Biomedical subjects
C Agalar
Publications and source records attributed to C Agalar.
Resuscitation with modified gelatin causes higher bacterial translocation in experimental sublethal hemorrhagic shock.
The effect of colloidal solutions on bacterial translocation was studied. Sublethal hemorrhagic shock was established by blood withdrawal until the mean arterial pressure fell to 40 mmHg within 15 min on 36 adult Wistar Albino rats. Resuscitation was performed using four different solutions with the same amount of blood. Group I (n = 9) 0.9% NaCl, Group II (n = 9) 10% dextran 40, Group III (n = 9) 6% hydroxyethyl starch, Group IV (n = 9) 4% modified fluid gelatin. Before resuscitation and after anesthesia blood samples were drawn to analyze pH, PCO2, PO2, SaO2, HCO3 and ABE values. Twenty-four hours after anesthesia laparotomy was performed to obtain tissue samples of the liver, spleen and mesenteric lymph nodes. Samples were cultured on EMB and blood agar media. Results were analyzed with the one-way ANOVA and Post-hoc test (Tukey's HSD). The translocated bacteria were mainly Eschericia coli and three grew in Group I, two in Group II, three in Group III and six in Group IV. Although there was a trend in difference in bacterial translocation rates among groups, statistical analyses revealed no difference among groups (p < 0.05). It can be concluded that resuscitation with modified gelatin causes higher bacterial translocation in an experimental sublethal hemorrhagic shock model.
Effect of teicoplanin and G-CSF on survival in experimental MRSA pneumonia in neutropenic mice.
AIM: To evaluate the effects of Teicoplanin and/or Granulocyte-Colony Stimulating Factor (G-CSF) on survival in an experimental model of MRSA pneumonia. MATERIAL AND METHOD: Seventy five Swiss Albino mice weighing 35 gr (32-43) were used. 50 microl of clinical isolate of MRSA (3 x 10(8) CFU/ml in saline solution) was administered by tracheal puncture to neutropenic mice. Neutropenia was achieved by using Cyclophosphamide 200 mg per kg intraperitoneally. The groups were consisted of tracheal puncture control in neutropenic mice (group 1) (n = 15), pneumonia in neutropenic mice (group II) (n = 15), Teicoplanin therapy for pneumonia in neutropenic mice (group III) (n = 15), G-CSF therapy for pneumonia in neutropenic mice (group IV) (n = 15), Teicoplanin and G-CSF combined therapy for pneumonia in neutropenic mice (group V) (n = 15). Differences in the survival rates within 72 hours among the groups, microbiological analysis of various tissue samples were accomplished and white blood cell counts were obtained. Kaplan-Meier statistics was used for survival analysis. Subgroup comparisons were done by using Breslow statistics. RESULTS: Teicoplanin therapy increased the survival rate (p = 0.0001) whereas G-CSF therapy did not in comparison to other groups. Teicoplanin and G-CSF combination therapy improved survival rate when compared with groups II, III, IV (p = 0.0001, p = 0.003, p = 0.0001, respectively). CONCLUSION: Teicoplanin and G-CSF combination therapy seems effective in reducing mortality rates in MRSA pneumonia in an experimental setting. Further animal and clinical studies must be done to achieve success in the treatment of nosocomial MRSA pneumonia.
Ciprofloxacin and rifampicin versus doxycycline and rifampicin in the treatment of brucellosis.
The present study was undertaken to evaluate the efficacy, safety, and patient tolerability of two antibiotic regimens for the treatment of brucellosis: rifampicin 600 mg/day and doxycycline 200 mg/day for 45 days (group 1), versus rifampicin 600 mg/day and ciprofloxacin 1 g/day for 30 days (group 2). Forty patients were diagnosed with brucellosis based on clinical and microbiological findings. The two groups were comparable regarding age and sex distribution. The average number of days without fever and symptoms was lower in group 2 patients than in group 1 patients (mean+/-SD: 3.85+/-1.98 for group 1 vs. 2.78+/-1.03 for group 2, P=0.044). During the 1-year follow-up period, three (15%) patients in group 2 and two (10%) patients in group 1 had clinical relapses; these rates were not significantly different. Ciprofloxacin and rifampicin treatment for brucellosis is as effective as the standard regimen of doxycycline and rifampicin and offers the advantage of a shorter duration of treatment.
The effects of G-CSF treatment and starvation on bacterial translocation in hemorrhagic shock.
BACKGROUND: Bacterial translocation is thought to be responsible for infectious complications after hemorrhagic shock. The aim of this study is to investigate the effects of granulocyte colony-stimulating factor (G-CSF) treatment on bacterial translocation in starved or fed animals subjected to hemorrhagic shock. MATERIALS AND METHODS: Fifty Wistar albino rats (200-275 g) were divided into six groups such as naive control (n = 7), G-CSF treatment (n = 7), hemorrhagic shock in starved rats (n = 9), hemorrhagic shock in fed rats (n = 9), G-CSF treatment 24 h before hemorrhagic shock in starved rats (n = 9), and G-CSF treatment 20 min after hemorrhagic shock in fed rats (n = 9). Hemorrhagic shock was induced by withdrawal of 2.1 ml/100 g blood via a carotid arterial cannulae placed under sodium pentobarbital anesthesia. Twenty-four hours later, mesenteric lymph nodes, liver, spleen, and peripheral blood samples were evaluated by using a quantitative microbiological technique and the numbers of colony-forming units were compared between groups. RESULTS: No bacteria was detected in samples from naive controls or G-CSF-treated unshocked rats. In animals subjected to hemorrhage, Escherichia coli was the predominant pathogen together with Streptococcus faecalis, Pseudomonas, and Lactobacillus species. In this model, starvation augmented the magnitude of bacterial translocation while G-CSF treatment has virtually abolished it. CONCLUSION: Under experimental conditions, preshock starvation increases gut-derived bacterial translocation and administration of G-CSF before or after hemorrhagic insult significantly reduces it.
Evidence that aminoguanidine inhibits endotoxin-induced bacterial translocation.
BACKGROUND: The role of inducible nitric oxide synthase (iNOS) in endotoxin-induced bacterial translocation was investigated by using its specific blocker aminoguanidine in 46 albino mice (25-35 g) allocated into four groups. METHODS: The first group received intraperitoneal saline (control; 0.9 per cent w v(-1) sodium chloride 1 ml kg(-1); n=6), the second group intraperitoneal endotoxin (Escherichia coli lipopolysaccharide 055:B5 20 mg kg(-1); n=19), the third group intraperitoneal aminoguanidine (20 mg kg(-1), 20 min before and 12 h after saline; n=6) and the fourth group both endotoxin and aminoguanidine intraperitoneally (n=15). Some 24 h later, the animals were anaesthetized with ether and blood samples were collected by cardiac puncture together with mesenteric lymph node (MLN), spleen and liver specimens under aseptic conditions. Specimens were then cultured to determine the presence of colony-forming units as an index of bacterial translocation. RESULTS: No bacterial growth was detected in samples from the first and third groups. Colony-forming bacteria were found in ten of 14 MLN samples, eight of 14 spleens, four of 14 livers and three of 14 peripheral blood samples in the second group, with E. coli being the predominant pathogen. In contrast, in the fourth group, colony-forming bacteria were found in only three of 14 MLN samples (P=0.02 versus the second group), three of 14 spleens and one of 14 liver specimens. None of the values in the fourth group was significantly different from those in the saline control group. CONCLUSION: The inhibition of iNOS during endotoxaemia by its specific blocker aminoguanidine attenuates the incidence of bacterial translocation in mice. These results may be exploited clinically for the prophylaxis and treatment of septic states.
Comparison of two regimens for ciprofloxacin treatment of enteric infections.
A clinical trial was conducted in 50 patients with blood cultures positive for Salmonella typhi or Salmonella paratyphi to compare treatment with ciprofloxacin for seven days, 500 mg b.i.d. (Group 1, 25 patients), with treatment for ten days, 750 mg b.i.d. (Group 2, 25 patients). Clinical cure was defined as defervescence of fever by day 5 of treatment, with an absence of complications and no clinical relapse. The clinical cure rate was 84% for group 1 and 96% for group 2; the difference in these rates was not statistically significant. The blood cultures of all patients were sterile by day 2 of treatment and remained so until the sixth month of follow-up. It was concluded that ciprofloxacin treatment for ten days in enteric fever is not necessary. Further studies are needed to evaluate the efficacy of shortening the duration of antibiotic therapy.
Factors that may increase morbidity in a model of intra-abdominal contamination caused by gallstones lost in the peritoneal cavity.
OBJECTIVE: To assess the effect of intraperitoneal gallstones with and without Escherichia coli and sterile bile on the incidence of intraperitoneal complications in mice. DESIGN: Prospective randomised study. SETTING: Teaching hospital, Turkey. MATERIAL: 180 Swiss albino mice in five groups, n = 20 in the control group, and n = 40 in each of the experimental groups. INTERVENTIONS: Group A laparotomy alone (controls); group B, laparotomy amd intraperitoneal instillation of E. coli 4 x 10(6) 0.1 ml; group C, laparotomy and insertion of sterilised gallstones; group D, laparotomy, insertion of gallstones and instillation of E. coli 4 x 10(6) 0.1 ml; and group E, laparotomy, insertion of gallstones, and instillation of E. coli 4 x 10(6) 0.1 ml and sterile bile 0.1 ml. A quarter of each group was killed after 1, 2, 4, and 8 weeks. MAIN OUTCOME MEASURES: Intra-peritoneal abscesses, adhesions, perforations, fistula, or obstruction. RESULTS: No mice died. Adhesions were found in 3(15%), 7(18%), 30(75%), 25(63%), and 24(60%) in the five groups, respectively. No mice in groups A, B, or C developed an abscess, but 8 did in each of groups D and E (20%). One mouse in group D developed obstruction. Logistic regression showed that abscess formation was significantly increased by the addition of gallstones and E. coli to the peritoneal cavity (p < 0.001) but the addition of bile had no effect. Gallstones increased the rate of adhesions more than nine fold (p < 0.001) but E. coli with or without bile had no effect (p = 0.75). CONCLUSIONS: Free gallstones within the peritoneal cavity with or without E. coli or sterile bile, or both, increased the rate of formation of both abscesses and adhesions in mice. These results suggest that efforts should be made retrieve gallstones that are dropped into the peritoneal cavity during laparoscopic cholecystectomy, particularly in patients with acute cholecystitis.
A case of peritonitis due to Rothia dentocariosa in a CAPD patient.
Explore the source record for details and available documents.
The role of HBV DNA and liver histopathology in HBsAg carriers.
BACKGROUND/AIMS: In this study, we evaluated the association among serum transaminase values, seropositivity of HBV DNA and liver histopathology of patients with positive HBsAg and HBe antibodies. METHODOLOGY: Thirty-five patients were placed in two groups according to their serum transaminase values. Patients with normal transaminase values were evaluated in the first group. The patients with above normal transaminase values were subjected in the second group. RESULTS: In the first group of patients with normal transaminase values, biopsy-proven moderate or severe chronic hepatitis was not observed. HBV DNA seropositivity was 53.3% in this group. Forty-five percent of the patients with above normal transaminase values had moderate chronic hepatitis and seropositivity for HBV DNA in this group was 55%. Our results supported the association between transaminase values and liver pathology, but no statistically significant association was shown between seropositivity of HBV DNA and liver pathology. CONCLUSION: There is much to be studied to understand the function of HBV DNA in the follow up of HBsAg carriers, and liver biopsy has to be used routinely in the follow up of asymptomatic carriers when they happen to have high transaminase values.