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PubMed1995

Gadolinium-enhanced magnetic resonance imaging assessment of hydroxyapatite orbital implants.

PURPOSE: Successful prosthesis attachment depends on complete vascularization of porous coralline hydroxyapatite when it is used as an orbital implant. We retrospectively assessed the utility of gadolinium-enhanced magnetic resonance imaging to evaluate and characterize the temporal progression of this fibrovascular process, which has been histologically documented elsewhere. METHODS: Serial T1-weighted gadolinium-enhanced orbital magnetic resonance examinations were performed in five patients receiving hydroxyapatite orbital implants. Retrospective evaluation of the enhancement patterns was performed. Magnetic resonance imaging enhancement patterns guided timing of final drilling for prosthesis fixation. RESULTS: Serial gadolinium-enhanced T1-weighted sequences consistently demonstrated centrally advancing, peripheral enhancement centered on the drilled access channels. Progression over time varied, with the following two patterns demonstrated: (1) rapid peripheral enhancement, which led to diffuse enhancement (three patients); and (2) enhancement limited to the periphery, which failed to advance centrally. CONCLUSIONS: The temporal enhancement seen on magnetic resonance imaging is identical to the histologically proven fibrovascular ingrowth pattern and most likely reflects this process. Magnetic resonance imaging can identify progression of fibrovascular ingrowth into the hydroxyapatite orbital implants and guide surgical planning. It may also identify implants that fail to vascularize, thereby preventing the morbidity encountered by drilling into an avascular hydroxyapatite implant.

Adolescent↗

PubMed2000

Enhancing effect of saccharides on the mutagenicity of 2-chloro-4-methylthiobutanoic acid.

The mutagenicity of 2-chloro-4-methylthiobutanoic acid (CMBA), a nitrite-treated Sanma fish mutagen, in Salmonella typhimurium TA100 was enhanced by addition of D-glucose during the CMBA-treatment. Several other monosaccharides also enhanced the mutagenicity of CMBA, and the order of the enhancing potency was found to be D-mannose, D-glucose>D-fructose, D-ribose, D-galactose. A disaccharide, maltose, showed only little enhancement. No enhancement was found with L-glucose. We investigated whether saccharides affect uptake of [methyl-14C]CMBA into S. typhimurium TA100. Saccharides which enhanced CMBA-induced mutagenesis increased the uptake. L-Glucose did not enhance the uptake. There was good correlation between the enhanced mutagenesis and increased radioactivity in Salmonella, suggesting that the enhancing effect of monosaccharide on the CMBA-induced mutagenesis results from the enhanced uptake of the mutagen into bacteria.

Butyrates↗

PubMed1998

Development and evaluation on transdermal delivery of enoxacin via chemical enhancers and physical iontophoresis.

Iontophoresis and enhancers were performed to enhance percutaneous absorption of enoxacin so as to compare the enhancement between these two enhancing methods. The cationic surfactant of benzalkonium chloride showed the highest enhancing activity for enoxacin for all pH values of buffer vehicles. The enhancement factor of sodium laurylsulfate showed a dose-dependent property between the range of 0.1% to 3.0% concentration. Nonionic surfactant of Polysorbate 80 did not exhibit any enhancing effect on the percutaneous absorption of enoxacin. The highest enhancement factor of iontophoretic delivery was observed at pH 5.0 solution of anodal iontophoresis for cationic enoxacin. The cathodal iontophoresis of negative molecules and anodal iontophoresis of neutral molecules showed lower enhancing effect for enoxacin. The fact that the skin residuals of enoxacin after iontophoresis showed both tremendous and current density-dependent amounts for cationic enoxacin suggested local skin and soft tissue infections might be treated by this physical enhancement method. Combination of benzalkonium chloride and iontophoresis exerted a synergistic effect for anionic enoxacin in pH 10.0, which was possibly due to the shielding of negative charge in skin and the water molecules carried by chloride.

Administration, Cutaneous↗

PubMed2001

Hypoxic enhancement of evoked noradrenaline release from the human neuroblastoma SH-SY5Y.

The effects of chronic hypoxia (2.5% O(2), 24 h) on [3H]noradrenaline ([3H]NA) release evoked from human neuroblastoma SH-SY5Y cells by depolarisation and by activation of muscarinic receptors was investigated. Depolarization of cells with 100 mM K(+) evoked [3H]NA release, and chronic hypoxia enhanced this release significantly. In fluorimetric studies, the K(+)-evoked rises of [Ca(2+)](i) observed in response to 100 mM K(+) were also significantly enhanced. Muscarine-evoked [3H]NA release was also dramatically enhanced by chronic hypoxia. However, muscarine-induced release of Ca(2+) from intracellular stores and subsequent capacitative Ca(2+) entry was unaffected. The protein kinase C inhibitors GF 109 203X and RO-31-8220 did not prevent the enhancement of muscarine-evoked release caused by chronic hypoxia. These findings indicate that chronic hypoxia increases release of [3H]NA from human neuroblastoma SH-SY5Y cells. Enhancement of K(+)-evoked release was attributable to an enhancement of depolarisation-mediated Ca(2+) influx. In contrast, the larger enhancement of muscarine-evoked [3H]NA release was not due to greater release of Ca(2+) from internal stores, nor due to enhanced Ca(2+) influx. Furthermore, it was not attributable to activation of protein kinase C. These findings suggest that enhancement of sympathetic output, known to occur following prolonged hypoxia, may be mediated in part by enhancement of exocytosis.

Calcium↗

PubMed2001

Enhancement of VP1-specific immune responses and protection against EMCV-K challenge by co-delivery of IL-12 DNA with VP1 DNA vaccine.

It has been reported that co-delivery of IL-12 DNA with a DNA vaccine further enhances antigen (Ag)-specific protective immunity in pathogenic challenge models. However, the enhancing effects of antibody by IL-12 have been controversial. To clarify this issue, we constructed an IL-12 expression vector, co-immunized IL-12 DNA with an encephalomyocarditis virus (EMCV)-D VP1 plasmid vaccine, and then evaluated immune modulatory effects and protection against lethal EMCV-K challenge. We observed that VP1-specific IgG production, as well as seroconversion rates, were significantly enhanced by IL-12 co-injection, indicating that IL-12 can enhance antibody responses in this model system. In particular, co-injection with VP1 plus IL-12 DNA into the same leg enhanced systemic Ag-specific IgG production to a significantly greater extent than either the separate leg injection of VP1 and IL-12 DNA or VP1 DNA vaccine alone. This suggests that local co-expression of IL-12 along with antigens is more important for enhanced antibody production. Furthermore, IgG2a isotype was significantly enhanced by IL-12 DNA co-injection, indicating a Th1 bias. In addition, co-delivery of IL-12 DNA was demonstrated to enhance VP1-specific Th cell proliferative responses. When animals were challenged with a lethal dose of EMCV-K, IL-12 DNA-co-immunized animals exhibited enhanced survival, as compared to VP1 DNA vaccine alone. These studies suggest that IL-12 plays an important role in increasing Ag-specific Th1 type antibody and cellular responses, resulting in enhanced protection against lethal EMCV-K challenge.

Animals↗

PubMed2002

Improved sonographic imaging of hepatic hemangioma with contrast-enhanced coded harmonic angiography: comparison with MR imaging.

The aim of this study was to compare peripheral nodular enhancement with centripetal progression on contrast-enhanced coded harmonic angio (CHA) with those as seen on magnetic resonance imaging (MRI) scan. A total of 20 patients with 24 hemangiomas confirmed by dynamic contrast-enhanced MRI were included in this study. All 20 patients were examined with CHA in conjunction with a galactose-based microbubble contrast agent (SH U 508A) and with interval delay scanning. The pattern and the time of contrast enhancement were recorded on CHA images. We compared CHA images with MRI in terms of the similarity of contrast-enhanced peripheral nodules. The significance of size of tumor and baseline echogenicity on the ability to see peripheral nodular enhancement was independently assessed. Peripheral nodular enhancement was shown on CHA in 22 (92%) of 24 hemangiomas. Of 22 hemangiomas, 21 (95%) with peripheral nodular enhancement had progressive centripetal fill-in on CHA images. In 4 (80%) of 5 hemangiomas less than 1.5 cm in diameter, contrast-enhanced peripheral nodules were depicted on CHA images. In terms of the similarity of peripheral nodules, CHA images showed the similarity more than "similar" grade with MRI in 21 (95%) of 22 hemangiomas. This study shows that CHA is approximately equal to MRI in its ability to show peripheral nodular enhancement with centripetal progression, even in small hemangiomas.

Adult↗

PubMedDate not supplied

Prolongation of TCD-enhanced Doppler signal by continuous infusion of levovist.

This study evaluated the effects of two different rates of infusion of echo-contrast agents (ECA) on signal enhancement. A total of 15 patients with insufficient Doppler signal due to inadequate transtemporal acoustic bone window were examined. Signal from the middle cerebral artery was recorded during the IV infusion of Levovist (300 mg/mL). Increment of signal enhancement in dB, time to signal enhancement appearance, time to clinically useful signal enhancement appearance, and duration of clinically useful signal enhancement were assessed during two infusions at the rate of 1 and 0.66 mL/min, respectively. Increment of signal enhancement was similar at the rate of 1 and 0.66 mL/min (p = 0.4). Mean time to signal enhancement appearance and mean time to clinically useful signal enhancement appearance were not significantly different with the two rates of infusion (p = 0.9 and p = 0.3, respectively). Mean duration of clinically useful signal enhancement was significantly higher with the infusion rate of 0.66 mL/min as compared to 1 mL/min (p < 0.0001). Levovist injected at the infusion rate of 0.66 mL/min prolonged the mean duration of signal enhancement, maintaining its effectiveness.

Aged↗

PubMed2003

The value of dynamic contrast enhanced power Doppler ultrasound imaging in the localization of prostate cancer.

OBJECTIVES: The objective of this study is to define enhancement characteristics that correlate to the presence of prostate cancer (PCa) and to evaluate the value of these characteristics in the localization of prostate cancer. METHODS: 29 patients with proven prostate malignancy, scheduled for radical prostatectomy, underwent an ultrasound examination prior to surgery. A bolus injection of contrast agent was administered intravenously. The distribution of the contrast enhanced blood to the prostate was monitored using Transrectal Contrast Enhanced Power Doppler Ultrasound. Fixed protocols and settings were used for all patients. The percentage of a selected area that showed enhancement was observed in time. The resulting enhancement curves were described using the parameters time to start, time to the maximum of the enhancement, the maximum value of the enhancement, and the rise time of the enhancement. Three evaluation-protocols divided the prostate into a number of areas of interest: into two areas using the Left-Right (LR) and Dorsal-Ventral (DV) protocols and into four areas using the Quadrant-protocol (Q). The enhancement parameters of the areas of interest were compared to identify the most affected area. The results were compared to the histopathological findings. RESULTS: For the LR-protocol, the minimal time to peak proved to be the most predictive parameter for selecting the major malignant area. 78% of the patients were diagnosed correctly (N=23). Accurate localization of the major malignancy in either the ventral or dorsal side of the prostate was not feasible using the current protocol. CONCLUSIONS: Malignancies can be accurately localized in either the left or the right side of the prostate based on the time to the maximum of the enhancement. An accurate discrimination between malignancies in either the dorsal or ventral side of the prostate cannot be performed. This is most likely due to anatomical differences between the dorsal and ventral area.

Contrast Media↗

PubMed1999

Role of ecto-kinase in phorbol ester-enhanced growth hormone-binding protein release from human IM-9 cells.

Previously we reported that a phorbol ester, phorbol 12, 13-dibutyrate (PDBu), increased the release of human growth hormone-binding protein (hGH-BP) in IM-9 cells, and that this phorbol ester-enhanced release was mediated by protein kinase Ca (PKCalpha). In the present study, the mechanisms of the phorbol ester-enhanced hGH-BP release were further investigated. Treatment of IM-9 cells with PDBu did not increase hGH-BPs (55-60 kDa) in the intracellular soluble fraction. When the cells were treated with trypsin to remove human growth hormone receptors (hGHRs) on the cell surface after stimulation, no hGH-BPs were detected in the culture supernatants, nor did treatment with bafilomycin A1 or chloroquine affect the PDBu-enhanced hGH-BP release. These results suggest that hGH-BPs released by PDBu stimulation are derived from cell surface hGHRs and not generated within the cells. Protein kinase inhibitors with broad specificities, K-252a and K-252b, inhibited the PDBu-enhanced release with almost the same dose-dependency, although only a trace amount of K-252b was incorporated into IM-9 cells than K-252a, suggesting that K-252b probably inhibits an ecto-kinase extracellularly. PDBu actually enhanced the phosphorylation of several extracellular proteins, and this enhanced phosphorylation was completely inhibited by K-252b treatment. Moreover, the PKCalpha-specific inhibitor bisindolylmaleimide III which inhibits PDBu enhanced hGH-BP release inhibited the PDBu-enhanced phosphorylation of extracellular proteins. On the other hand, the impermeable PKC inhibitor PKC inhibitor peptide 19-31 did not inhibit PDBu-enhanced release, suggesting that the target PKCalpha for PDBu is not present on the extracellular surface. Taken together, these results suggest that, in addition to intracellular PKCalpha, activation of an undefined ecto-kinase may also be involved in the PDBu-enhanced hGH-BP release.

Carbazoles↗

PubMed2000

Enhanced bioavailability by buccal administration of triamcinolone acetonide from the bioadhesive gels in rabbits.

The pharmacokinetics and bioavailability of triamcinolone acetonide were determined to investigate buccal absorption from the mucoadhesive gels in rabbits. The enhancing effect of sodium deoxycholate as an enhancer on the buccal absorption of triamcinolone acetonide from the mucoadhesive gels was evaluated in rabbits. Thus, 2 mg/kg of triamcinolone acetonide was administered from the mucoadhesive gels containing an enhancer (enhancer group) or not (control group) via the buccal routes and compared with intravenous routes (1 mg/kg, i.v. group). AUC of the control, enhancer and i.v group were 2374+/-915, 3778+/-1721 and 3945+/-2085 h ng/ml, respectively, and the absolutive bioavailability of enhancer or i.v to control group were 159.14 or 332.35%, respectively. The average C(max) of control and enhancer group were 263+/-159 and 362+/-201 ng/ml, and the mean T(max) of the control group and enhancer group were 5.00+/-1.67 and 4.33+/-0.82 h, respectively, but there was no significant difference. As the triamcinolone acetonide gels containing sodium deoxycholate as an enhancer was administered to rabbits via the buccal routes, the relative bioavailability showed about 1.59-fold compared with the control group. Buccal administration of triamcinolone acetonide gels containing sodium deoxycholate as an enhancer to rabbits showed a relatively constant, sustained blood concentration with minimal fluctuation.

Adhesives↗

PubMed2003

In vitro and in vivo evaluations of the efficacy and safety of skin permeation enhancers using flurbiprofen as a model drug.

The efficacy and safety of commonly used enhancers were systemically evaluated by in vitro and in vivo methods in this study. Flurbiprofen was used as the model drug to examine the enhancing capacity of these enhancers. Both in vitro permeation by Franz cells and in vivo kinetics of skin disposition were performed to determine the flurbiprofen permeation by enhancers. Unsaturated fatty acids showed the greatest enhancement of flurbiprofen permeation. The enhancing effect of D-limonene was slightly lower than that of the fatty acids. Azone and L-alpha-lecithin even reduced the skin deposition by flurbiprofen application. In vitro prostaglandin E(2) (PGE(2)) release by cell culture, in vivo transepidermal water loss (TEWL) and colorimetry, and skin morphological changes were determined to examine the irritation of the skin by enhancers. The results showed that skin disruption and inflammation did not necessary correspond to the enhancing efficiency of the enhancers. Moreover, some discrepancies were observed in these irritant profiles when using various methods. The fatty acids generally showed the most irritating properties, followed by Azone, D-limonene, and L-alpha-lecithin. A complete portrait of the efficacy and safety of commonly used enhancers was therefore established in this study.

Adjuvants, Pharmaceutic↗

PubMed1994

Pharmacokinetic analysis of the absorption enhancing action of decanoic acid and its derivatives in rats.

The enhancing action of decanoic acid (C10) and its derivatives on mucosal absorption of phenolsulfonphthalein (PSP) in the jejunum or colon was analyzed using pharmacokinetics in rats. After administration of a solution containing PSP and an enhancer [C10, 2-hydroxydecanoic acid (2-OHC10), or 3-hydroxydecanoic acid (3-OHC10)] into the jejunal or colonic loop, the amounts of PSP and enhancer remaining in the loop and/or plasma PSP concentration were determined periodically. 2-OHC10 exhibited a greater absorption enhancing potency than C10, while 3-OHC10 was less effective. Disappearance of residual PSP from the loop ceased after complete absorption of the enhancer. The enhancer-induced disappearance rate constant of PSP correlated well with the product of the enhancer disappearance rate and its capacity to sequester calcium ions. In conclusion, the enhancement of PSP mucosal absorption by C10 and its derivatives is consistent with a pharmacokinetic model, assuming that the enhanced membrane permeability of PSP depends on the enhancer disappearance kinetics from the loop and its calcium ion sequestration capacity.

Animals↗

PubMed2000

MRI changes in myocarditis--evaluation with spin echo, cine MR angiography and contrast enhanced spin echo imaging.

AIM: Myocarditis is probably under-diagnosed with clinical criteria generally used for diagnosis. Magnetic resonance imaging (MRI) has shown promise in detecting heart muscle disorders and we set out to assess the role of cine magnetic resonance angiography (MRA) and contrast enhancement in myocarditis, as there is a need for a non-invasive tool that can aid prognosis and follow-up. MATERIALS AND METHODS: Twenty patients were evaluated with T1 SE pre- and post-gadolinium enhancement and cine MRA. Four patients were histologically proven to have myocarditis, eight others were diagnosed as having myocarditis by clinical criteria and eight did not have myocarditis. Images were evaluated in a blinded fashion for regional wall motion abnormality and contrast enhancement pattern. Analysis of contrast enhancement by signal intensity measurement was also performed. RESULTS: Focal myocardial enhancement with associated regional wall motion abnormality correlated with myocarditis in 10 out of 12 patients, two patients with abnormal focal enhancement alone also clinically had myocarditis. None of the non-myocarditis patients showed abnormal focal enhancement. Enhancement analysis suggests that focal corrected myocardial enhancement of > 40% is abnormal. CONCLUSION: In the correct clinical context, focal myocardial enhancement on spin echo MRI strongly supports a diagnosis of myocarditis, especially when associated with regional wall motion abnormality.Roditi, G. H. (2000). Clinical Radiology55, 752-758.

Adult↗

PubMed2001

Technical report: lymph node enhancement at MRI with MnDPDP in primary hepatic carcinoma.

AIMS: To report two cases of lymph node enhancement in primary hepatic carcinoma following the administration of Mangafodipir trisodium (MnDPDP, Teslascan(R), Nycomed Amersham U.K.), an hepatocyte specific magnetic resonance imaging (MRI) contrast agent. To review our experience with this contrast agent and the literature to establish if such enhancement occurs in normal lymph nodes or has been previously described in hepatocellular carcinoma (HCC) or other lesions. MATERIALS AND METHODS: The radiological reports of all MnDPDP enhanced abdominal MRI examinations were reviewed for lymph node enlargement. The MR images from examinations with reported nodal enlargement were re-evaluated for evidence of nodal enhancement and the hospital notes and histological reports were reviewed. Nodal enhancement was considered present if lymph node signal intensity was greater than that of the spleen following MnDPDP. Literature searches were performed on Medline and PubMed for previous descriptions of lymph node enhancement following MnDPDP. RESULTS: The reports of 90 MnDPDP abdominal MRI examinations were reviewed. Of 18 cases of lymph node enlargement, two had evidence of lymph node enhancement following MnDPDP. These two cases had hepatocellular carcinoma and fibrolamellar hepatocellular carcinoma, respectively, confirmed on liver biopsy. No reports of lymph node enhancement following MnDPDP were identified in the literature. CONCLUSION: Two cases of lymph node enhancement following MnDPDP have been presented. Although histological confirmation of the lymph nodes was not obtained, the authors propose that the lymph node enhancement was due to functioning hepatocytes in lymph node metastases from the patients' histologically confirmed hepatocellular carcinomas. Burkill, G. J. C., Mannion, E. M. & Healy, J. C. (2001). Clinical Radiology56, 67-71.

Adult↗

PubMed2006

Gadolinium-enhanced magnetic resonance imaging after percutaneous vertebroplasty does not improve the short-term prediction of new compression fractures.

PURPOSE: To investigate the relationships between contrast-enhanced magnetic resonance imaging (MRI) findings and new compression fractures occurring after percutaneous vertebroplasty (PVP) in order to determine the necessity of contrast-enhanced MRI. MATERIAL AND METHODS: The material comprised 13 consecutive patients (27 vertebrae) with compression fractures who underwent vertebroplasty. Twenty-nine adjacent vertebrae were monitored for new compression fractures. We performed contrast-enhanced MRI within the 5 days following PVP. RESULTS: The 29 adjacent vertebrae displayed 10 enhanced lesions and 19 vertebral bodies without enhancement-unenhanced lesions on MRI within the 5 days after PVP. In 4 out of 10 vertebrae, enhanced lesions were seen within the 5 days after PVP, but no abnormalities were seen on preoperative MRI. In these 4 vertebrae, new compression fractures were seen within the 1 month following PVP. In the other 6 vertebrae, enhanced lesions were seen within the 5 days after PVP, and these signal changes were detected by preoperative MRI in the same area. In 3 of these 6 vertebrae, new compression fractures occurred at 4, 8, and 9 months after PVP, respectively. However, all of the enhanced lesions were detectable on unenhanced MRI, which was conducted at the same time as enhanced MRI. CONCLUSION: New compression fractures after PVP may be predicted with early postoperative MRI. Contrast-enhanced MRI does not improve detection of the new lesions.

Aged↗

PubMed1997

Tumoural portal vein thrombosis. Enhancement with MnDPDP.

PURPOSE: Intrahepatic thrombus is usually associated with either cirrhosis or hepatocellular carcinoma (HCC). Most HCCs enhance after the administration of MnDPDP (Teslascan). Our objective was to analyze the enhancement characteristics of tumour portal vein thrombi. MATERIAL AND METHODS: Thrombi affecting the main or segmental portal veins (17 cases) and the suprahepatic inferior vena cava (1 case) were retrospectively selected from a series of 128 patients studied with MR imaging before and after the administration of MnDPDP. Enhancement was assessed qualitatively and quantitatively. RESULTS: All tumour thrombi enhanced after MnDPDP administration. The enhancement was more conspicuous in the GRE images. On the quantitative evaluation, the portal thrombus enhancement was greater for GRE images than SE images. Portal thrombi enhanced more than the liver and the HCCs. There was a significant difference between the enhancement of the HCCs and the thrombi with both MR imaging techniques. CONCLUSION: The greater enhancement of the tumour thrombus associated with the liver and HCC may suggest that other mechanisms, apart from accumulation of the contrast medium within the hepatocytes inside the thrombi, are involved in thrombus enhancement.

Aged↗

PubMed2005

Memory enhancing effect of low-dose sevoflurane does not occur in basolateral amygdala-lesioned rats.

BACKGROUND: Certain anesthetics might enhance aversive memory at doses around 0.1 minimum alveolar concentration. This issue was investigated in a rat model of learning and memory. In addition, evidence for basolateral amygdala (BLA) involvement in mediating memory enhancement was sought. METHODS: First, the memory-enhancing potential of various anesthetics was determined. Rats underwent single-trial inhibitory avoidance training (0.3 mA shock/1 s) during exposure to air, 0.11% sevoflurane, 0.10% halothane, 0.77% desflurane, or 0.12% isoflurane. Memory was assessed at 24 h. Second, the BLA contribution to sevoflurane memory enhancement was determined. Rats received bilateral excitotoxic N-methyl-D-aspartate (12.5 mg in 0.2 microl per BLA) lesions of the BLA 1 week before training. Memory of lesioned and control rats was compared 24 h after training in air or sevoflurane. RESULTS: Sevoflurane exposure during training significantly enhanced 24-h retention performance for both nonoperated and sham-operated rats (P < 0.005 for both vs. their respective controls). Halothane, but not desflurane or isoflurane, also enhanced retention performance (P < 0.05). However, halothane-induced hyperalgesia during learning clouds interpreting enhanced retention performance solely as a memory consolidation effect. BLA lesions significantly reduced and equalized retention performance for both sevoflurane- and air-exposed animals. Lesions blocked memory enhancement without also causing a generalized inability to learn, because additional training revealed essentially normal task acquisition and 24-h memory. CONCLUSIONS: Sevoflurane enhances aversive memory formation in the rat. The BLA likely contributes to this effect. The risk of aversive memory formation may be enhanced during exposure to low-dose sevoflurane.

Amygdala↗

PubMed2006

Oral glutamine enhances heat shock protein expression and improves survival following hyperthermia.

No pharmacologic agent has shown benefit in treating heatstroke. Previous data indicate that enhanced heat shock protein 70 (HSP-70) expression can improve survival postexperimental heatstroke. Glutamine (GLN) can enhance HSP-70 expression in other injury models. This study assessed if orally administered GLN could enhance tissue HSP expression and could improve survival following whole body hyperthermia. Intestinal permeability and plasma endotoxin were assayed to determine if enhanced HSP expression correlated with improved organ function. GLN (0.65 g/kg) or an iso-nitrogenous control (Travasol; T) was given to rats via gavage twice daily for 5 days pre-heatstroke. Hyperthermia was performed in anesthetized rats by heating animals to 42 degrees C (rectal temperature) for 30 min. HSP-70 analyzed via Western blot. Gut permeability was measured 6 and 24 h post-hyperthermia. Plasma endotoxin was measured 24 h post-hyperthermia. Survival was analyzed for 5 days post-hyperthermia. GLN administration enhanced gut and lung HSP-70 post-hyperthermia. GLN administration led to significantly enhanced gut heat shock factor 1 (HSF-1) activation before heatstroke and at 1 h postheat stress. GLN decreased gut permeability at 6 and 24 h post-hyperthermia versus T. Plasma endotoxin also decreased in GLN-treated rats 24 h post-hyperthermia. Oral GLN therapy significantly improved survival (P < 0.05). Our results indicate that oral GLN can enhance tissue HSP-70 and HSF-1 activation post-hyperthermia. These results also indicate that enhanced HSP-70 may have functional significance as GLN-treated animals had decreased gut permeability, plasma endotoxin, and improve survival following lethal hyperthermia. Enhanced expression of HSP-70 may be an important mechanism leading to enhanced survival via GLN. These data indicate that oral GLN may useful in prevention of mortality from heatstroke in at risk populations.

Administration, Oral↗