotic NT2-N neurons were exposed to 3 h of hypoxia and glucose deprivation and reoxygenated for 21 h. After 3 h of hypoxia with neutral medium, IL-8 was significantly increased compared to controls (150 (100-250)% vs. 100 (85-115)%, p=0.023). After 21 h of neutral reoxygenation, both IL-8 (380 (110-710)% vs. 150 (85-260)%, p=0.041) and monocyte chemoattractant protein-1 (MCP-1) (650 (440-2000)% vs. 310 (230-340)%, p=0.007) were significantly increased compared to controls. After 3 h of hypoxia, both IL-8 (p=0.002) and MCP-1 (p=0.008) were significantly lower in cells with acidotic compared with cells with neutral medium. Acidosis during reoxygenation, however, significantly increased IL-8 release, whereas MCP-1 release was diminished. Similar effects of acidosis were seen in normoxic controls. The cells also secreted RANTES and IP-10, but not 8 other cytokines tested. We found no effect on cell death, measured by MTT assay, of addition of IL-8, MCP-1 or antibodies to these. We conclude that human NT2-N neurons release IL-8 and MCP-1 during 21 h of reoxygenation after 3 h of hypoxia. Acidosis led to a differential effect on IL-8 and MCP-1, with increased IL-8 and decreased MCP-1, both during reoxygenation and in normoxic controls. IL-8 and MCP-1 had no effect on cell death.

Acidosis↗
PubMed2005

Acidosis, lactate, electrolytes, muscle enzymes, and other factors in the blood of Sus scrofa following repeated TASER exposures.

Repeated exposure to electro-muscular incapacitating devices could result in repetitive, sustained muscle contraction, with little or no muscle recovery period. Therefore, rhabdomyolysis and other physiological responses, including acidosis, hyperkalaemia, and altered levels of muscle enzymes in the blood, would be likely to occur. Experiments were performed to investigate effects of repeated exposures of TASER International's Advanced TASER X26 on muscle contraction and resultant changes in blood factors in an anaesthetized swine model. A total of 10 animals were used. Six swine were exposed for 5 s, followed by a 5-s period of no exposure, repeatedly for 3 min. (In five of the animals, after a 1-h delay, a second 3-min exposure period was added.) The remaining four animals were used for an additional pilot study. All four limbs of each animal exhibited contraction even though the electrodes were positioned in areas at some distances from the limbs. The degree of muscle contraction generated during the second exposure period was significantly lower than that in the first exposure series. This finding was consistent with previous studies showing that prolonged activity in skeletal muscle will eventually result in a decline of force production. There were some similarities in blood sample changes in the current experiments with previous studies of muscular exercise. Thus problems concerning biological effects of repeated TASER exposures may be related, not directly to the "electric output" per se, but rather to the resulting contraction of muscles (and related interruption of respiration) and subsequent sequelae. Transient increases in hematocrit, potassium, and sodium were consistent with previous reports in the literature dealing with studies of muscle stimulation or exercise. It is doubtful that these short-term elevations would have any serious health consequences in a healthy individual. Blood pH was significantly decreased for 1h following exposure, but subsequently returned toward a normal level. Leg muscle contractions and decreases in respiration each appeared to contribute to the acidosis. Lactate was highly elevated, with a slow return (time course greater than 1 h) to baseline. Other investigators have reported profound metabolic acidosis during restraint-associated cardiac arrest. Since restraint often occurs immediately after TASER exposure, this issue should be considered in further development of deployment concepts. On the basis of the results of the current studies, the repeated use of electro-muscular incapacitating devices in a short period of time is, at least, feasible, with the caveat that some medical monitoring of subjects may be required (to observe factors such as lactate and acidosis).

Acidosis↗
PubMed2005

Acidosis affects tumor cell survival through modulation of nitric oxide release.

The influence of environmental pH on the production of tumoricidal free radical nitric oxide (NO) was investigated in mouse fibrosarcoma L929 and rat glioma C6 cell lines. A combination of IFN-gamma and IL-1 induced a significant NO release and subsequent reduction of cell viability in tumor cell lines. Acidification of cell culture medium reduced tumor cell NO production in a pH-dependent manner. While the inhibitory effect of acidosis on NO production in C6 cells was associated with a further decrease in cell viability, it completely rescued L929 cells from NO-dependent apoptotic and necrotic death. Acidic pH diminished IFN-gamma+ IL-1-induced expression of inducible NO synthase (iNOS) mRNA and protein, and abolished the activation of iNOS transcription factor IRF-1 in L929 cells. Moreover, extracellular acidosis significantly impaired cytokine-induced phosphorylation of MAP kinase p44/42 (ERK1/2) and subsequent expression of transcription factor c-Fos in L929 cells. Finally, mild acidosis (pH 6.8) augmented, while severe acidosis (pH 6.0) reduced, IFN-gamma-induced iNOS activation/NO release and NO-dependent anticancer activity of rat and mouse macrophages. Taken together, our findings indicate that modulation of macrophage and tumor cell iNOS by an acidic microenvironment might influence the progression of NO-sensitive solid tumors.

Acidosis↗
PubMed2004

Fatal metabolic acidosis caused by thiamine deficiency.

Acute thiamine deficiency, an uncommon cause of hemodynamic instability in Western countries, may be manifested by acute heart failure and neurological deficits. Severe metabolic acidosis is one of its least recognized features. We present a report of foreign workers who complained of weakness and lower limb edema and were found to have acute thiamine deficiency. One died of refractory metabolic acidosis and shock, and the diagnosis was reached post mortem. Thiamine deficiency should be considered in every case of severe lactic acidosis without an obvious cause, especially in high-risk populations (malnourished, alcoholics, Far-East workers, etc). Whenever it is suspected, empiric treatment with thiamine should be initiated immediately. Physicians who care for populations at risk should be familiar with the clinical spectrum of nutritional deficits, and monitor the nutritional habits of these patients carefully. The treatment is inexpensive and devoid of adverse effects. Moreover, delaying thiamine administration in patients with deficiency may cause severe life-threatening metabolic acidosis and affect recovery. The prophylactic use of thiamine in a high-risk population, even before blood levels are received, may be cost effective.

Acidosis↗
PubMed2005

Metabolic acidosis: differentiating the causes in the poisoned patient.

Metabolic acidosis may arise from several drugs and toxins through a variety of mechanisms. Differentiating the causes of metabolic acidosis in the poisoned patient is an indispensable skill in clinical practice. Comprehension of toxin-induced metabolic acidosis, combined with a thorough history, physical examination, appropriate use of laboratory tests, and a stepwise approach, should aid the clinician in determining the cause of metabolic acidosis in the poisoned patient. When confronted with such a patient, it is imperative that one administer appropriate antidotal therapy, when necessary, and provide the patient with exceptional supportive care.

Acidosis↗
PubMed2005

Mitochondrial tRNA gene mutations in patients having mitochondrial disease with lactic acidosis.

Lactic acidosis has been associated with a variety of clinical conditions and can be due to mutation in nuclear or mitochondrial genes. We performed mutations screening of all mitochondrial tRNA genes in 44 patients who referred as hyperlactic acidosis. Patients showed heterogeneous phenotypes including Leigh disease in four, MELAS in six, unclassified mitochondrial myopathy in 10, cardiomyopathy in five, MERRF in one, pure lactic acidosis in six, and others in 12 including facio-scaplo-femoral muscular dystrophy (FSFD), familial cerebellar ataxia, recurrent Reye syndrome, cerebral palsy with mental retardation. We measured enzymatic activities of pyruvate dehydrogenase complex, and respiratory chain enzymes. All mitochondrial tRNA genes and known mutation of ATPase 6 were studied by single strand conformation polymorphism (SSCP), automated DNA sequence and PCR-RFLP methods. We have found one patient with PDHC deficiency and six patients with Complex I+IV deficiency, though the most of the patients showed subnormal to deficient state of respiratory chain enzyme activities. We have identified one of the nucleotide changes in 29 patients. Single nucleotide changes in mitochondrial tRNA genes are found in 27 patients and one in ATPase 6 gene in two patients. One of four pathogenic point mutations (A3243G, C3303T, A8348G, and T8993G) was identified in 12 patients who showed the phenotype of Leigh syndrome, MELAS, cardimyopathy and cerebral palsy with epilepsy. Seventeen patients have one of the normal polymorphisms in the mitochondrial tRNA gene reported before. SSCP and PCR-RFLP could detect the heteroplasmic condition when the percentage of mutant up to 5, however, it cannot be observed by direct sequencing method. It is important to screen the mtDNA mutation not only by direct sequence but also by PCR-RFLP and the other sensitive methods to detect the heroplasmy when lactic acidosis has been documented in the patients who are not fulfilled the criteria of mitochondrial disorders.

Acidosis, Lactic↗
PubMed2005

Acidosis of severe falciparum malaria: heading for a shock?

Severe Plasmodium falciparum malaria encompasses a complex syndrome affecting many organs and causing physiological perturbations that have many features in common with children with sepsis. Among these, metabolic acidosis has emerged as a central feature of severe malaria and is the best independent predictor of a fatal outcome in both adults and children. There is now clear evidence that intravascular hypovolaemia (shock) is common in children with malarial acidosis. How it should be treated presents a therapeutic dilemma because acidosis often coexists with impaired consciousness (cerebral malaria). We summarize the results of recent clinical trials examining the safety and efficacy of volume expansion in children with 'cerebral malaria' complicated by acidosis.

Acidosis↗
PubMed2005

Carbon dioxide pneumoperitoneum-mediated attenuation of the inflammatory response is independent of systemic acidosis.

BACKGROUND: The purpose of this study was to determine if systemic acidosis induced by peritoneal absorption of carbon dioxide (CO2 ) during laparoscopy plays a role in CO2 pneumoperitoneum-mediated attenuation of the acute phase inflammatory response associated with perioperative sepsis. The influence of hepatic polymorphonuclear (PMN) leukocyte infiltration on this phenomenon was also investigated. METHODS: Forty-five rats were randomized into 5 groups: anesthesia control, open cecal ligation and puncture (OCLP), laparoscopic cecal ligation and puncture using helium for insufflation (He LCLP), LCLP using CO2 with continued spontaneous ventilation (LCLP-SV), and LCLP using CO2 with intubation and positive pressure ventilation (LCLP-PPV). RESULTS: After 30 minutes, arterial blood gas parameters remained normal in control, OCLP rats, and He LCLP rats, while CO2 LCLP-SV rats developed significant hypercarbic acidosis. This acidosis was corrected in CO2 LCLP-PPV rats ( P < .0001 vs CO2 LCLP-SV for both). Expression of the rat acute phase gene alpha 2 -macroglobulin was greater after OCLP and He LCLP than after either CO2 LCLP-SV or CO2 LCLP-PPV ( P < .0001 vs either CO2 OCLP-SV for both). However, levels of alpha 2 -macroglobulin were not significantly different between the acidotic (LCLP-SV) and normocarbic (LCLP-PPV) CO2 groups. Infiltration of the hepatic parenchyma by PMNs did not differ significantly between groups. CONCLUSIONS: CO2 insufflation-induced systemic acidosis is not responsible for the reduction in the acute phase inflammatory response observed in laparoscopic animal models of sepsis. Hepatic PMN infiltration also does not appear to mediate this effect.

Acidosis↗
PubMed2002

Lactic acidosis after cardiac surgery is associated with polymorphisms in tumor necrosis factor and interleukin 10 genes.

BACKGROUND: Lactic acidosis after cardiac surgery is a manifestation of excess cytokine production. Cytokine-related genetic polymorphisms account for variability in cytokine response and may predispose to the development of lactic acidosis after cardiac surgery. METHODS: Routine postoperative cardiac surgery patients were studied. Lactic acid levels were greater than 4 mmol/L in study patients and less than 4 mmol/L in controls. Polymerase chain reaction-based techniques were used to examine carriage of tumor necrosis factor beta (TNF-beta), TNF G-308A, and interleukin 10 (IL-10) G-1082A alleles. RESULTS: Demographic characteristics and details of surgery were similar for 30 control and 21 study patients. Lactic acid levels after intensive care admission changed over time and were related to both TNF-beta and IL-10 G-1082A polymorphisms. All 4 study patients homozygous for TNF-beta1 and carrying an IL-10-1082A allele developed lactic acidosis (p = 0.02). There was no relation between the rate of epinephrine infusion or duration of cardiopulmonary bypass and lactic acid levels. CONCLUSIONS: Genetic factors have a role in the development of lactic acidosis after cardiac surgery.

Acidosis, Lactic↗
PubMed1994

Protein and acidosis alter calcium-binding and fluorescence spectra of the calcium indicator indo-1.

The fluorescent indicator indo-1 is widely used to monitor intracellular calcium concentration. However, quantitation is limited by uncertain effects of the intracellular environment on indicator properties. The goal of this study was to determine the effects of protein and acidosis on the fluorescence spectra and calcium dissociation constant (Kd) of indo-1. With 350 nm excitation light, the ratio of indo-1 fluorescence in the absence versus the presence of saturating Ca2+ at wavelength lambda (S lambda) and Kd increased with [protein]. At pH 7.3, Kd, S400, and S470, which were 210 nM, 0.033, and 1.433 in the absence of protein, increased to 808 nM, 0.161, and 2.641, respectively, by adding proteins from frog muscle and to 638 nM, 0.304, and 3.039, respectively, by adding proteins from rat heart. Effects of protein on indo-1 fluorescence were reduced at higher [indo-1]. Acidosis (pH 6.3) had separate effects, which were additive to those of protein: in the absence of protein, acidosis increased Kd to 640 nM; frog muscle proteins further increased Kd to 1700 nM. Acidosis also changed S lambda slightly. In summary, interaction with protein or protons alters indo-1 calcium-binding and fluorescence. These findings are consistent with several previous studies and suggest that indo-1 calibration constants need to be derived in the presence of appropriate types of protein, ratio of [indo-1]/[protein], and pH.

Acidosis↗
PubMed1988

Effects of hypoxia with mild acidosis and reoxygenation on slow response action potentials in canine myocardial tissues.

We studied slow response action potentials (SRAP) in canine ventricular muscle tissue during hypoxia (and mild acidosis) and reoxygenation. Slow responses were initiated by perfusing the tissue with a solution containing 27 mM KCl and 10(-6) M norepinephrine. The tissue was stimulated at 0.5 Hz, 20V and 4ms (duration of the pulse). Microelectrode techniques were used to record action potential and mechanical activity was recorded with a force displacement transducer. Hypoxia and mild acidosis progressively diminished the amplitude and duration of these SRAPs, whereas reperfusion/reoxygenation progressively increased their amplitude even more than that in the control (prehypoxic value). Action potential duration (APD) increased (at all levels) during reperfusion compared to that in hypoxia and mild acidosis but APD remained shorter than the control (prehypoxic level). The effects of hypoxia (and mild acidosis) and subsequent reoxygenation seem similar to that of elevating the extracellular calcium (increased inward current). From these experiments one cannot, however, distinguish the effects of hypoxia on inward current from those on the outward currents.

Acidosis↗
PubMed1985

The relative sensitization by acidosis of five calcium blockers in cat papillary muscles.

We have previously reported that the negative inotropic effects of both verapamil and nifedipine on cat papillary muscles are enhanced as pH is lowered from 7.4 to 6.8 and 6.0. These studies have now been extended to compare the relative sensitization by acidosis of verapamil, nifedipine, lidoflazine, perhexilene and diltiazem. Developed tension was recorded in cat papillary muscles and the calcium concentration was adjusted over the range 2 to 10 mM. At pH 7.4, addition of all five drugs moved the dose response curve to the right with pA2 values from 4.82 (lidoflazine) to 9.94 (nifedipine). At pH 6.0, there was eight-fold sensitization by acidosis for verapamil, but four, three, and two-fold sensitization for nifedipine, lidoflazine and perhexilene. Diltiazem, however, was not sensitized by acidosis. The differential effects of acidosis on the negative inotropic properties of the five drugs may reflect their ancillary properties opposite gating of the calcium channel, local anaesthesia, intracellular calcium movement or Na+/Ca2+ exchange, but also suggest that diltiazem may have the property of inhibiting the effects of low pH on cell membranes.

Acidosis↗
PubMed1988

Ouabain inhibits intracellular pH recovery from acidosis in cultured mouse heart cells.

Myocardial ischaemia induces cytosolic acidification, which promotes cardiac damage, dysfunction or arrhythmia. In this study, we investigated the effect of ouabain on the intracellular pH (pHi) in cultured mouse ventricular cells, using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The average resting pHi in myocytes was 7.19. After myocytes were acid-loaded with NH4Cl, the pHi recovered from acidosis to the resting level within a few minutes via amiloride-sensitive Na+/H+ exchange. Ouabain inhibited this pHi recovery dose-dependently with half-maximal inhibition at 3 X 10(-5) M, but did not suppress the ionophore monensin-induced pHi elevation. The inhibition of the pHi recovery from acidosis by ouabain is possibly caused by an inhibition of amiloride-sensitive Na+/H+ exchange, which is secondary to a suppression of Na+ efflux through (Na+, K+) pump. Above results demonstrate the possibility that digitalis promotes intracellular acidosis or inhibits the pHi recovery from acidosis in ischaemic myocardium.

Acidosis↗
PubMed1988

Sodium deficit causing decreased weight gain and metabolic acidosis in infants with ileostomy.

The records of 11 infants, 25 to 38 weeks' gestation, with metabolic abnormalities induced by ileostomy fluid losses were reviewed. At operation for necrotizing enterocolitis (NEC) (9) or meconium ileus (MI) (2), they weighed between 1,100 and 3,100 g and were from one to 41 days old. All developed total body sodium depletion and metabolic acidosis from ileostomy bicarbonate loss. In seven, sodium depletion was severe enough to require supplementation; six initially lost or failed to gain weight despite being fed adequate diet and calories. However, after receiving sodium supplementation (three with NaCl and three with NaHCO3), these six patients gained weight and improved their metabolic acidosis. The other five subjects did not initially receive sodium supplementation. Four gained weight; one of these later received supplemental NaHCO3 for a metabolic acidosis. The fifth patient failed to thrive until his ileostomy was closed. All infants initially had urine Na less than 10 mEq/L and normal serum Na. All infants whose urine Na rose above 10 mEq/L and had serum HCO3- greater than or equal to 20 mEq/L grew adequately. A direct relationship existed between ileostomy output and sodium intake required for growth. This expressed mathematically (Na intake = 1.2 + [0.13 x ileostomy output] shows a basal sodium need (with no ileostomy output) of 1.2 mEq/kg/d and an additional requirement of 0.13 mEq/kg/d of sodium for each mL/kg/d of ileostomy output. We conclude that infants with ileostomies are at extreme risk of total body sodium depletion with resultant metabolic acidosis and inadequate weight gain. These infants require sodium supplementation with a combination of NaCl and NaHCO3.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1977

Neonatal lactic acidosis and renal failure: the role of peritoneal dialysis.

Lactic acidosis accompanied by acute renal failure in the newborn period was studied in two infants with circulatory insufficiency and hypoxia. Peritoneal dialysis was necessitated by anuria and serum potassium concentrations of 12.0 and 8.9 mEq/1. Plasma lactate concentration was 35 and 50 mM/1 and blood pH 7.23 and 7.18, respectively, at the time dialysis was instituted. Because of the uncontrollable anaerobic metabolism in these two patients, and the attendant inability to metabolize lactate, the use of commercial lactate-containing dialysates as a source of base was shown to be ineffective in correcting the acidosis and hypothesized to cause a worsening of metabolic acidosis due to a loss of bicarbonate from extracellular fluid into dialysate. Stabilization or improvement in the metabolic acidosis occurred with the utilization of a dilaysate containing bicarbonate with a gradient favoring movement of bicarbonate into, and lactate out of, extracellular fluid.

Acidosis↗
PubMed1984

Renal tubular acidosis type 4 in neonatal unilateral kidney diseases.

Three neonates, two with unilateral renal vein thrombosis and one with unilateral dysplastic kidney, developed type 4 renal tubular acidosis, manifested by nonazotemic hyperkalemic metabolic acidosis with alkaline urine pH and reduced potassium excretion. Normal plasma concentrations of sodium, aldosterone, and renin activity, together with normal renal fractional excretion of sodium, supported the diagnosis of renal tubular acidosis type 4, subtype 5. Arginine HCl loading studies showed that despite their ability to bring the urine pH to less than 5.8, net acid excretion was inadequate relative to the corresponding plasma bicarbonate concentration. Treatment with oral bicarbonate resulted in sustained normalization of blood acid-base status and accelerated linear growth in the first two infants, in whom spontaneous recovery occurred by ages 8 and 15 months, respectively. At that time, the affected kidneys were extremely small with distorted collecting systems; the contralateral kidneys showed compensatory hypertrophy. In the third infant, persistent acidosis and growth failure resulted from medical noncompliance; the removal of the dysplastic kidney at 7 months of age was followed by the return to normal blood acid-base status and normalized tubular hydrogen and potassium excretion. We conclude that neonatal unilateral kidney disease can result in renal tubular subtype 5. Spontaneous recovery can be expected, presumably because of " autonephrectomy " of the affected kidney plus the compensatory hypertrophy of the contralateral kidney.

Acidosis, Renal Tubular↗
PubMed1998

D-lactic acidosis: pathologic consequence of saprophytism.

In this report, we describe a 50-year-old woman with a short bowel who had recurrent episodes of weakness, ataxia, slurred speech, confusion, and nausea. D-Lactic acidosis was diagnosed on the basis of a D-lactate level of 8.2 mmol/L (normal, 0 to 0.25) obtained during an episode of confusion. D-Lactic acidosis is a potentially fatal clinical condition seen in patients with a short small intestine and an intact colon. Excessive production of D-lactate by abnormal bowel flora overwhelms normal metabolism of D-lactate and leads to an accumulation of this enantiomer in the blood. This disorder provides insight into the role of intestinal flora in human metabolism and demonstrates the manner in which altered intestinal flora can produce disease in humans. Increased awareness of D-lactic acidosis is necessary for prompt and appropriate treatment. The pathophysiology and treatment of D-lactic acidosis are reviewed.

Acidosis, Lactic↗
PubMed2003

Intrapartum computerized fetal heart rate parameters and metabolic acidosis at birth.

OBJECTIVE: To estimate to what extent computerized fetal heart rate (FHR) parameters are affected by labor and to estimate the relationship between FHR parameters and the degree of fetal metabolic acidosis in laboring patients at term. METHODS: Fifty-one women between 37 and 42 weeks' gestational age were recruited prospectively in the following groups: 1) nonlaboring women, and 2) laboring women requiring fetal scalp electrode for continuous electronic FHR monitoring. Computerized FHR analysis was performed for 1 hour within 6 hours of delivery in the nonlaboring group and continuously throughout labor in the laboring group. Multiple linear regression analysis was used to determine the relationship between individual FHR parameters during the last hour before delivery and the degree of metabolic acidosis at birth. RESULTS: The umbilical cord artery base excess and pH did not show any significant correlation with any of the computer-derived FHR parameters studied. Both umbilical cord venous base excess and pH were inversely related to the number of large FHR decelerations (r = -.46, P <.01 and r = -.56, P <.01, respectively). Labor was associated with a 31% increase in both short- and long-term FHR variation in the reassuring FHR tracing group when compared with nonlaboring women. Although this increase in FHR variation was not seen in the nonreassuring FHR tracing group, there was no relationship to the degree of metabolic acidosis at birth. CONCLUSION: In term pregnant women with reassuring FHR tracing, labor causes an increase in both short- and long-term FHR variation, which was abolished in the presence of nonreassuring FHR tracing. Computer-derived FHR parameters studied during the last hour of labor were not correlated with the degree of metabolic acidosis as measured in the umbilical artery at birth.

Acidosis↗