A comparison of survival of moulded monoblock and modular tibial components of 751 AGC total knee replacements in the treatment of rheumatoid arthritis.

We evaluated the survival of moulded monoblock and modular tibial components of the AGC total knee replacement in patients with rheumatoid arthritis. Between 1985 and 1995, 751 knees with this diagnosis were replaced at our institution. A total of 256 tibial components were of the moulded design and 495 of the modular design. The mean follow-up of the moulded subgroup was 9.6 years (0.5 to 14.7), and that of the modular group 7.0 years (0.1 to 14.7). The groups differed significantly from each other in Larsen grade, cementing of components and patellar resurfacing, but no statistically significant difference between the survival of the components was found (Log rank test, p = 0.91). The cumulative success rate of the moulded group was 96.8% (95% confidence interval 93.6% to 98.4%) at five years and 94.4% (95% confidence interval 90.4% to 96.7%) at ten years, and of the modular group 96.2% (95% confidence interval 94% to 97.6%) and 93.6% (95% confidence interval 89.7% to 96%), respectively. Revision was required in 37 total knee replacements, the main causes were infection, pain, loosening of the tibial component and patellar problems. Survival rates for both components were satisfactory.

Comparison of the effect of gluconate, lactose, and xylitol on bone recalcification in calcium-deficient rats.

The therapeutic value of three calcium absorption promoting carbohydrates, lactose, gluconate and xylitol, in bone calcification was evaluated in 7-week-old male rats which were fed on a semisynthetic Ca-deficient diet for 3 weeks. Lactose + CaCO3, xylitol + CaCO3, Ca-gluconate, or CaCO3 alone were administered to the Ca-deficient rats for 2 weeks; the carbohydrate and Ca contents of the diets were 5% and 0.5%, respectively. The Ca-deficient rats showed a decrease in serum total Ca and ionized Ca2+ and in tibial Ca, Mg, P and density, with a concomitant increase in bone hydroxyproline concentration. Bone and serum tartrate-resistant acid phosphatase activities were increased 2-fold and the serum 1,25(OH)2D3 level 5-fold. Smaller increases were found in serum calcitonin, PTH, alkaline phosphatase and osteocalcin levels. These changes (except calcitonin) were reversed by the administration of Ca and the carbohydrates. It was observed that all three agents improved the recalcification of bones compared with the effect of CaCO3 alone. The effect of lactose and xylitol was superior to that of gluconate. These results suggest advantages in the use of xylitol in Ca-supplements.

The rostroventromedial medulla is not involved in alpha 2-adrenoceptor-mediated antinociception in the rat.

The aim of the current study was to investigate the role of the rostroventromedial medulla (RVM) in alpha 2-adrenoceptor-mediated antinociception. Medetomidine or clonidine, selective alpha 2-adrenoceptor agonists were microinjected into the RVM in unanesthetized rats with a chronic guide cannula. The antinociceptive effects were evaluated using the tail-flick and hot-plate tests. For comparison, medetomidine was microinjected into the cerebellum or the periaqueductal gray (PAG). To study the role of medullospinal pathways, the tail-flick latencies were also measured in spinalized rats. The reversal of the antinociception induced by intracerebral microinjections of medetomidine was attempted by s.c. atipamezole, a selective alpha 2-adrenoceptor antagonist. The reversal of the antinociception induced by systemic administration of medetomidine was attempted by microinjections of 5% lidocaine or atipamezole into the RVM. When administered into the RVM, medetomidine produced a dose-dependent (1-30 micrograms) antinociception in the tail-flick and hot-plate tests, which antinociceptive effect was completely reversed by atipamezole (1 mg/kg, s.c.). Also clonidine produced a dose-dependent (3-30 micrograms) antinociception following microinjection into the RVM. Microinjections of medetomidine into the cerebellum or the PAG produced an identical dose-response curve in the tail-flick test as that obtained following microinjection into the RVM. In spinalized rats the antinociceptive effect (tail-flick test) induced by medetomidine microinjected into the RVM was not less effective than in intact rats. Lidocaine (5%) or atipamezole (5 micrograms) microinjected into the RVM did not attenuate the antinociception induced by systemically administered medetomidine (100 micrograms/kg, s.c.).(ABSTRACT TRUNCATED AT 250 WORDS)

Involvement of nitric oxide and serotonin in modulation of antinociception and pressor responses evoked by stimulation in the dorsolateral region of the periaqueductal gray matter in the rat.

In rats anaesthetized with alphaxalone/alphadolone, electrical stimulation in the periaqueductal gray matter in the region lying lateral and dorsolateral to the aqueduct produced a pressor response and an increase in the latency of the tail flick response to noxious heat applied to the tail. The antinociception and the pressor response were significantly attenuated following microinjection of 15 nmol 5-hydroxytryptamine at the site of stimulation in the periaqueductal gray matter. Microinjection of an equal volume of 165 mM saline had no effect. The inhibitory effects of 5-hydroxytryptamine were blocked by prior intracerebroventricular administration of 100 microg of the nitric oxide synthase inhibitor L-nitroarginine methyl ester. Neither 5-hydroxytryptamine or L-nitroarginine methyl ester had any effect on resting arterial pressure or on the baseline latency of the tail flick reflex. It is suggested that the inhibitory effects of 5-hydroxytryptamine in the dorsolateral periaqueductal gray matter are normally dependent on the functional integrity of local nitric oxide synthase-containing interneurons. Nitric oxide may act in association with 5-hydroxytryptamine to control the excitability of the aversive system in the midbrain.

Myometrial estrogen and progesterone receptor binding in pregnancy: inhibition by the detergent action of phospholipids.

We characterized the phospholipid inhibition of estradiol and progesterone binding to guinea-pig and human myometrial receptors. Of twelve compounds studied, phosphatidylinositol (PI), lysophosphatidic acid and lysophosphatidylcholine (lyso-PC) were the most active inhibitors (50% inhibition at 10(-5) M). Lyso-PC with fatty acid chain length C14:0 inhibited ligand binding both to estrogen receptor (ER) and progesterone receptor (PR), C16:0 only to PR and C18:0 neither to ER nor to PR. The lyso-derivates were more inhibitory than the parent compounds. The ionic detergent (sodium taurocholate) inhibited both ER and PR binding, but the non-ionic detergent (Triton X-100) only PR. Triton X-100 enhanced the PI-induced inhibition of ER binding by a factor of 10. PR was more sensitive to inhibition than ER in all cases. The type of inhibition was non-competitive. At term pregnancy, ligand binding to myometrial ER or PR was low or absent in humans, but moderate in the guinea-pig. Phospholipid extracts of human decidua and fetal membranes contained PI and phosphatidylserine rather than lyso-PC. The extract was a potent inhibitor of ligand binding to PR (50% inhibition at 10(-6) M phospholipid phosphorus), but not to ER. The physicochemical environment, modulated by phospholipids acting as detergents, may regulate sex steroid function also in vivo. This might have special significance for pregnancy maintenance.

Carrageenan-induced changes in spinal nociception and its modulation by the brain stem.

Carrageenan was used to study inflammation-induced changes in spinal nociception and its brain stem modulation in the pentobarbitone-anesthetized rat. Carrageenan was administered intraplantarly into one hindpaw 2 h before the start of electrophysiological single unit recordings of wide-dynamic range (WDR) neurons of the spinal dorsal horn. Carrageenan produced a significant leftward shift in the stimulus-response function for mechanical stimuli, whereas that for noxious heat stimuli was short of statistical significance. Conditioning electrical stimulation in the rostroventromedial medulla (RVM) significantly attenuated noxious heat-evoked, but not mechanically evoked, responses to spinal dorsal horn WDR neurons in the control (contralateral) side. However, in the carrageenan-treated side RVM stimulation had no significant effect on mechanically or noxious heat-evoked responses. Following direct spinal administration of neuropeptide FF (NPFF), noxious heat-evoked responses, but not mechanically evoked responses, were attenuated by RVM-stimulation also in the carrageenan-treated side. This selective NPFF-induced enhancement of brain stem-spinal inhibition was not reversed by naloxone. The results indicate that carrageenan-induced inflammation significantly changes the response properties of spinal nociceptive neurons and their brain stem-spinal modulation. During inflammation, NPFF in the spinal cord produces a submodality-selective potentiation of the antinociceptive effect induced by brain stem-spinal pathways, independent of naloxone-sensitive opioid receptors.

RT-PCR from eosinophil-depleted leukocytes without RNA extraction: cell selection using streptavidin PCR tubes.

OBJECTIVES: The major RNase activity of leukocytes has been attributed to eosinophil-derived neurotoxin EDN. Depletion of eosinophils enables RT-PCR from 10(5) leukocytes without RNA extraction. In this study we introduced streptavidin-coated PCR tube strips for the selection of eosinophil-free leukocytes for RT-PCR analysis. DESIGN AND METHODS: Polypropylene 0.2 ml PCR tube strips were coated with streptavidin and biotinylated antibodies against cell surface antigens were attached to the tubes. CD7-positive T-lymphocytes, CD19-positive B-lymphocytes and CD16-positive cells (mainly neutrophils and monocytes) were positively selected by incubating of 1-2 x 10(5) leukocytes in the antibody-coated PCR tubes for 30 min at 23 degrees C. RESULTS: The mean amount of cells bound into a tube was 31,500 (CV25%) T-cells and 8,600 (CV61%) B-cells from 12 blood samples, and 23,600 (CV22%) CD16+ cells from 17 samples. The influence of selected cell lysate on the RT-PCR analysis of Philadelphia chromosome (bcr/abl translocation) from 100 K562 cells was small: 78% (CV28%) of the leukocyte-free signal was obtained in the presence of CD16+ cells or 89% (CV15%) and 99% (CV11%) and in the presence of T-cells and B-cells, respectively. CONCLUSIONS: These results suggest that through the introduction of eosinophil-free cell population into RT-PCR a reproducible method with reasonable leukocyte yield and avoiding RNA extraction was developed.

Role of nitric oxide and serotonin in modulation of the cardiovascular defence response evoked by stimulation in the periaqueductal grey matter in rats.

In rats anaesthetised with alphaxalone/alphadolone, electrical stimulation (10 s trains of 1 ms pulses at 80 Hz, 40-80 microA) in the dorsolateral and lateral periaqueductal grey matter (PAG), the midbrain defence area, evoked a pressor response with tachycardia and vasodilatation in the hindlimb. Microinjection of 200 nl 0.66 mM 5HT, but not 200 nl 165 mM NaCl, at the site of stimulation attenuated the components of the PAG-evoked response by 75-98%. The effect of 5HT was significantly reduced by prior intracerebroventricular injection of 100 microg N-nitro-L-arginine methyl ester (an inhibitor of nitric oxide synthase) but not N-nitro-D-arginine methyl ester. Resting cardiovascular parameters did not change significantly following any of these manipulations. The results suggest that serotonin exerts an inhibitory modulation on the excitability of the midbrain defence area by a mechanism which involves nitric oxide.

Lidocaine in the rostroventromedial medulla and the periaqueductal gray attenuates allodynia in neuropathic rats.

In the present study we attempted to find out if the rostroventromedial medulla (RVM) or the periaqueductal gray (PAG) might contribute to chronic allodynia induced by unilateral ligation of two spinal nerves in the rat. Lidocaine was microinjected in the RVM or PAG and allodynia was quantitatively determined by measuring the hindlimb withdrawal thresholds to mechanical stimulation of the paw. For comparison, lidocaine was also injected systemically (s.c.). Lidocaine in the RVM produced a dose-related (20 and 40 micrograms) antiallodynic effect. Lidocaine (20 micrograms) in the PAG produced identical antiallodynic effect as in the RVM. With systemic administrations of lidocaine, a considerably higher dose (> > 40 micrograms) was needed to produce a significant antiallodynic effect. Naloxone, an opioid-antagonist (1 mg/kg s.c.), did not attenuate the antiallodynic effect of lidocaine in the RVM. An antiallodynic dose of lidocaine (20 micrograms) in the RVM or the PAG did not influence the withdrawal response in the unoperated hindlimb nor the heat-induced tail-flick reflex. The results indicate that the RVM and the PAG have a facilitatory influence on the spinal segmental mechanisms underlying chronic allodynia. The selective attenuation of allodynia induced by lidocaine in the RVM and the PAG is independent of opiate receptors, and it can not be explained by a systemic spread of the drug.

Can the alpha 2-adrenoceptor agonist-mediated suppression of nocifensive reflex responses be due to action on motoneurons or peripheral nociceptors?

To exclude the possibility that the suppression of nocifensive reflex responses induced by alpha 2-adrenergic agents is due to action on alpha-motoneurons or peripheral nociceptors, we studied the effect of medetomidine, an alpha 2-adrenoceptor agonist, on the monosynaptic reflex and on the primary afferent nociceptor-mediated antidromic vasodilator response in rats. Additionally, the effect on the dorsal root potential, an index of a transient excitability change in the central terminals of primary afferent fibers, was determined. Medetomidine was applied systemically at doses (100 and 300 micrograms/kg) which have proven strongly antinociceptive in previous studies. The amplitudes of a submaximal monosynaptic reflex volley or a submaximal dorsal root potential were not changed by medetomidine. Medetomidine induced a decrease of cutaneous blood flow but did not abolish the vasodilatatory response to antidromic stimulation of the sciatic nerve at C-fiber intensity as determined by the laser Doppler flow method. The results indicate that the alpha 2-adrenoceptor-mediated suppression of nocifensive reflex responses is not caused by a decreased excitability of motoneurons or peripheral nociceptors. An alpha 2-adrenoceptor agonist does not modulate the transient stimulus-evoked change in the excitability of central terminals of primary afferent fibers.

The antinociceptive action of an alpha 2-adrenoceptor agonist in the spinal dorsal horn is due to a direct spinal action and not to activation of descending inhibition.

In this electrophysiological study we tried to find out whether the spinal antinociceptive effect of a supraspinally administered alpha 2-adrenoceptor agonist is due to a direct spinal effect or to activation of descending inhibition. The responses to wide-dynamic range (WDR) neurons of the spinal dorsal horn were studied following application of medetomidine, a selective alpha 2-adrenergic agonist, into the rostroventromedial medulla (RVM) or directly onto the spinal cord of the intact and in spinal rats. The noxious electrical stimuli were applied to the ipsilateral receptive field in the plantar region of the hind paw, and responses mediated by A- and C-fibers to WDR neurons were separately evaluated. The reversal of medetomidine-induced effects was attempted by a systemic administration of atipamezole, a selective alpha 2-adrenoceptor antagonist. Medetomidine injection into the RVM produced a dose-dependent, atipamezole-reversible attenuation of the C-fiber-mediated responses to WDR neurons of the spinal dorsal horn in both intact and spinal rats. Paradoxically, the spinal antinociceptive effect of supraspinally administered medetomidine was stronger in spinal rats. The A-fiber-mediated responses were significantly less attenuated by medetomidine than the C-fiber-mediated responses to the WDR neurons. Also a direct application of medetomidine onto the spinal cord produced a dose-dependent, atipamezole-reversible attenuation of the C-fiber-mediated responses, and this effect was identical in intact and in spinal rats. The medetomidine doses producing spinal antinociception were considerably lower with a direct spinal application than with a supraspinal application.(ABSTRACT TRUNCATED AT 250 WORDS)

A noninvasive method for studying quantitatively heat-evoked nocifensive hindlimb withdrawal reflexes in lightly anesthetized rats.

We have developed a noninvasive method for studying quantitatively the magnitude of hindlimb withdrawal reflexes induced by noxious heat in lightly anesthetized rats. The amplitude, latency, and duration of the hindlimb withdrawal was determined by a very small piezoceramic device placed on the hamstring muscle while the glabrous skin of the hindpaw was stimulated using a feedback-controlled contact thermostimulator. An increase in the amplitude and duration of the withdrawal response, concomitant with a decrease in the response latency, was found with increasing stimulus temperature. The sensitivity of the method was verified using morphine, which produced a dose-related (3.5-7.0 mg/kg) attenuation of all these response components. The use of a piezoceramic device for measuring the withdrawal response provides a quantitative, noninvasive method for evaluating the magnitude of various components of the nocifensive withdrawal reflexes induced by noxious stimuli in lightly anesthetized rats.

The effect of a selective alpha2-adrenoceptor antagonist on pain behavior of the rat varies, depending on experimental parameters.

Effects of atipamezole, an alpha2-adrenoceptor antagonist, in various acute pain tests were studied in the rat. Atipamezole (at doses > or = 0.1 mg/kg I.P.) and idazoxan, another alpha2-adrenoceptor antagonist (2.5 mg/kg, I.P.), increased licking latency in the hot-plate test. Bilateral administration of atipamezole (10 microg) into the locus coeruleus did not increase licking latency in the hot-plate test. Medetomidine (an alpha2-adrenoceptor agonist; 1-3 mg/kg) or repeated pre-exposures to the testing apparatus reversed the effect of atipamezole (1.5 mg/kg) in the hot-plate test. Atipamezole also increased the latency to mechanically induced licking/biting response at a dose of 1.5 mg/kg, but not at lower doses. In the heat-induced tail-flick test, in contrast, atipamezole at doses of 0.1 and 1.5 mg/kg produced a medetomidine-reversible decrease of response latencies. This facilitation of the tail-flick response disappeared if the intensity of the heat stimulus was high. At a dose range from 0.03 to 1.5 mg/kg atipamezole did not significantly alter the paw withdrawal latency to noxious mechanical stimulation, nor pain behavior in the formalin test. Responses to nociceptive spinal dorsal horn neurons were not modulated by atipamezole (1 mg/kg) in anesthetized spinalized rats. The results indicate that an alpha2-adrenoceptor antagonist may have variable effects in behavioral pain tests, depending on habituation of the experimental animals to the testing conditions, the dose of the drug, the type of behavioral response and the submodality or the intensity of the noxious test stimulus. The atipamezole-induced changes in pain behavior observed in this study may rather be explained due to action on motor expression of pain than due to modulation of nociception.

Survivorship of the Charnley total hip arthroplasty in juvenile chronic arthritis. A follow-up of 186 cases for 22 years.

Between 1971 and 1991 we performed Charnley low-friction arthroplasty (LFA) on 116 patients (186 hips) with juvenile chronic arthritis (JCA). We have now carried out a survival study, taking endpoints as revision, death or the end of the year 1993. Overall survival was 91.9% at ten years and 83.0% at 15 years. That of the femoral component was 95.6% at ten years and 91.9% at 15 years and of the acetabulum 95.0% and 87.8%, respectively. Only the use of steroids significantly impaired the survival. We therefore recommend the use of Charnley LFA for young patients with JCA requiring total hip replacement.

Improved method for detecting knee replacement infections based on extended combined 99mTc-white blood cell/bone imaging.

The purpose of this study was to evaluate whether an extension of the imaging time to 24 h post-injection improves the diagnostic accuracy of technetium-99m-hexamethylpropyleneamine oxime (99mTc-HMPAO) leucocyte imaging in detecting knee replacement infections. Thirty patients were studied, with infection confirmed in eight (27%) and excluded in 22 on the basis of clinical and microbiological findings. Leucocyte imaging was carried out at 2-4 h (routine images) and at 24 h (late images) post-injection. For comparison, bone imaging with technetium-99m-hydroxydiphosphonate (99mTc-HDP) was carried out at arterial, soft tissue and metabolic phases. Late leucocyte imaging was found to be more sensitive (100% vs. 87.5%) and more specific (82% vs. 77%) than routine leucocyte imaging in detecting infections. All the bone imaging methods showed a sensitivity of 100%, whereas the specificity varied from only 5% to 23%. All procedures had high negative predictive values (NPVs) (94 to 100%) for excluding infection. However, the positive predictive value (PPV) was only 28 to 32% for bone imaging and 58% for routine leucocyte imaging, whereas late leucocyte imaging showed a PPV of 67% and a diagnostic accuracy of 87%. The data indicate that late leucocyte imaging may be superior to routine leucocyte imaging for examining patients with symptomatic knee replacements.

Comparison of 99mTc ciprofloxacin, 99mTc white blood cell and three-phase bone imaging in the diagnosis of hip prosthesis infections: improved diagnostic accuracy with extended imaging time.

The purpose of this study was to compare the utility of 99mTc labelled ciprofloxacin (Infecton) imaging with the 99mTc white blood cell and three-phase bone imaging procedures for identifying hip prosthesis infection. We studied 30 symptomatic patients in whom infection was confirmed in eight and excluded in 22 cases based on clinical and microbiological findings. 99mTc ciprofloxacin images were obtained at 1, 4 and 24 h after the injection of the tracer, and the data were compared to those obtained from 99mTc leukocyte and three-phase bone imaging. The 99mTc ciprofloxacin imaging correctly identified all true infections. In 13 (59%) of the non-infected patients, non-specific uptake of 99mTc ciprofloxacin was found in the 1-h and 4-h images, which disappeared, however, in the 24-h images. When the early and late 99mTc ciprofloxacin images were compared, the specificity was found to improve from 41% to 95%, positive predictive value from 38% to 89%, and the diagnostic accuracy from 57% to 97%. The accuracy of the conventional 99mTc leukocyte imaging was 90%. Dynamic bone imaging also yielded abnormal findings in all the infected patients although also in 23% of the non-infected patients. Current data indicate that 99mTc ciprofloxacin is a useful method for confirming hip prosthesis infection. The diagnostic efficiency of this method is improved when the imaging time is extended to 24 h post-injection of the tracer.

99m Tc-ciprofloxacin (Infecton) imaging in the diagnosis of knee prosthesis infections.

The purpose of this study was to evaluate the usefulness of 99mTc labelled ciprofloxacin imaging in detecting the presence of infection in patients with symptomatic knee prostheses. Among 16 randomly selected patients of whom seven had infection based on clinical and microbiological findings and nine did not, 99mTc-ciprofloxacin images were obtained at 1, 4 and 24h after the injection of the tracer. While there was some diffuse non-specific accumulation of 99mTc-ciprofloxacin in large synovial joints and in prosthetic knee joints, the infected knee prostheses were found to show more intensive focal uptake, which also extended outside the synovial cavity. The infection related uptake remained visible in the 24h images, whereas non-specific uptake had a fading tendency at this time point. 99mTc-ciprofloxacin imaging showed diagnostic sensitivity of 86% and a specificity of 78% for correctly classifying the presence of infection. The data indicate that 99mTc-ciprofloxacin imaging may be used in the diagnosis of knee prosthesis infections. Infection-related uptake remains visible in the 24h images and is typically found also outside the synovial cavity, which should be noted in the evaluation of the images.

Organic aciduria in rats fed high amounts of xylitol or sorbitol.

The acidification of urine during polyol feeding was investigated with 27 Long-Evans male rats (aged 12 weeks) which were fed a xylitol diet (X), a sorbitol diet (S), or a basal diet for 4 weeks. The amount of polyols in the diet was increased from 5% to the final 20% level within 3 weeks. The polyol-fed animals showed reduced weight gain, lowered urine pH (from 6.5 to 5.6), and a 4-fold increase in the titratable acid excretion. X and S increased the daily urine volumes by 49 and 63%, respectively, but did not affect the wet weight or the pH values of the feces. as chromatographic-mass spectrometric analyses of organic acids revealed highly increased amounts of methylmalonic acid (13- to 20-fold) and 2-oxoglutaric acid (4- to 5-fold) in the urine of polyol-fed rats. The urinary excretion of citric acid and malic acid was also increased significantly (2- to 4-fold). The acidity of urine was not reflected in the blood acid-base balance of the animals. The increases in the levels of urinary organic acids in the polyol-fed rats were explained in terms of impaired mitochondrial oxidation of these acids and of impaired conversion of methylmalonic acid to succinic acid.

Bone repair in calcium-deficient rats: comparison of xylitol+calcium carbonate with calcium carbonate, calcium lactate and calcium citrate on the repletion of calcium.

The potential value of xylitol in calcium therapy was evaluated by comparing the effect of dietary xylitol (50 g/kg diet) + calcium carbonate with the effects of calcium carbonate, calcium lactate and calcium citrate on bone repair of young male rats after the rats consumed for 3 wk a calcium-deficient diet (0.2 g Ca/kg diet). After this calcium-depletion period, the rats were fed for 2 wk one of four diets, each containing 5 g Ca/kg diet as one of the four dietary calcium sources. The diet of the control animals was supplemented with CaCO3 (5 g Ca/kg diet) throughout the study. The Ca-deficient rats showed low bone mass, low serum calcium and high serum 1,25-dihydroxycholecalciferol, parathyroid hormone (1-34 fraction) and osteocalcin concentrations. They also excreted magnesium, phosphate and hydroxyproline in the urine in high concentrations, and had high bone alkaline phosphatase and tartrate-resistant acid phosphatase activities. Most of these changes were reversed by the administered of the calcium salts. The highest recoveries of femoral dry weight, calcium, magnesium and phosphate were observed in the groups receiving xylitol+CaCO3 and calcium lactate. Calcium lactate and calcium citrate caused low serum phosphate concentration compared with rats receiving CaCO3 and with the age-matched Ca-replete controls. Xylitol-treated rats excreted more calcium and magnesium in urine than did the other rats, probably due to increased absorption of these minerals from the gut. These results suggest that dietary xylitol improves the bioavailability of calcium salts.

Retention of calcium from various xylitol-calcium combinations in rats.

Previous studies have shown that xylitol, the five-carbon sugar alcohol, increases the intestinal absorption of Ca in the rat. In this study an optimum xylitol:Ca molar ratio for Ca absorption and retention was determined in 10-week-old Long-Evans male rats. Xylitol was intubated with 20 mg of 45Ca (as 45CaCl2 or 45CaCO3) into the stomach of fasted rats in 1 ml water using xylitol:Ca molar ratios of 0:1, 0.5:1, 1:1, 1.5:1 or 2:1. Radioactivity of urine, feces and humerus was determined from 48-hr samples. The highest retention rate of 45Ca in the whole body or in the humerus was found when 114 mg of xylitol was given with Ca (xylitol:Ca molar ratio 1.5). Xylitol affected humeral retention more significantly than whole body retention. For comparison, the retention of 45Ca was determined from four lactose:CaCl2 combinations and from Ca-lactate and Ca-citrate salts. None of these combinations increased Ca retention significantly, although lactose at 114 mg dose showed slight positive effect. The results favor the use of a xylitol:Ca molar ratio of 1.5 in Ca supplements.