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PubMed2001

A sustainable community-based arsenic mitigation pilot project in Bangladesh.

A sustainable community-based arsenic mitigation pilot project has been successfully operating for 22 months in the Chapainawabganj arsenic hot spot (Bangladesh) where safe treated drinking and cooking water derived from tubewells is being supplied below the Bangladesh maximum permissible limit (0.05 ppm total arsenic). There has been close community involvement in all stages and the arsenic removal mechanism used adapted from the simple process of adsorption by natural ferric oxyhydroxide. Supplemented ferric oxyhydroxide produces daily de-contaminated water batches until replaced at the end of the cycle. A regional renewal/recycling centre supplies new, and safely stores used, ferric oxyhydroxide. Recycling is beginning where adsorbed arsenic can be separated prior to ferric oxyhydroxide reuse. The mechanism is flexible regarding water volumes, cycle lengths, pre and post-treatment arsenic concentrations, tubewell chemistries and is cost-effective. Pilot project parameters were set at 60 l per day ( < 0.05 ppm total arsenic) and 16 day cycles per tank for each of the four selected families with pretreatment concentrations up to 1.1 ppm. A maximum of ~ 24 g of arsenic is produced from the approximately 900 g (dry) of ferric oxyhydroxide used per tank per year. Anecdotal evidence possibly suggests positive health effects within a few months and villagers report an improved water taste. The project should contribute to coping with such arsenicosis crises and expansion is planned.

Arsenic↗
PubMed2005

Prescribed burns and wildfires in Colorado: impacts of mitigation measures on indoor air particulate matter.

Wildfires and prescribed burns are receiving increasing attention as sources of fine particulate matter (PM2.5). The goal of this research project was to understand the impact of mitigation strategies for residences impacted by scheduled prescribed burns and wildfires. Pairs of residences were solicited to have PM2.5 concentrations monitored inside and outside of their houses during four fires. The effect of using air cleaners on indoor PM2.5 was investigated, as well as the effect of keeping windows closed. Appropriately sized air cleaners were provided to one of each pair of residences; occupants of all of the residences were asked to keep windows shut and minimize opening of exterior doors. Additionally, residents were asked to record all of the activities that may be a source of particulate matter, such as cooking and cleaning. Measurements were made during one prescribed burn and three wildfires during the 2002 fire season. Outdoor 24-hr average PM2.5 concentrations ranging from 6 to 38 microg/m3 were measured during the fires, compared with levels of 2-5 microg/m3 during background measurements when no fires were burning. During the fires, PM2.5 was < 3 microg/m3 inside all of the houses with air cleaners installed. This corresponds with a decrease of 63-88% in homes with the air cleaners operating when compared with homes without air cleaners. In the homes without the air cleaners, measured indoor concentrations were 58-100% of the concentrations measured outdoors.

Air Pollution, Indoor↗
PubMedDate not supplied

Performance analysis of a medical decision algorithm to mitigate spread of SARS due to interfacility patient transfers.

OBJECTIVE: To determine performance of a medical decision algorithm to mitigate spread of severe acute respiratory syndrome (SARS) from interfacility patient transfers during the Toronto SARS outbreak. METHODS: Records from the Provincial Transfer Authorization Centre and Toronto Public Health from April 1 to July 31, 2003, were linked using probabilistic methods. Authorization decision (transfer authorized or denied) and SARS status (probable case, suspect case, or patient under investigation for SARS; or non-SARS case) were obtained for linked records. Primary outcome was the number of patients where correct authorization decisions were made based on SARS status at the time of request. Secondary outcome was the number for whom, in retrospect, authorization decision was correct knowing final SARS status. Algorithm sensitivity, specificity, and predictive values were determined. RESULTS: There were 14,571 requests for transfer and 2,132 patients investigated for SARS during the study period. The algorithm authorized 14,551 and did not authorize 20 requests. Sensitivity and specificity to make appropriate authorization decisions at the time of request were 100% (95% confidence interval [CI], 77.2%-100%) and 99.95% (95% CI, 99.9-100%), respectively. Positive and negative predictive values were 65% (95% CI, 44.1%-85.9%) and 100% (95% CI, 98.4%-100%), respectively. Sensitivity and specificity, in retrospect, within ten days of the transfer request were 100% (95% CI, 80.6%-100%) and 99.97% (95% CI, 99.9%-100%), respectively. Positive and negative predictive values were 80% (95% CI, 62.5%-97.5%) and 100% (95% CI, 98.4%-100%), respectively. Seven of the 20 patients with nonauthorized requests were not known to have SARS at the time of request. Within ten days, three of seven were under investigation for, a suspect case of, or a probable case of SARS. CONCLUSIONS: The medical decision algorithm was highly sensitive and specific in correctly authorizing transfers. Despite its highly sensitive and specific algorithm, it did incorrectly deny authorization to a very small number of patients without SARS.

Algorithms↗
PubMed1986

Mitigation of residential formaldehyde contamination by indoor climate control.

The effectiveness of indoor climate as a mitigation measure for indoor formaldehyde contamination was studied in a mobile home. The effects of nine indoor climate regimes on formaldehyde levels were evaluated for the temperature and humidity ranges of 20 degrees C to 30 degrees C and 30% RH to 70% RH. Formaldehyde levels at the lowest combination of temperature and relative humidity (20 degrees C, 30% RH) were only 20% of those measured at the highest combination of temperature and relative humidity (30 degrees C, 70% RH) evaluated. Reducing temperature alone (from 30 degrees C to 20 degrees C) was shown to result in an approximate 70% reduction in formaldehyde levels. Reducing relative humidity alone (from 70% to 30%) resulted in an approximate 40% reduction in formaldehyde levels. A high linear correlation was observed between formaldehyde levels and temperature and between formaldehyde levels and relative humidity. Analysis of energy consumption and associated costs indicated that temperature reduction from 25 degrees C to 20 degrees C during the cooling season would increase energy usage costs by about 20%; temperature reduction in the heating season would result in both reduced formaldehyde levels and reduced energy costs. Although effective, humidity control--particularly to 30% under summertime conditions--appears to be prohibitively costly. The relationship between temperature and formaldehyde levels suggests that climate control also may be appropriate for reducing indoor levels of other continuously generated contaminants.

Environmental Exposure↗
PubMed2003

Groundwater arsenic contamination, its health impact and mitigation program in Nepal.

About 47% of Nepal's total population is living in Terai region and 90% of them are relying on groundwater as their major source of drinking water. About 200,000 shallow tubewells have been installed by different agencies in 20 Terai districts, serving 11 million people. Recently, arsenic contamination of groundwater has been recognized as a public health problem in Nepal. This has sensitized government, national and international nongovernment organizations working on water quality sector to carry out water quality assessment for arsenic in the affected communities. So far, 15,000 tubewells has been tested where 23% samples exceeded World Health Organization guideline value of 10 microg/L and 5% exceeded "Nepal Interim Arsenic Guideline" of 50 microg/L. It is estimated that around 0.5 million people in Terai are living at risk of arsenic poisoning (>50 microg/L). Some recent studies have reported the prevalence of dermatosis related to arsenicosis from 1.3 to 5.1% and the accumulation of arsenic in biological samples like hair and nail much higher than the acceptable level. Though some steps are being taken by government and private organizations to combat the problem, it has not been able to cover all the affected communities. Nepal still needs more research work on arsenic occurrence and effects and mitigation programs simultaneously.

Adolescent↗
PubMed1998

The cost-effectiveness of radon mitigation in schools in Northamptonshire.

A comprehensive radon survey of 2372 rooms in 348 Northamptonshire schools is reported, together with results of the successful mitigation of the raised radon levels found in 20 schools. From analysis of the occupancy of affected rooms and the costs of remediation a total cost of 19,400 Pounds per man-sievert saved annually was derived. This is around four times more cost-effective than the radon remediation in Health Service premises in Northamptonshire, and slightly more cost-effective than a domestic programme where all householders with radon levels above the Action Level carry out remediation. As only a small percentage of householders undertook remediation, a schools' remediation programme is the most cost-effective programme to reduce radon in an Affected Area.

Adolescent↗
PubMed2000

Immune response to adenovirus-delivered antigens upregulates utrophin and results in mitigation of muscle pathology in mdx mice.

The upregulation of endogenous utrophin in skeletal muscle may lead to a new approach to the treatment of Duchenne muscular dystrophy (DMD). We found that injection of an E1, E3-deleted adenovirus vector expressing beta-galactosidase (beta-Gal) or green fluorescent protein (GFP) into the skeletal muscle of neonatal dystrophin-deficient mdx mice alleviated dystrophic pathology. In the adenovirus-infected muscles, an evaluation of sarcolemma stability showed low permeability and immunohistochemistry revealed utrophin upregulation at the extrasynaptic sarcolemma of mature muscle fibers. This utrophin upregulation was concomitant with endomysial cellular infiltration from a host immune reaction. There was no evidence of active muscle regeneration. In normal C57BL/10 mice, utrophin was also upregulated in adenovirus-injected skeletal muscles, where upregulated utrophin often coexisted with dystrophin. FK506 and anti-CD4 antibody administration decreased utrophin expression in adenovirus-injected mdx muscles and prevented the dystrophic phenotype from being mitigated, suggesting that an immune reaction is involved in utrophin upregulation. This is the first report demonstrating the improvement of the dystrophic phenotype as a result of the acquired overexpression of endogenous utrophin. Our findings provide an important clue to understanding the mechanism of utrophin expression and the development of an effective treatment for DMD.

Adenoviridae↗
PubMed2000

A novel murine anti-human Fas mAb which mitigates lymphadenopathy without hepatotoxicity.

Defects in Fas-mediated apoptosis are implicated in autoimmune diseases including rheumatoid arthritis (RA). Although induction of Fas-mediated apoptosis could have therapeutic effects on these diseases, it might cause deleterious effects in liver as Fas ligand or an agonistic anti-murine Fas antibody Jo2 causes severe hepatic injury in mice. We report here on the interesting characteristics of the newly obtained anti-Fas mAb, HFE7A, which cross-reacts with the Fas molecules of various species ranging from human to mouse and mitigates autoimmune symptoms without hepatotoxicity in mice. The administration of HFE7A to mice induced apoptosis in the thymocytes, although administration of HFE7A to mice or to marmosets did not induce any sign of hepatitis. The effect of HFE7A on liver is different from that of anti-murine Fas antibody Jo2, which causes acute and lethal hepatic injury to mice. Administration of HFE7A reduced lymphadenopathy and abnormal T cells in MRL-gld/gld mice. HFE7A induced apoptosis in synovial cells prepared from RA patients. Surprisingly, HFE7A protected mice from fulminant hepatitis induced by Jo2. Therefore, HFE7A is a potential therapeutic antibody not only for autoimmune diseases including RA but also for fulminant hepatitis.

Animals↗
PubMed2003

Peptides based on the complementarity-determining regions of a pathogenic autoantibody mitigate lupus manifestations of (NZB x NZW)F1 mice via active suppression.

Two peptides based on the complementarity-determining regions (CDR) 1 and 3 (pCDR1 and pCDR3) of a murine monoclonal anti-DNA autoantibody that expresses the common idiotype 16/6Id were shown to down-regulate systemic lupus erythematosus (SLE)-associated T cell responses and to prevent the development of clinical symptoms in the SLE-prone mice, (NZB x NZW)F(1). In the present study the ability of the CDR-based peptides to treat an already established disease was tested. Mice were given 10 weekly injections of peptides either i.v. or s.c. The treatment led to a moderate reduction in the anti-DNA autoantibody titer, and a significant decrease in proteinuria and kidney pathology. The CDR-based peptides affected the pathogenic isotypes (IgG2a and IgG3) of the anti-DNA antibodies in the serum and in immune complexes in the kidneys. Both peptides mitigated disease manifestations and prolonged the survival of mice that were treated starting at the age of 7 months when full-blown disease was already developed. Furthermore, some beneficial effects of treatment with the CDR-based peptides could be adoptively transferred to diseased recipients. A reduction in the secretion of IL-2, IFN-gamma, IL-4 and IL-10 was detected in supernatants of splenocytes of the treated mice. In contrast, treatment up-regulated the immunosuppresive cytokine-transforming growth factor-beta. Thus the ameliorating effect of the CDR-based peptides on SLE manifestations is at least partially via the immunomodulation of the cytokine profile.

Adjuvants, Immunologic↗
PubMed2006

Iodine deficiency mitigates growth retardation and osteopenia in selenium-deficient rats.

Selenium deficiency is associated with impaired bone metabolism and osteopenia in rats. However, it is not known how combined selenium and iodine deficiency affects bone metabolism. Therefore, we investigated the effect of selenium and iodine deficiency on bone metabolism in 2nd-generation selenium- and iodine-deficient rats. Selenium-deficient (Se-), iodine-deficient (I-), selenium- and iodine-deficient (Se-/I-), and control rats (Se+/I+), were pair-fed their respective diets until they were 74 d old. Each pair-fed rat was fed a selenium-adequate diet in the same amount as that consumed the day before by its selenium-deficient counterpart, taking food spillage into account. The skeletal phenotype was analyzed by dual energy X-ray absorptiometry, histomorphometry, and bone metabolism markers. Erythrocyte glutathione peroxidase activity (Gpx) and plasma thyroid hormones were measured to assess selenium and iodine status, respectively. In both Se-/I+ and Se-/I- rats, Gpx was reduced by 99% compared with pair-fed Se+/I+ and Se+/I- rats (P < 0.001). Iodine deficiency reduced plasma thyroxine by 64% in the 2 iodine-deficient groups (P < 0.001). Body weight, tail length, plasma insulin-like growth factor, pituitary growth hormone concentration, and femur and tibia bone mineral density were significantly greater in the Se-/I- rats than in the Se-/I+ rats. This study shows that iodine deficiency mitigated growth retardation and osteopenia in 2nd-generation selenium-deficient rats and suggests that adequate selenium status should be ensured before measures are taken to correct iodine deficiency.

Animal Feed↗
PubMed2006

Ornithine restores ureagenesis capacity and mitigates hyperammonemia in Otc(spf-ash) mice.

We showed that Otc(spf-ash) mice, a model of ornithine transcarbamylase deficiency, were able to sustain ureagenesis at the same rate as control mice, despite reduced enzyme activity, when a complete mixture of amino acids was provided. An unbalanced amino acid mixture, however, resulted in reduced ureagenesis and hyperammonemia. To study the effect of ornithine supplementation [316 micromol/(kg.h)] on urea and glutamine kinetics in conscious Otc(spf-ash) mice under a glycine-alanine load [6.06 mmol/(kg.h)], a multiple tracer infusion protocol ([(13)C(18)O]urea, [5-(15)N]glutamine, [2,3,3,4,4 D(5)]glutamine and [ring-D(5)] phenylalanine) was conducted. Ornithine supplementation increased ureagenesis [3.18 +/- 0.88 vs. 4.56 +/- 0.51 mmol/(kg.h), P < 0.001], reduced plasma ammonia concentration (1125 +/- 621 vs. 193 +/- 94 micromol/L, P < 0.001), and prevented acute hepatic enlargement (P < 0.006) in Otc(spf-ash) mice. Ornithine supplementation also increased [96 +/- 20 vs. 120 +/- 16 micromol/(kg.h), P < 0.001] the transfer of (15)N from glutamine to urea, to values observed in the control mice [123 +/- 17 micromol/(kg.h)]. De novo amido-N glutamine flux was higher [1.57 +/- 0.37 vs. 3.04 +/- 0.86 mmol/(kg.h); P < 0.001] in Otc(spf-ash) mice, but ornithine supplementation had no effect (P < 0.56). The flux of glutamine carbon skeleton was affected by both genotype (P < 0.0001) and by ornithine (P 0. 036). In conclusion, ornithine supplementation restored ureagenesis, mitigated hyperammonemia, prevented liver enlargement, and normalized the transfer of (15)N from glutamine to urea. These data strongly suggest that ornithine has the potential for the biochemical correction of OTCD in Otc(spf-ash) mice.

Amino Acids↗
PubMed2005

Distortion of quantitative genomic and expression hybridization by Cot-1 DNA: mitigation of this effect.

Cross-hybridization of repetitive sequences in genomic and expression arrays is reported to be suppressed with repeat-blocking nucleic acids (C(o)t-1 DNA). Contrary to expectation, we demonstrated that C(o)t-1 also enhanced non-specific hybridization between probes and genomic targets. When added to target DNA, C(o)t-1 enhanced hybridization (2.2- to 3-fold) to genomic probes containing conserved repetitive elements. In addition to repetitive sequences, C(o)t-1 was found to be enriched for linked single copy (sc) sequences. Adventitious association between these sequences and probes distort quantitative measurements of the probes hybridized to desired genomic targets. Quantitative microarray hybridization studies using C(o)t-1 DNA are also susceptible to these effects, especially for probes that map to genomic regions containing conserved repetitive sequences. Hybridization measurements with such probes are less reproducible in the presence of C(o)t-1 than for probes derived from sc regions or regions containing divergent repeat elements, a finding with significant ramifications for genomic and expression microarray studies. We mitigated the requirement for C(o)t-1 either by hybridizing with computationally defined sc probes lacking repeats or by substituting synthetic repetitive elements complementary to sequences in genomic probes.

DNA↗
PubMed1999

Effect of growth hormone therapy in mitigating hypoxia-induced and food restriction-induced growth retardation in the newborn rat.

OBJECTIVE: Hypoxia may alter the neuroendocrine control of catabolic and anabolic states early in postnatal life by modulating the growth hormone-insulin-like growth factor-I (GH-IGF-I) system. We wondered: a) to what extent hypoxia effects on the GH-IGF-I axis differed from those of food deprivation alone; and b) whether administration of exogenous GH mitigates alterations of the GH-IGF-I axis caused by hypoxia or food restriction. DESIGN: Prospective laboratory investigation using nursing dams and suckling pups. Experimental groups included: a) room air control subjects; b) hypoxia-exposed subjects (FIO2, 0.12); or c) room air breathing subjects whose dam food intake was matched to that of hypoxic dams. Half of the pups in each group were administered rat GH (100 microg subcutaneously each day), and the remaining received vehicle alone. The intervention lasted 18 days. SETTING: Research laboratory in a university medical center. SUBJECTS: Twelve litters of 1-day-old Sprague-Dawley rat pups and nursing dams. INTERVENTIONS: Hypoxia exposure, food restriction, GH administration. MEASUREMENTS AND MAIN RESULTS: By the end of the study, body weights of the hypoxic and pair-fed pups were significantly lower than the weights of control animals (p < .001 for both groups), and weight gain correlated significantly with total dam food consumption (r2 = .85, p < .0001). GH administration increased weight gain only in hypoxic animals (p < .001) but it increased tail lengths significantly in both hypoxic and control pups (p < .001). Serum IGF-I levels in both hypoxic and pair-fed pups were significantly lower than in control animals. Serum IGF-binding protein-3 (IGFBP-3) was significantly lower in the hypoxic compared with the control animals. GH administration resulted in significant increases in serum levels of IGFBP-3 in both the control (p < .05) and the hypoxic (p < .01) pups compared with their vehicle-treated litter mates. CONCLUSIONS: Exogenous GH attenuates growth impairment associated with hypoxia but not with food restriction, and these effects may be mediated in part by IGFBP-3.

Animals↗
PubMed1993

Methods for mitigating soft-tissue injury after subcutaneous injection of water soluble contrast media.

RATIONALE AND OBJECTIVES: Water soluble contrast media may cause tissue injury by extravasation during intravenous injection during various radiologic examinations. The authors attempted to find out what kind of management could mitigate tissue injury when extravasation of water soluble contrast media occurs. METHODS: Sodium and meglumine ioxithalamate was injected subcutaneously into 240 hind feet of 120 rats that were divided into six groups according to the methods of experimental management. Experimental managements included the following: no further management (control), injection of distilled water, injection of normal saline, injection of hydrocortisone, hot water application, and cold water application. Gross morphologic changes in each group were compared with those in the control group. RESULTS: Only the saline injection group showed statistically significant decrease of tissue injury compared with the control group. CONCLUSIONS: Saline injection lessens the degree of soft-tissue injury at contrast media extravasation sites in rats.

Animals↗
PubMed2002

Astrocytic activation and delayed infarct expansion after permanent focal ischemia in rats. Part II: suppression of astrocytic activation by a novel agent (R)-(-)-2-propyloctanoic acid (ONO-2506) leads to mitigation of delayed infarct expansion and early improvement of neurologic deficits.

A novel agent, (R)-(-)-2-propyloctanoic acid (ONO-2506), has a unique property in that it modulates functions of activated cultured astrocytes, including pronounced inhibition of S-100beta synthesis. The present study examined whether administration of this agent would mitigate the delayed expansion of infarct volume and the neurologic deficits after permanent middle cerebral artery occlusion (pMCAO) in rats. Daily intravenous administration of ONO-2506 (10 mg/kg) abolished the delayed infarct expansion between 24 and 168 hours after pMCAO, whereas the acute infarct expansion until 24 hours was unaffected. The agent significantly reduced the expression of S-100beta and glial fibrillary acidic protein in the activated astrocytes and the number of terminal deoxynucleotidyl transferase-mediated 2;-deoxyuridine 5;-triphosphate-biotin nick end labeling-positive cells in the periinfarct area. The neurologic deficits were significantly improved, compared with the vehicle-treated groups, as early as 24 hours after the initial administration of ONO-2506. The agent had a wide therapeutic time window of 0 to 48 hours after pMCAO. These results indicate that because of the pharmacologic modulation of astrocytic activation induced by ONO-2506, symptoms can regress whereas delayed expansion of the lesion is arrested. Pharmacologic modulation of astrocytic activation may confer a novel therapeutic strategy against stroke.

Animals↗
PubMed1976

Mitigation of graft-versus-host disease in lethally irradiated mice grafted with spleen cells adherent to glass beads.

Murine spleen cells were separated on the basis of adherence to glass beads into distinct subpopulations that differ in their ability to produce acute graft-versus-host disease (GVHD). Nonadherent CBA spleen cells produce acute GVHD in 6-10 days in lethally irradiated (C57BL/6 X CBA)F1 mice as do unfractionated spleen cells. Spleen cells which are adherent to glass beads, however, enable 71% of the mice to survive without symptomatology of acute GVHD. The low proliferative response of these cells to phytohemagglutinin (PHA) correlated with the mitigated GVHD seen in animals grafted with this fraction. Proliferative cells as determined by the spleen colony assay and the in vitro agar colony-forming assay are present in this fraction as are cells responsive to mitogenic stimulation with lipopolysaccharide (LPS). B6CBF1 mice grafted with CBA adherent cells exhibit a gradual return over a period of 5 months to normal PHA and LPS stimulation levels as shown by splenic cell responses of these mice to mitogens. Surviving mice grafted with adherent cells were chimeric as determined by electrophoretic hemoglobin pattern analysis and serial bone marrow transplantation.

Animals↗
PubMed2000

Use of allochimeric proteins to mitigate graft-versus-host and host-versus-graft immune responses to rat small bowel allografts.

BACKGROUND: We aimed to identify the polymorphic epitopes that mitigate graft-versus-host disease (GvHD) and host-versus-graft response (HvGR) toward rat small bowel allografts in rats. METHODS: We tailored class I major histocompatibility complex (MHC) allochimeric antigens encoding 10 al-helical (alpha(1h)l58-80-RT1.Aa) or 4 (alpha(1h)l/u62-69-RT1.Aa) polymorphic amino acids. In the GvHD model, ACI (RT1a) donors were pretreated (day -14) with an intrathymic injection of alpha(1h)l58-80-RT1.Aa, alpha(1h)l/u62-69-RT1.Aa, or RT1.Al protein, with or without simultaneous intravenous injection of anti-T-cell receptor R73 monoclonal antibodies. Wistar-Furth (WF; RT1u) donors were tested with a similar protocol. In the HvGR model, ACI recipients were treated with a protocol designed to induce transplantation tolerance toward WF heart allografts: a portal vein injection of alpha(1h)l/u62-69-RT1.Aa protein and cyclosporine (4 mg/kg, intramuscular; days 0-6). RESULTS: GvHD was prevented in all (ACI x LEW) F1 recipients (RT1a/l) by pretreating ACI donors with R73 monoclonal antibody and recipient RT1.Al or alpha(1h)l58-80-RT1.Aa protein. Similarly, pretreatment of WF donors with RT1.Aa protein also prevented GvHD in (ACI x WF) F1 recipients. However, in a combined GvHD/HvGR model, ACI recipient perioperative treatment designed to prevent HvGR only modestly prolonged WF small bowel allograft survival (27.7+/-5.3 days compared to 17.4+/-4.6 days in the cyclosporine-alone group). In contrast, application of the two protocols significantly prolonged WF allograft survival (55.6+/-34.6 days), with two of seven recipients surviving more than 100 days. CONCLUSION: Simultaneous inhibition of GvHD and HvGR significantly prolongs small bowel allograft survival.

Animals↗
PubMed2004

A lazaroid mitigates postresuscitation myocardial dysfunction.

OBJECTIVE: Lazaroids, a series of 21-aminosteroids, reduce free radical mediated injury after ischemia and reperfusion. We hypothesized that the lazaroid U-74389G would minimize postresuscitation myocardial dysfunction and thereby improve neurologically meaningful survival in a rodent model after resuscitation from 8 mins of ventricular fibrillation. DESIGN: Randomized, controlled laboratory study. SETTING: University-affiliated research institute. SUBJECTS: Sprague-Dawley rats. INTERVENTIONS: Ventricular fibrillation was electrically induced in ten anesthetized Sprague-Dawley rats. The lazaroid agent U-74389G in a dose of 1 mg.kg-1 or its vehicle serving as a placebo was injected into the right atrium after 7 mins of untreated ventricular fibrillation. One minute after injection of the compound, precordial compression was begun together with mechanical ventilation and continued for 6 mins before attempted electrical defibrillation. MEASUREMENTS AND MAIN RESULTS: All animals were successfully resuscitated. Postresuscitation cardiac index, left ventricular end-diastolic pressure, the rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg, and the maximum rate of left ventricular pressure decline were significantly less impaired in lazaroid-treated animals. This contrasted with control animals, which had significantly greater myocardial impairment, greater neurologic deficit, and lesser duration of survival. CONCLUSIONS: The lazaroid compound U-74389G, administered during cardiac arrest, mitigated postresuscitation myocardial dysfunction and improved survival.

Animals↗