BACKGROUND:

Partial portal vein ligation causes an increase in portal pressure that remains stable even after the appearance of collateral circulation, with functional adaptation to prolonged decrease in portal blood flow.

AIM:

To assess whether different constriction rates produced by partial ligation of the vein interfere with the results of this experimental model in rats.

METHODS:

Three groups of five rats each were used; in group 1 (sham-operated), dissection and measurement of portal vein diameters were performed. Portal hypertension was induced by partial portal vein ligation, reducing its size to 0.9 mm in the remaining 10 animals, regardless of the initial diameter of the veins. Five animals with portal hypertension (group 2) underwent reoperation after 15 days and the rats in group 3 after 30 days. The calculation of the constriction rate was performed using a specific mathematical formula (1 - π r 2 / π R2) x 100% and the statistical analysis with the Student t test.

RESULTS:

The initial diameter of the animal's portal vein was 2.06 mm, with an average constriction rate of the 55.88%; although the diameter of the veins and the constriction rate in group 2 were lower than in group 3 (2.06 mm - 55,25% and 2.08 mm - 56.51%, respectively), portal hypertension was induced in all rats and no significant macroscopic differences were found between the animals that were reoperated after 15 days and after 30 days respectively, being the shorter period considered enough for the evaluation. Comparing the initial diameter of the vein and the rate of constriction performed in groups 2 and 3, no statistic significance was found (p>0.05).

CONCLUSION:

Pre-hepatic portal hypertension in rat can be induced by the reduction of the portal vein diameter to 0.9 mm, regardless the initial diameter of the vein and the vessel constriction rate.

BACKGROUND:

The negative result of a research does not always indicate failure, and when the data do not permit a proper conclusion, or are contrary to the initial project, should not simply be discarded and archived.

AIM:

To report failure after performing experimental model of liver ischemia and reperfusion normothermic, continuous or intermittent, in small animals aiming at the study of biochemical and histological parameters after postoperative recovery.

METHODS:

Fifteen Wistar rats were divided into three groups of five animals each; all underwent surgery, the abdomen was sutured after the proposed procedures for each group and the animals were observed for 6 h or until they died, and then were reoperated. In Group 1, control (sham-operated): dissection of the hepatic hilum was performed; in Group 2: clamping of the hepatic hilum for 30 m; in Group 3: clamping of the hepatic hilum for 15 m, reperfusion for 5 m and another 15 m of clamping. Data from Groups 2 and 3 were compared with Student's t test.

RESULTS:

All animals of Group 1 survived for 6 h. Two animals in Group 2 died before the 6 h needed to validate the experiment; two did not recover from anesthesia and one survived until the end. In Group 3, four animals died before the 6 h established and one of them survived the required time. Only one animal in Group 2 and one in Group 3 survived and were able to accomplish the study. There was no statistical significance when the results of Groups 2 and 3 were compared (p>0.05).

CONCLUSION:

The death of six animals before the necessary period of observation turned the initial proposal of the experiment unfeasible.

BACKGROUND:

Animal models are useful to evaluate the efficacy of antimicrobials in experimental sepsis.

AIM:

To elucidate the steps of producing an experimental model for the treatment of extended-spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae sepsis

METHODS:

Several ESBL inoculums ranging from 1.5x109 colony-forming units per milliliter (CFU/mL) to 2.0x1010CFU/mL were administered by peritoneal injection in adults Wistar rats. Outcomes and microbiological data of quantitative peritoneal and blood cultures were observed in untreated animals. Animals which received 2.0x1010CFU/mL inoculums were treated with single meropenem dose (30mg/kg) after one hour and those which received 1.0x1010CFU/mL inoculums were treated immediately with three doses of meropenem 50 mg/kg. Outcomes were observed for 24 hours after inoculation.

RESULTS:

Solutions with 1.5 x109 and 6.0x109 CFU/mL were not lethal within 24 hours. Inoculums of 1.0x1010CFU/mL were lethal in 80% and solutions with 2.0x1010 CFU/mL were lethal in 100% of animals. ESBL lethal sepsis (1.0x1010CFU/mL) was treated immediately with 50 mg/kg of meropenem every eight hours for 24 hours and presented 40% mortality compared with 80% mortality of the control group (p=0.033). Quantitative cultures of peritoneal fluid presented 104CFU/mL or less for treated animals compared to more than 105 for untreated animals (p=0.001).

CONCLUSION:

Inoculums of 1.0x1010CFU/mL achieved the best results to study a model of lethal sepsis and this model of treatment of carbapenem-susceptible Enterobacteriaceae can serve as control to further evaluation of treatment of carbapenemase-producing Enterobacteriaceae models.

BACKGROUND:

The number of malignancies increased alarmingly. Surgery constitutes one of the most efficient therapeutic modalities for the treatment of solid tumors. The neoplastic implant in surgical wound is a complication whose percentage of occurrence reported in the literature is variable, but sets with high morbidity and therapeutic difficulties. Protecting the wound is one of the recommended principles of oncologic surgery.

AIM:

To evaluate the influence of wound protection in the development of tumor implantation.

METHODS:

Sarcoma 180 tumor cells were used, with intraperitoneal inoculation in Swiss mice. After the establishment of neoplastic ascites, animals were randomized into two groups of 10, each group consisting of five males and five females. In both groups, laparotomy and manipulation of intra-abdominal organs was performed. In a group laparotomy was performed using the protection of the abdominal wound and the other group without it. On the 9th postoperative day macroscopic evaluation of the operative scar was performed, which was later removed for microscopic evaluation.

RESULTS:

There was microscopic infiltration of tumor cells in the wound of all animals. However, the group that held the protection, infiltration was less intense when compared to the group without it. The infiltration was also more severe in females than in males of the same group.

CONCLUSION:

Tumor infiltration into the wound was more intense in the group in which the protection of the surgical site was not performed, and in females when compared to males of the same group.

Introduction:

Colorectal cancer is a very frequent sort of neoplasm among the population, with a high mortality rate. It develops from an association of genetic and environmental factors, and it is related to multiple cell signaling pathways. Cell cultures and animal models are used in research to reproduce the process of disease development in humans. Of the existing animal models, the most commonly used are animals with tumors induced by chemical agents and genetically modified animals.

Objective:

To present and synthesize the main animal models of colorectal carcinogenesis used in the research, comparing its advantages and disadvantages.

Method:

This literature review was performed through the search for scientific articles over the last 18 years in PubMed and Science Direct databases, by using keywords such as “animal models”, “colorectal carcinogenesis” and “tumor induction”.

Results:

1,2-dimethylhydrazine and azoxymethane are carcinogenic agents with high specificity for the small and large intestine regions. Therefore, the two substances are widely used. Concerning the genetically modified animal models, there is a larger number of studies concerning mutations of the APCp53 and K-ras genes. Animals with the APC gene mutation develop colorectal neoplasms, whereas animals with p53 and K-ras genes mutations are able to potentiate the effects of the APC gene mutation as well as the chemical inducers.

Conclusion:

Each animal model has advantages and disadvantages, and some are individually efficient as to the induction of carcinogenesis, and in other cases the association of two forms of induction is the best way to obtain representative results of carcinogenesis in humans.

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