Evaluation of hematological, biochemical and oxidative stress profile in calves under propofol anesthesia.

Propofol is a widely used drug in veterinary medicine to induce anesthesia; as well as the chosen compound for protocols of intravenous anesthesia. The present study aimed to describe the hematological, biochemical and oxidative stress alterations in calves kept under anesthesia by propofol in different dosages. In order to achieve this, eight Holstein calves were induced using propofol in a 5 mg/kg dosage and maintained under continuous propofol infusion for 60 min, having being administered 0.6 mg/kg/h or 0.8 mg/kg/h in crossover design with seven days interval. Blood samples were collected immediately before the anesthesia induction (baseline), and 30 min, 1, 2, 3, 4 and 5 h after the procedure started. Statistically relevant propofol influence was observed both in blood and biochemical parameters, with differences between dosages according to the time of infusion. The drug action over oxidative stress was also observed, causing a raise of the total antioxidant capacity (TAC) with an uric acid increase. Additionally, the increase of triglycerides, induced by the anesthesia maintenance with propofol, caused lipemia in the samples, which was capable of interfering directly in the measurements made by refractometry and spectrophotometry. It was concluded that, in spite of propofol induced alterations in blood and biochemical parameters, such alterations are subtle. In addition to that, the drug presented an antioxidative effect, which reinstates the safety of anesthesia maintenance with propofol in calves.

Omega-3 Fatty Acids Alter Systemic Inflammatory Mediators Caused by Apical Periodontitis.

INTRODUCTION: This study investigated the effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) on serum inflammatory mediators of rats with pulp exposure-induced apical periodontitis. METHODS: Forty male Wistar rats were divided into the following groups: control, untreated rats (C); control rats treated with ω-3 PUFAs (C-O); rats with pulp exposure-induced apical periodontitis (AP); and rats with pulp exposure-induced apical periodontitis treated with ω-3 PUFAs (AP-O). ω-3 PUFAs were administered orally once a day for 15 days before pulp exposure and continued for 30 days after pulp exposure. The rats were sacrificed, and then blood and jaw samples were collected. Blood analysis was conducted to determine the total number of leukocytes including neutrophils, monocytes, and lymphocytes. Proinflammatory cytokines tumor necrosis factor alpha, interleukin (IL) 6, and IL-17 were quantified by enzyme-linked immunosorbent assay. Histologic analysis was performed to confirm the development of apical periodontitis. The data were statistically evaluated using analysis of variance and the Tukey posttest. The significance level was set at 5%. RESULTS: The development of apical periodontitis was confirmed in all infected groups. Bone destruction was larger in the AP group compared with the AP-O group (P < .05). Blood analysis showed that the AP and AP-O groups showed higher numbers of lymphocytes, leukocytes, monocytes, eosinophils, and expressions of tumor necrosis factor alpha and IL-6 compared with the C and C-O groups (P < .05). In contrast, the presence of leukocytes, lymphocytes, and the expression of IL-6 decreased in the AP-O group compared with the AP group (P < .05). CONCLUSIONS: ω-3 PUFA supplementation influences the systemic effects caused by apical periodontitis, decreasing the number of leukocytes, lymphocytes, and IL-6 in rat blood.

Systemic oxidative stress in Suffolk and Santa Ines sheep experimentally infected with Haemonchus contortus.

The mechanisms responsible for the imbalance between oxidants and antioxidants in sheep infected with Haemonchus contortus are not well established. This study aimed to prove the hypothesis that oxidative stress occurring during infection by H. contortus varies according to breed, and that the parasite burden correlates with hypoalbuminaemia and anaemia. Thus, after deworming and confirming the absence of infection, two different sheep breeds, Suffolk (n = 15) and Santa Ines (n = 22), were orally inoculated with a single dose of 5,000 L3 of H. contortus. The egg counts per gram of faeces (EPG), packed cell volume (PCV) and concentrations of several plasma markers of oxidative stress (lipid peroxidation, albumin, uric acid, total bilirubin, total antioxidant capacity [TAC], total oxidant concentration [TOC] and the oxidative stress index [OSI]) were quantified before (control group) and during the experimental infection (28, 34 and 42 days post-inoculation). In both breeds, TOC increased at 28 days and TAC increased at 42 days. In Suffolk sheep, there was a positive correlation of EPG with oxidant components (28 days) and a negative correlation of EPG with PCV (42 days). In Santa Ines sheep, there was a positive correlation of EPG with bilirubin (r = 0.492; p = 0.020). H. contortus infection caused oxidative stress, which varied according to the breed. Parasite burden was not associated with hypoalbuminaemia, whereas there was a negative correlation with PCV. This research provides the first evidence that the antioxidant status contributes more to the resilience to H. contortus in Santa Ines sheep compared to Suffolk sheep.

Omega 3 Fatty Acids Reduce the Triglyceride Levels in Rats with Apical Periodontitis.

The aim of this study was to evaluate the influence of the prophylactic and therapeutic supplementation with omega 3 polyunsaturated fatty acids (w-3 PUFAs) on the lipid profile and periapical bone resorption in rats with apical periodontitis. Forty male rats were divided into groups: control rats (C), rats treated with w-3 PUFAs (C+O), rats with pulp exposure-induced apical periodontitis (AP), and rats with AP treated with w-3 PUFAs (AP+O). The administration of w-3 PUFAs was carried out orally once a day for 15 days before pulp exposure and, subsequently, for an additional 30 days after pulp exposure. AP was induced by exposing pulpal tissues to the oral environment. The samples were collected after 30 days. Triglycerides and cholesterol levels were enzymatically measured using the Trinder method. The jaws were collected and submitted for histological analysis. Two-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at p<0.05. The triglyceride levels of the AP group were significantly higher than those of the C, C+O and AP+O groups (p<0.05). However, the difference in the cholesterol levels among the groups was not significant (p>0.05). Rats with AP showed larger areas of bone resorption as well as higher inflammatory intensity compared with rats with AP supplemented with w-3 PUFAs. It may be concluded that the presence of multiple AP foci increased the triglyceride levels. In addition, omega 3 supplementation might reduce these levels in rats with AP, as well as the bone resorption areas of periapical tissues.

Endodontic infections increase leukocyte and lymphocyte levels in the blood.

OBJECTIVES: The aim of this study was to determine whether the presence of single or multiple apical periodontitis (AP) alters blood cell counts and cytokine production. MATERIAL AND METHODS: Thirty rats were divided into three groups: a control group comprising rats without AP, a group called 1AP comprising rats with AP in one tooth, and a group called 4AP comprising rats with AP in four teeth. Endodontic infection was induced by pulp exposure of the first right maxillary molar in the 1AP group or by exposing the first and second right maxillary and mandibular molars in the 4AP group. A blood count and cytokine levels were obtained 30 days after infection by collecting blood by cardiac puncture. The maxillae were dissected and stained with hematoxylin and eosin to evaluate the inflammatory infiltrate. The data were tabulated and subjected to statistical analysis (P < 0.05). RESULTS: Histological analysis showed a predominance of mononuclear inflammatory cells. In blood, significant increase of leukocytes, lymphocytes, and tumor necrosis factor alpha (TNF-α) in 4AP compared with the control and 1AP groups (P < 0.05) was observed. In addition, significant decrease of interleukin-4 (IL-4) in 1AP and 4AP groups compared with the control was observed (P < 0.05). CONCLUSIONS: In the rat model, the presence of multiple AP can affect health by increasing lymphocyte and TNF-α levels in the blood. CLINICAL RELEVANCE: The presence of endodontic infections can interfere with the blood profile, altering systemic health.

Influence of Apical Periodontitis on Stress Oxidative Parameters in Diabetic Rats.

INTRODUCTION: In this study, we investigated if apical periodontitis (AP) associated with diabetes influenced the levels of endogenous antioxidants, the total antioxidant capacity (TAC), and the oxidant parameter in the serum of Wistar rats. METHODS: Forty male rats were divided into 4 equal groups: normal rats (N), rats with AP (AP), diabetic rats (D), and diabetic rats with AP (D + AP). Diabetes was induced by alloxan (150 mg/kg). AP was induced by exposing the pulpal tissue to the oral environment. After 36 days, blood and maxillae were collected. Albumin, bilirubin, uric acid, TAC, and malondialdehyde (MDA) levels were measured, and histologic analysis of the maxillae was performed. P < .05 was set as the threshold for statistical significance. RESULTS: Uric acid levels were higher in the D + AP group when compared with that of the N, D, and AP groups (P < .05). The MDA concentration was higher in the D and D + AP groups when compared with the N and AP groups (P < .05). The level of albumin was lower in the D + AP group when compared with the N, AP, and D groups. Inflammatory infiltration was more intense in the periapical region in the D + AP group compared with that in the AP group (P < .05). CONCLUSIONS: Our findings indicate that diabetes may change the antioxidant status, increase the concentration of MDA and uric acid, and decrease albumin levels in the serum. In addition, AP can potentiate the effects of diabetes by reducing the levels of albumin and increasing the levels of uric acid.

The effects of increased heme oxygenase-1 on the lymphoproliferative response in dogs with visceral leishmaniasis.

Canine visceral leishmaniasis (CVL) is known to affect the cellular immunity of infected dogs, through impairing lymphoproliferation and microbicidal mechanisms. This study examined heme oxygenase-1 (HO-1) and its metabolites, oxidative stress and IL-10 levels in CVL and investigated correlations between these parameters. Additionally, the effects of HO-1 inhibition on the lymphoproliferative response and cytokine production in lymph node cells (LNCs) from infected dogs were evaluated. Forty-four dogs, 24 controls and 20 dogs with CVL were selected. Plasma and splenic levels of HO-1, haptoglobin, soluble CD163 receptor, ferritin and IL-10 were determined using capture ELISA. The HO-1 levels and relative gene expression in peripheral blood and bone marrow mononuclear cells were also determined. LNCs proliferation was evaluated with an HO-1 activator and with an HO-1 inhibitor, in the presence of the Leishmania infantum soluble antigen (SAgL), using flow cytometry. HO-1, IL-2, IFN-gamma and IL-10 were also determined in these cultures using capture ELISA. Infected dogs presented oxidative stress and increased HO-1 levels and relative gene expression, with correlation between oxidative stress and HO-1. The substances from heme metabolism and IL-10 were also elevated in the plasma and spleens of infected dogs. IL-10 and HO-1 levels were positively correlated with one another. Inhibition of HO-1 increased LNCs proliferation and decreased IL-10 and IL-2 production in the presence of SAgL. The increased HO-1 metabolism observed in CVL is probably associated with oxidative stress and increased IL-10, which could be one of the mechanisms responsible for inhibition of the lymphoproliferative response in sick dogs.

Free p-Cresol Alters Neutrophil Function in Dogs.

To achieve a clearer understanding of the mechanisms responsible for neutrophil dysfunction recently described in dogs with chronic renal failure (CRF), the plasma concentrations of free p-cresol in healthy dogs (n = 20) and those with CRF (n = 20) were compared. The degree of correlation was determined between plasma levels of p-cresol and markers of oxidative stress and function of neutrophils in these dogs. The effect of this compound on oxidative metabolism and apoptosis was assessed in neutrophils isolated from 16 healthy dogs incubated in RPMI 1640 supplemented with p-cresol (0.405 mg/L) and compared with medium supplemented with uremic plasma (50%). To achieve this, the plasma concentration of p-cresol was quantified by liquid phase high-performance liquid chromatography. The neutrophil oxidative metabolism was determined using the probes hydroethidine and 2',7'-dichlorofluorescein diacetate and apoptosis was measured using Annexin V-PE by capillary flow cytometry. Compared with the healthy dogs, uremic dogs presented higher concentrations of free p-cresol, greater oxidative stress, and neutrophils primed for accelerated apoptosis. The free p-cresol induced in neutrophils from healthy dogs increased apoptosis and decreased reactive oxygen species production. We conclude that the health status presented during uremia concomitant with the increase in plasma free p-cresol can contribute to the presence of immunosuppression in dogs with CRF.

Blood profile and histology in oral infections associated with diabetes.

INTRODUCTION: We aimed to investigate the relationship between blood profile and histologic findings in both apical periodontitis (AP) and periodontal disease (PD) associated with diabetes. METHODS: Wistar rats (N = 80) were assigned to the following 8 groups: control, AP, PD, AP associated with PD, diabetes, diabetes with AP, diabetes with PD, and diabetes with AP and PD. Diabetes mellitus (DM) was induced with streptozotocin, AP was induced by exposure to the oral environment, and PD was induced using periodontal ligature. After 30 days, blood samples were collected, and the rats were euthanized. Subsequently, the maxillae were processed for light microscopy. Hematologic examinations were conducted to determine the total number of erythrocytes and leukocytes, erythrocyte constant, and blood glucose level. One-way analysis of variance and Kruskal-Wallis tests were used for statistical analysis, and the significance was set at P < .05. RESULTS: A significant correlation was found between the histologic findings and blood parameters. CONCLUSIONS: In conclusion, diabetes accelerated the development and progression of AP and PD in the rats and caused an increase in the average erythrocyte volume as well as the leukocyte and neutrophil counts. Oral infections increase the total number of leukocytes, the number of neutrophils and lymphocytes, and blood glucose concentrations in DM rats.

Apical periodontitis and periodontal disease increase serum IL-17 levels in normoglycemic and diabetic rats.

OBJECTIVES: This study aimed to evaluate the influence of apical periodontitis (AP) and/or periodontal disease (PD) on serum interleukin-17 (IL-17) levels in a rat model of diabetes mellitus (DM). METHODS: Eighty male Wistar rats were divided into eight groups of ten animals each: normoglycemic, AP, PD, AP+PD, DM, DM+AP, DM+PD, and DM+AP+PD. DM was induced using streptozotocin, AP by dental pulp exposure to the oral environment, and PD by periodontal ligature. The animals were sacrificed after 30 days, and venous blood samples were collected via cardiac puncture to determine the serum IL-17 and neutrophil levels. The maxillae were dissected and processed for radiographic analysis. The periapical lesion areas were quantified in pixels. The total assessed values were tabulated according to each experimental group and were statistically analyzed using Spearman's correlation and Kruskal-Wallis test (p < 0.05). RESULTS: A significant difference in the serum IL-17 levels was observed between the groups without oral infections and the groups with AP+PD-associated lesions, regardless of the presence of DM (p < 0.05). Diabetes increased the neutrophil levels, regardless of the presence of oral infection. However, a combination of two oral infections increased the neutrophil levels in DM rats (p < 0.05). The level of bone resorption lesions was greater in DM rats than in normoglycemic rats (p < 0.05). CONCLUSION: The combination of AP and PD increased the serum IL-17 levels in DM and normoglycemic rats and increased the neutrophil levels in DM rats. Diabetes increased the neutrophil levels and bone resorption in rats. CLINICAL SIGNIFICANCE: AP is capable of potentiating systemic inflammatory changes when associated with PD, and increases in blood glucose can accelerate the pathogenesis of oral infections.

Pulpal and periodontal diseases increase triglyceride levels in diabetic rats.

OBJECTIVES: The aim of this study was to evaluate triglyceride and cholesterol levels in diabetic rats and their relationship with pulpal and periodontal diseases. METHODS: Eighty male rats (Rattus norvegicus albinus, Wistar) were divided into the following eight groups comprising ten animals each: normal rats (G1), rats with pulpal diseases (G2), rats with periodontal diseases (G3), rats with both pulpal and periodontal diseases (G4), diabetic rats (G5), diabetic rats with pulpal diseases (G6), diabetic rats with periodontal diseases (G7), and diabetic rats with both periodontal and pulpal diseases (G8). Diabetes was induced by injecting streptozotocin, periapical lesions were induced by exposing pulpal tissue to the oral environment, and periodontal diseases were induced by periodontal ligature. The animals were killed after 30 days, and lipid profile was enzymatically measured using Trinder's method. The total assessed values were statistically analyzed by analysis of variance and Tukey test (p < 0.05). RESULTS: The triglyceride levels of diabetic rats with periodontal disease and of diabetic rats with both periodontal and pulpal diseases were significantly higher than those of normal rats and nondiabetic group rats, respectively. The differences in the cholesterol levels among the groups were not significant. CONCLUSIONS: We found that the association of pulpal and periodontal diseases with diabetes increased triglyceride levels in rats. CLINICAL SIGNIFICANCE: Changes in lipid profile may be related to the presence of oral infections and diabetes.