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PubMed1978

Treating heartburn in pregnancy: comparison of acid and alkali mixtures.

A randomised crossover trial was performed in 55 pregnant women who complained of heartburn to see whether alkali or acid treatment alleviated it. Each woman was given a week's treatment with an acid mixture, an alkali mixture, and a placebo in randomised order. Both acid and alkali mixtures were better than placebo, but there was no significant difference between the acid and alkali treatments. Together with the inconsistent reports of some patients, these findings suggest that both acid reflux and bile regurgitation may cause heartburn in pregnant women and that other factors may also play a part. Because the cause of heartburn may be difficult to determine, treatment should be empirical. If the patient does not respond to seven days' acid treatment an alkali mixture should be prescribed; there is a 98% chance that one of these treatments will relieve symptoms.

Bicarbonates↗
PubMed1987

Vasoactive intestinal peptide stimulates alkali excretion in turtle urinary bladder.

The turtle urinary bladder possesses an active transport mechanism for the electrogenic secretion of alkali. This process is independent of exogenous Cl and Na, induced by cyclic AMP (cAMP), and potentiated in bladders from NaHCO3-loaded (alkalotic) turtles. In the present study, it is shown that the serosal addition of vasoactive intestinal peptide (VIP) induces rapidly developing parallel increases in alkali secretion and in the short-circuiting current carried by this secretion. The VIP-induced increment in alkali secretion is greater in the presence than in the absence of an exogenously added phosphodiesterase inhibitor. Additions of a cAMP analog subsequent to the VIP-induced alkali secretion fail to induce any further increase in alkalinization. These results provide evidence for the action of VIP as a hormonal up regulator of alkali excretion in the turtle urinary bladder.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Physiological disposal of the potential alkali load in diet of the rat: steps to achieve acid-base balance.

The purpose of this study was to provide a better understanding of the physiological role of endogenous net organic acid production in rats consuming their usual diet. Balance studies were performed over 24 h, and urine was collected in the day and night portions of the diurnal cycle. A supplemented low-electrolyte diet(LED) was fed to determine whether urinary organic anions were identical to those in the diet. A titration procedure was developed to determine the pK of titratable groups in the urine of rats studied with and without an acid load. Although normal rats excreted net acid (NAE), the latter was inversely related to the amount of food consumed. The rates of excretion of bicarbonate (HCO3), citrate, unmeasured organic anions, and NH+4 were higher in the night portion of the diurnal cycle. NAE rose dramatically when alkali intake was decreased by consuming the LED. Dietary and urinary organic anions were not identical because rats fed the LED supplemented with potassium citrate excreted <10% of this alkali load as citrate and <25% as HCO3. In the 24 h after 3,000 ¿mol NH4Cl was given intraperitoneally, H+ did not appear to be retained, yet NAE rose by only close to 2,000 ¿eq. The rate of excretion of titratable groups with a pK in the 3 to 5 pH range fell by close to 1,000 ¿eq; most of these changes occurred in the first 7 h after NH4Cl was given. We conclude that rat chow provides a large net alkali load. There appear to be two types of endogenous acid production, a form associated with a rise in NAE (e.g., sulfuric acid) and dietary alkali-driven endogenous net acid production, which titrates this alkali. Renal excretion of organic anions makes these acids end products of metabolism.

Acid-Base Equilibrium↗
PubMed1998

Retinal cytokine response in mouse alkali-burned eye.

The kinetics of inflammatory cytokines in sensory retina of mice with corneal alkali-burned eyes were examined. Retinal samples were collected from ICR mice with unburned and alkali-burned eyes from day 3 to day 14. Enzyme-linked immunosorbent assay was used to quantitate the expression levels of interleukin-1 alpha (IL-1 alpha), IL-1 beta and IL-6. Concentrations of IL-1 beta and IL-6 were significantly elevated at day 3 after alkali burn, and reduced to normal level by day 7. The concentration of IL-1 alpha was below assay sensitivity at all times. A significant elevation of IL-1 beta and IL-6 in the sensory retina may contribute to the retinal inflammatory response in the alkali-burned eyes. This is the first report suggesting that the retina is involved in the damage process of alkali burn.

Animals↗
PubMed2005

Accelerated wound healing of alkali-burned corneas in MRL mice is associated with a reduced inflammatory signature.

PURPOSE: The present study was conducted to investigate healing of alkali-burned corneas in MRL/MpJ (MRL) mice. METHODS: Gross, clinical, and histologic criteria were used to compare healing of alkali-burned corneas in MRL and control C57BL/6J (B6) mice. Effects of neutrophil depletion of B6 mice and allogeneic reconstitution of B6 mice with MRL bone marrow on wound healing were evaluated. Gene expression patterns in normal and wounded corneas were surveyed with array-based quantitative real-time RT-PCR (AQPCR). RESULTS: MRL mice showed accelerated reepithelialization and decreased corneal opacity compared with B6 mice after alkali wounding. Marked inflammatory cell infiltration and fibrosis were evident in the corneas and anterior chambers of B6 mice. MRL mice showed less severe lesions, except for stromal edema. Rapid reepithelialization and reduced keratitis/iritis were also observed in neutrophil-depleted B6 mice, but not in B6 mice reconstituted with MRL bone marrow. AQPCR showed transcriptional changes of fewer genes associated with inflammation and corneal tissue homeostasis in alkali-burned corneas from MRL mice. Increased expression of an anti-inflammatory gene, Socs1, and a gene associated with healing, Mmp1a, were evident in MRL corneas. CONCLUSIONS: Alkali-burned corneas heal faster and more completely in MRL mice than in B6 mice, by means of rapid reepithelialization, reduced inflammation, and reduced fibrosis. Reduced inflammation, including decreased neutrophil infiltrates and the lack of a robust proinflammatory gene expression signature correlates with the rapid healing. However, the rapid-healing phenotype is not intrinsic to MRL hematopoietic progenitor cells.

Animals↗
PubMed1991

Expression and distribution of renal vacuolar proton-translocating adenosine triphosphatase in response to chronic acid and alkali loads in the rat.

Renal hydrogen ion excretion increases with chronic acid loads and decreases with alkali loads. We examined the mechanism of adaptation by analyzing vacuolar proton-translocating adenosine triphosphatase (H+ ATPase) 31-kD subunit protein and mRNA levels, and immunocytochemical distribution in kidneys from rats subjected to acid or alkali loads for 1, 3, 5, 7, and 14 d. Acid- and alkali-loaded rats exhibited adaptive responses in acid excretion, but showed no significant changes in H+ ATPase protein or mRNA levels in either cortex or medulla. In contrast, there were profound adaptive changes in the immunocytochemical distribution of H+ ATPase in collecting duct intercalated cells. In the medulla, H+ ATPase staining in acid-loaded rats shifted from cytoplasmic vesicles to plasma membrane, whereas in alkali-loaded rats, cytoplasmic vesicle staining was enhanced, and staining of plasma membrane disappeared. In the cortical collecting tubule, acid loading increased the number of intercalated cells showing enhanced apical H+ ATPase staining and decreased the number of cells with basolateral or poorly polarized apical staining. The results indicate that both medulla and cortex participate in the adaptive response to acid and alkali loading by changing the steady-state distribution of H+ ATPase, employing mechanisms that do not necessitate postulating interconversion of intercalated cells with opposing polarities.

Acid-Base Equilibrium↗
PubMed1993

[The effect of long-term alkali therapy for recurrent calcium stone patients with distal renal tubular acidosis].

Alkali therapy is widely accepted as a treatment for recurrent calcium stone patients with distal renal tubular acidosis (dRTA). Nine patients, five with complete and four with incomplete type of dRTA, were treated with alkali agents for more than three years; an average period of 10.8 years. In five patients, new stone formation and stone growth were completely prevented by this treatment. Among the four failed cases, three did not take enough alkali agents (in spite of our medication), and the other had recurrent urinary tract infection resulting in infectious stone formation. In conclusion, the long-term efficacy of alkali therapy for prevention of recurrent stone formation with dRTA is confirmed when the patient takes enough alkali agents and the urinary tract infection is well controlled.

Acidosis, Renal Tubular↗
PubMed2003

Animal study on expression of laminin and fibronectin in cornea during wound healing following alkali burn.

OBJECTIVE: To observe the expression of laminin and fibronectin in alkali-burned corneas in rats. METHODS: A total of 18 normal Wistar rats were randomly divided into 6 groups (n = 3 in each group). For each rat, one eye was injured by alkali burn, the other one was taken as the normal control. Then all the corneas were surgically removed and the expression of laminin and fibronectin was observed with immunohistochemistry respectively at 7 hours, 1 day, 3 days, 7 days, 14 days and 28 days after alkali burn. RESULTS: Compared with that of the normal controls, the expression of laminin and fibronectin of the burned eyes was dramatically higher at 7 hours, reached peak at 14 days and decreased to the normal level at 28 days after alkali burn. CONCLUSIONS: In the process of wound healing after alkali burn, the expression of laminin and fibronectin increases dramatically, which suggests that laminin and fibronectin may participate in the process of corneal wound healing.

Animals↗
PubMed2003

[Effect of overall alkali of Tongbiling on CD69 expression activated mouse T lymphocytes].

AIM: To investigate the effect of overall alkali of Tongbiling(TBL) on CD69 expression on activated mouse T lymphocytes and its possible mechanism. METHODS: Phorbol 12,13-dibutyrate(PDB) or concanavalin (ConA) were added successively into mouse lymphocytic culture with various concentration of overall alkali TBL. After 24 hours, CD69 expression rate on mouse T lymphocytes activated with PDB or ConA was analyzed by flow cytometry. RESULTS: Overall alkali TBL could significantly down-regulate CD69 expression in a dose-dependent manner. CONCLUSION: Overall alkali TBL can significantly inhibit CD69 expression on activated mouse T lymphocytes. This study provided an experimental basis for application of overall alkali TBL to treatment of rheumatoid arthritis.

Alkaloids↗
PubMed1987

Alkali-burned collagen produces a locomotory and metabolic stimulant to neutrophils.

Polymorphonuclear leukocytes (PMNs) invade the cornea following an alkali burn apparently undergoing a respiratory burst and degranulation, which is thought to lead to corneal ulceration. The supernatant obtained from burned Sigma collagen (Miller type 1) or from bovine cornea produced a significant locomotory stimulus to PMNs. Citrate inhibited this locomotory stimulus by 69.5% and 98%, respectively. PMNs were stimulated to undergo a respiratory burst without the concomitant release of beta-glucuronidase when exposed to the supernatant from alkali-burned commercial collagens, or from bovine or porcine corneas. This stimulation is reduced by 72% (Sigma collagen) or 89% (bovine cornea) when the supernatant is dialyzed against distilled water and reinstated when the osmolality is increased. The degree of the respiratory burst is partially dependent on the volume of the supernatant, the duration of alkali exposure, and/or the concentration of NaOH used. The respiratory burst of PMNs stimulated by alkali-burned Sigma collagen supernatant is inhibited by trifluoperazine but not by citrate or EDTA. Light and electron microscopy of these stimulated PMNs show many large blebs and hairlike projections. The authors hypothesize that collagen breakdown product(s) from alkali burning might be the initial, or one of the initial stimuli, for PMN invasion into the cornea and the subsequent activation of the respiratory burst.

Animals↗
PubMed1996

Electrospray tandem mass spectrometry of alkali metal-containing anionic complexes of tripeptide.

Collision-induced dissociation mass spectra of alkali metal-containing anionic tripeptides are reported. Both N-terminal and C-terminal product ions were observed from the precursor ions [M - 2H + X]- and [M - 3H + 2X]- where X stands for an alkali metal. The results are consistent with precursor ion structures in which an alkali metal ion is centrally located for bonding with the amino terminus, the amide nitrogen atoms, and an oxygen atom of the carboxylate terminus; the second alkali metal ion in [M - 3H + 2X]- is likely attached to the other oxygen atom of the carboxylate terminus.

Amino Acid Sequence↗
PubMed1999

Enhancement of bone-bonding strengths of titanium alloy implants by alkali and heat treatments.

The purpose of this study is to evaluate the bone-bonding ability of alkali- and heat-treated titanium alloys. Smoothed-surface rectangular plates of Ti6Al4V, Ti6Al2Nb1Ta, and Ti15Mo5Zr3Al were prepared. The plates were inserted transcortically into the proximal metaphyses of bilateral rabbit tibiae, with alkali- and heat-treated plates inserted on the right side, and untreated plates on the left. The tensile failure loads between the implants and the bones were measured after 8, 16, and 24 weeks by a detaching test. The untreated implants showed almost no bonding even at 16 weeks, and only weak bonding at 24 weeks. In contrast, treated implants showed bonding to bone at all time periods. Histological examination showed that alkali- and heat-treated alloys bonded directly to the bone. Conversely, the untreated implants had an intervening layer of fibrous tissue between the bone and the plate, or only partial direct contact with the bone. This study demonstrates that alkali and heat treatments enhance the bone-bonding strength of these titanium alloys. Although in this study even tentative conditions of the treatments enhance the bonding strength of the titanium alloys, further work is required to determine the optimum conditions for treatment to give the highest bonding strength. These new bioactive titanium alloys are available for weight-bearing and bone-bonding orthopedic devices.

Alkalies↗
PubMed2000

Bonding of alkali- and heat-treated tantalum implants to bone.

Alkali- and heat-treated tantalum (Ta) has been shown to bond to bone. The purpose of this study was to investigate the effects of chemical treatments on the bone-bonding ability of tantalum implants in rabbit tibiae. Miyazaki et al. reported in vitro that alkali- and heat-treated tantalum had an apatite forming ability in an acellular simulated body fluid (SBF). In this study, smooth-surfaced rectangular plates (15 x 10 x 2 mm) of pure tantalum and treated tantalum were prepared. The plates were implanted transcortically into the proximal metaphyses of bilateral rabbit tibiae, alkali- and heat-treated plates for one limb and untreated plates for the contralateral limb, which served as a paired control. Bone bonding at the bone/implant interface was evaluated by tensile testing and undecalcified histological examination, at 8 and 16 weeks after implantation. The treated implants showed weak bonding to bone at 8 weeks, and exhibited significantly higher tensile failure loads compared with untreated tantalum implants at 16 weeks. The untreated implants showed almost no bonding, even at 16 weeks. Histological examination by Giemsa surface staining, contact microradiography (CMR), and scanning electron microscopy (SEM) revealed that treated tantalum implants bonded directly to bone tissue. In contrast, the untreated tantalum implants had a intervening fibrous tissue layer between the bone and the plate and did not bond to bone at 8 and 16 weeks. It is clear from these results that alkali and heat treatment induce the bone-bonding ability of tantalum. This new bioactive tantalum should be an effective material for weight-bearing and bone-bonding orthopedic devices.

Alkalies↗
PubMed2003

Clustering of nucleosides in the presence of alkali metals: Biologically relevant quartets of guanosine, deoxyguanosine and uridine observed by ESI-MS/MS.

Electrospray ionization (ESI) mass spectra of nucleosides, recorded in the presence of alkali metals, display alkali metal ion-bound quartets and other clusters that may have implications for understanding non-covalent interactions in DNA and RNA. The tetramers of guanosine and deoxyguanosine and also their metaclusters (clusters of clusters), cationized by alkali metals, were observed as unusually abundant magic number clusters. The observation of these species in the gas phase parallels previous condensed-phase studies, which show that guanine derivatives can form quartets and metaclusters of quartets in solution in the presence of metal cations. This parallel behavior and also internal evidence suggest that bonding in the guanosine tetramers involves the bases rather than the sugar units. The nucleobases thymine and uracil are known to form magic number pentameric adducts with K+, Cs+ and NH4+ in the gas phase. In sharp contrast, we now show that the nucleosides uridine and deoxythymidine do not form the pentameric clusters characteristic of the corresponding bases. More subtle effects of the sugars are evident in the fact that adenosine and cytidine form numerous higher order clusters with alkali metals, whereas deoxyadenosine and deoxycytidine show no clustering. It is suggested that hydrogen bonding between the bases in the tetramers of dG and rG are the dominant interactions in the clusters, hence changing the ribose group to deoxyribose (and vice versa) generally has little effect. However, the additional hydroxyl group of RNA nucleosides enhances the non-selective formation of higher-order aggregates for adenosine and cytidine and results in the lack of highly stable magic number clusters. Some clusters are the result of aggregation in the course of ionization (ESI) whereas others appear to be intrinsic to the solution being examined.

Deoxyguanosine↗
PubMed1993

Quantitation of 2-amino-3-methylimidazo[4,5-f]quinoline and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline DNA adducts in specific sequences using alkali or uvrABC excinuclease.

2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MelQx) are carcinogens found in cooked meats that form DNA adducts upon metabolic activation. Purified DNA from Chinese hamster ovary (CHO) cells was reacted in vitro with the active metabolites N-acetoxy-IQ or N-acetoxy-MelQx, and the adduct levels in the 5' dihydrofolate reductase (DHFR) gene and downstream region were quantitated by Southern hybridization. Adducted and restricted DNA was treated with Escherichia coli uvrABC excinuclease or alkali (0.1 N NaOH, 37 degrees C, 60 min) to incise DNA at IQ and MelQx adduct sites. The DNA was then denatured with formamide, electrophoresed on a neutral agarose gel, transferred to a support membrane, and hybridized with sequence-specific DNA probes. Both uvrABC and alkali reduced the intensity of Southern hybridization in proportion to the number of IQ or MelQx adducts in DNA, indicating that these adducts are substrates for uvrABC and that they form alkali-labile lesions in DNA. IQ and MelQx adduct levels were the same in the 5' DHFR gene and in the downstream region. Southern hybridization analysis of pBR322 containing known levels of IQ or MelQx adducts showed that the efficiency of cutting IQ or MelQx adducts by uvrABC excinuclease and alkali was approximately 30% and 15%, respectively. 32P-postlabeling studies examining adduct level in bulk DNA further showed that the adduct profiles were identical in pBR322, CHO DNA, and cultured CHO cells exposed to the reactive metabolites of IQ or MelQx. The results indicate that IQ and MelQx adducts can be quantitated in specific genomic sequences and that this method should be directly applicable to studies of gene-specific repair of these adducts in cultured cells.

Alkalies↗
PubMed1982

Adenosine phosphate and glutathione levels in the regenerated corneal epithelium after abrasion and mild alkali burns.

After scraping away the corneal epithelium or after mild alkali burn, the regeneration of the cellular layers on the stromal surface was observed clinically. The average time of regeneration was 7 days after abrasion and 12 days after mild alkali burn. When the stromal surface was just covered by the newly regrown epithelium, the metabolite levels were determined. In the regenerated corneal epithelium after abrasion the ATP/ADP ratios were much higher than in the normal epithelium and much lower after the alkali burns. The GSH levels were diminished in both groups. The GSSG levels were elevated significantly only after the alkali burns resulting in a decreased redox ratio of the glutathione. The results seemed to be in accordance with morphological and enzymatical data of the regenerating corneal epithelium. Changes of the glutathione in the corneal endothelium were cautiously interpreted.

Adenine Nucleotides↗
PubMed1996

Mechanism of linoleic acid hydroperoxide reaction with alkali.

Treatment of (13S,9Z,11E)-13-hydroperoxy-9,11-octadecadienoic acid (13S-HPODE) with strong alkali resulted in the formation of about 75% of the corresponding hydroxy acid, (13S,9Z,11E)-13-hydroxy-9,11-octadecadienoic acid (13S-HODE), and the remaining 25% of products was a mixture of several oxidized fatty acids, the majority of which was formed from (9Z,11R,S,12S,R)-13-oxo-11,12-epoxy-9-octadecenoic acid by Favorskii rearrangement (Gardner, H.W., et al. (1993) Lipids 28, 487-495). In the present work, isotope experiments were completed in order to get further information about the initial steps of the alkali-promoted decomposition of 13S-HPODE. 1. Reaction of [hydroperoxy-18O2] 13S-HPODE with 5 M KOH resulted in the formation of [hydroxy-18O] 13S-HODE and [epoxy-18O](9Z,11R,S,12S,R)-13-oxo-11,12-epoxy-9-octadecenoi c acid; 2. treatment of a mixture of [U-14C] 13S-HODE and [hydroperoxy-18O2] 13S-HPODE with KOH and analysis of the reaction product by radio-TLC showed that 13S-HODE was stable under the reaction conditions and did not serve as precursor of other products; 3. reaction of a mixture of [U-14C] 13-oxo-9,11-octadecadienoic acid (13-OODE) and [hydroperoxy-18O2] 13S-HPODE with KOH resulted in the formation of [U-14C-epoxy-18O]99Z,11R,S,12S,R)-13-oxo-11,12-epoxy-9-octad ecenoic acid; 4. treatment of a mixture of [hydroperoxy-18O2] 13S-HPODE and [carboxyl-18O1] 13S-HPODE with KOH afforded (9Z,11R,S,12S,R)-13-oxo-11,12-epoxy-9-octadecenoic acid having an 18O-labeling pattern which was in agreement with its formation by intermolecular epoxidation. It was concluded that (9Z,11R,S,12S,R)-13-oxo-11,12-epoxy-9-octadecenoic acid is formed from 13S-HPODE by a sequence involving initial dehydration into the alpha, beta-unsaturated ketone, 13-OODE, followed by epoxidation of the delta 11 double bond of this compound by the peroxyl anion of a second molecule of 13S-HPODE. Rapid conversion of hydroperoxides by alkali appeared to require the presence of an alpha, beta-unsaturated ketone intermediate as an oxygen acceptor. This was supported by experiments with a saturated hydroperoxide, methyl 12-hydroperoxyoctadecanoate, which was found to be much more resistant to alkali-promoted conversion than 13S-HPODE.

Alkalies↗
PubMed2005

Preventive treatment of nephrolithiasis with alkali citrate--a critical review.

Using the keywords "urolithiasis and citrate treatment", "nephrolithaisis and citrate treatment", "kidney stones and citrate treatment", a Medline search revealed 635 articles published between 1 January 1966 and 1 December 2004. For the present analysis, only studies meeting all of the following criteria were included: (1) publications in English or German, (2) studies on preventive alkali citrate treatment in patients with calcium oxalate, uric acid and infection stone disease, (3) clinical studies including at least ten subjects, and (4) treatment phases of at least 1 week duration. A total of 43 studies met the inclusion criteria and were further subclassified according to intermediate or ultimate endpoints as well as to study design. With stone recurrence as the ultimate endpoint, 21 uncontrolled studies in almost 1,000 patients demonstrated a reduction in stone forming rate by 47-100%. In four randomized controlled trials including 227 patients, 53.5% on alkali citrate vs 35% on placebo remained stone-free after at least 1 year of treatment (P<0.0005). Similar values (66% vs 27.5% for alkali citrate vs placebo, P<0.0005) were obtained in 104 patients from two randomized trials with dissolution/clearance of residual stones as endpoint. Unfortunately, up to 48% of alkali citrate treated patients left the studies prematurely, primarily due to adverse effects such as eructation, bloating, gaseousness or frank diarrhea.

Alkalies↗