Mandibular bone density and calcium content affected by different kind of stress in mice.

OBJECTIVES: Stress is considered to affect many body and mental functions. This leads to activation of the hypothalamic-pituitary-adrenal axis and the adrenomedullary sympathetic system resulting to increased glucocorticoid release. Corticosteroids are known to cause systemic bone loss. The aim of the study was to investigate the role of different kinds of stress on the mandible bone mass of Wistar mice. METHODS: 75 male Wistar mice were divided into three groups (n=25 each). The animals of group C were submitted to stress by electroshock with 22-45 volts for a duration of 4 seconds each minute for one hour each day. Group B was submitted to isolation stress and group A was the control group. The duration of the experiment was 137 days. RESULTS: The adrenals weight was increased (group C vs group A, p<0.001; group B vs group A p<0.05), while urine hydroxyproline was reduced under stress. The calcium content of the mandible and the ratio between calcium content and mandible volume was decreased (p<0.05 for both groups). CONCLUSIONS: Mandibular bone mass was affected by different kinds of stress and may represent a considerable parameter for the diagnosis, prevention and treatment of bone mass deficiency.

Impact of hyperlipidaemia on the orbital bone cefotaxime levels in rats.

Facial injuries are critical conditions, leading to serious complications, such as occult facial infections. Infectious endophthalmitis occurs despite of antibiotics use during implantation of intraocular lenses and is generally resistant to antibiotic therapy. It is a crucial situation in ophthalmology, since it often induces a substantial reduction of visual acuity and in some cases the loss of the eye despite treatment. It is, therefore, important to obtain drug levels able to exert antimicrobial effect in the diseased organ. The distribution of a drug depends on the binding extent to both plasma proteins and tissues and only the free drug is capable to be transported/diffused across membranes from blood vessels into tissues, in order to achieve its effect on the target organ. Hyperlipidaemia and consequent enhanced concentration of free fatty acid can modify binding pharmacokinetics of antibiotics through antagonism for the same binding sites. Cefotaxime, the third generation cephalosporin with easy penetration in a variety of tissues and body fluids and low incidence of adverse effects, can obtain adequate concentration in blood, eye bulb, and in the orbital bones. Its levels are influenced by hyperlipidaemia with clinical impact.

Mandibular bone density and calcium content affected by long-term anticonvulsant treatment in rats.

OBJECTIVE: Bone is perpetually absorbed and reformed, serving also to electrolyte homeostasis, mainly for calcium and phosphorus. Anticonvulsant medications are traditionally considered harmful to bone because of their interaction with the metabolism of vitamin D, due to hepatic enzyme induction. A study of the effect of anticonvulsant medications on mandibular bone quality was undertaken. MATERIALS AND METHODS: 24 Wistar rats in three groups received diphenylhydantoin or diazepam or placebo intraperitoneally (i.p.). Absolute bone weight, bone to body weight ratio, specific bone weight, absolute calcium concentration, calcium to mandibular bone weight ratio and mineral element concentration were examined after animal sacrifice, three months later. From the results it may be concluded that diazepam and diphenylhydantoin administration affect the mandibular bone density and calcium content in terms of absolute weight and specific weight. Mandibular calcium concentration was affected only by diphenhylhydantoin treatment.

Biocompatibility of resin composites subcutaneously implanted in rats with experimentally induced arthritis.

OBJECTIVE: To evaluate the biocompatibility of resin composite specimens with different curing efficiency, subcutaneously implanted in rats with experimentally induced arthritis. METHODS: The amount of remaining CC bonds (%RDB) of hybrid resin composite specimens photopolymerized for 10s and 40s exposure time (n=3) was measured by micro-attenuated total reflectance Fourier transform infrared spectroscopy. Male Wistar rats (n=36) were classified in two groups (n=18) of healthy animals and of animals with experimentally induced arthritis. Resin composite specimens irradiated for 10s and 40s and calcium hydroxide control specimens were implanted subcutaneously in each animals' dorsum. Following 2-, 4- and 9-week periods the animals were sacrificed. The development of arthritis was defined by biochemical analysis and the changes in the relative weight of animals' organs (spleen, thymus, adrenals). Tissue reactions were examined histologically. RESULTS: %RDB per site and exposure time showed statistically significant differences. Lowest %RDB values were recorded on 40s exposed specimens. Biochemical indices and relative organ weights demonstrated statistically significant differences between healthy animals and animals with arthritis. The health status of the animals and the materials used did not influence tissue response. First and second periods of sacrifice showed reduced propensity of connective tissue development in comparison to the third period. The same applied for the second period regarding the presence of giant cells. SIGNIFICANCE: The materials tested and the animals' health status did not result in altered tissue response compared to control group. The period of sacrifice was associated with different tissue responses.

Clonidine changes lidocaine free concentrations in rat myocardium without affecting heart function measured by echocardiography.

Lidocaine is a local anaesthetic widely used in regional and epidural anaesthesia. Clonidine a alpha2-adrenergic agonist is an antihypertensive agent, regulating the production of catecholamines (epinephrine and norepinephrine) and added to local anesthetic infusions in order to improve postoperative analgesia. The aim of the study was to investigate the influence of clonidine co-administration on the binding of 14C lidocaine to rat serum and heart tissue protein as well as its pharmacodynamic effects in the heart. Four groups of Wistar rats (n=7) were used; Groups I and II received 4 mg/kg lidocaine i.m. Groups III and IV received lidocaine and 1 microg/kg clonidine i.m. In group I and III fifteen minutes and in groups II and IV thirty minutes after the initial treatment, ultrasound examination of heart function (heart rate, diameter of left ventricle in systole and diastole, ejection fraction) was performed. The animals were then sacrificed in all groups. Lidocaine free fraction in serum and heart was evaluated via ultrafiltration. The kinetics of lidocaine was altered by clonidine co-administration probably by mechanisms related to protein binding alterations. However, the pharmacokinetic interactions were not accompanied by changes of pharmacodynamic parameters including those of heart function as measured by echocardiography.

Morphological changes of gingiva in streptozotocin diabetic rats.

Gingivitis and periodontitis are chronic bacterial diseases of the underlying and surrounding tooth tissues. Diabetes mellitus is responsible for tooth deprivation both by decay and periodontal disease. The streptozotocin-induced diabetes results in a diabetic status in experimental animals similar to that observed in diabetes patients. The aim of the study was to investigate the relationship between the gingival lesions and the microangiopathy changes in streptozotocin-induced diabetes mellitus. Forty male Wistar rats were divided into two groups (control and experimental). Diabetes mellitus was induced by 45 mg/kg IV streptozotocin. The histological investigation of the marginal gingival and the relevant gingival papilla showed inflammation of the lamina propria and the squamous epithelium as well as marked thickness of the arteriole in the diabetic group, but no changes were observed in the control group. The results suggested a probable application of a routine gingival histological investigation in diabetic patients in order to control the progress of disease complications. It may be concluded that histological gingival investigation can be used as a routine assay for the control of the diabetic disease and prevention of its complications.

Thyroid hormone modulates the responsiveness of rat aorta to alpha1-adrenergic stimulation: an effect due to increased activation of beta2-adrenergic signaling.

AIM: The ability of the thyroid hormone to increase cardiac output and to lower systemic vascular resistance may provide a novel treatment for cardiovascular diseases. Therefore, understanding the mechanisms of thyroid hormone action on the heart and peripheral vasculature could be of clinical importance. We previously found that thyroid hormone modulates the alpha1-adrenergic effect on vascular reactivity of rat aortas. In the present study we further investigated possible mechanisms of this response. METHODS: Hyperthyroidism was induced on Wistar-Kyoto male rats with L-Thyroxine, (THYR) treatment for two weeks, N.=18 while untreated rats used as controls (NORM), N.=16. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to Potassium Chloride (KCl) and Phenylephrine (PE) in rings in the presence of Ritodrine, a beta-2 agonist (NORM-RITO, N:=8, THYR-RITO, N.=9), or in the absence of Ritodrine (THYR, N.=9, NORM, N.=8). RESULTS: With KCL, Tmax was not different between the THYR, NORM, NORM-RITO, and THYR-RITO groups. With PE, there was a difference in Tmax between NORM-RITO and NORM, 0.66 (0.056) g vs 1.00 (0.066) g, P<0.05 and THYR and NORM, 0.75 (0.055) g vs 1.00 (0.066) g, P<0.05. No significant difference was observed between THYR-RITO AND THYR. Furthermore, Relax % was not significantly different between the NORM and the THYR, NORM-RITO, and THYR-RITO groups, 64.5%(3.7) vs 67.3%(6.7), 73.5% (4.3) and 81.8 %(4.7), P>0.05. CONCLUSIONS: PE induced vasoconstriction in isolated rat aortic rings was reduced after both ritodrine and thyroxine treatment. However, co-administration of thyroid hormone and ritodrine did not result in a synergistic reduction of PE induced vasoconstriction. Thus, thyroxine may modulate the alpha1-adrenergic vascular responsiveness by enhancing beta2-adrenergic stimulation.

Anticoagulant-induced changes on antibiotic concentrations in the serum and bones.

The aim of this study was to determine whether the co-administration of acenocoumarin as anticoagulant and certain quinolones, i.e., cefapirin, pefloxacin and ciprofloxacin increased the levels of the given antibiotics and whether this resulted in a prolongation of prothrombin time. Seventy male albino Wistar rats aged 8-10 weeks and weighed 170 +/- 14 g were used and divided into seven groups (I, II, III, IV, V, VI, VII: n=10). The rats in group I received cefapirin via 1 g/kg/8h im injection. Group II received cefapirin via of 1 g/kg/8h im injection and 0.1 mg/kg/24h p.o. acenocoumarin. Group III received ciprofloxacin 0.18 mg/kg/24h im. Group IV received ciprofloxacin 0.18 mg/kg/24h im and 0.1 mg/kg/24h p.o. acenocoumarin. Group V received 10 mg/kg/24h pefloxacin im. Group VI received 10 mg/kg/24h pefloxacin im and 0.1 mg/kg/24h p.o. acenocoumarin while Group VII received only acenocoumarin 0.1 mg/kg/24h p.o. Drug administration was performed over a total of 5 doses in order to obtain steady state concentrations in the plasma and tissues. The animals were sacrificed by decapitation 2 h after the last antibiotic administration. Prothrombin time and antibiotic concentrations in the serum, femur and mandible were assessed. In the study, all the antibiotics were found to prolong prothrombine time following acenocoumarin administration. In addition, perfloxacin and ciproflaxin concentrations were increased in the serum and mandible after acenocoumarin treatment. Cepafirin levels remained unaffected after the administration of this anticoagulant. In conclusion, anticoagulant and quinolone co-administration led to significant pharmacokinetic interactions. Thus particular attention should be paid in the case of these drugs being used in combination in clinical practice.

Effect of L-carnitine administration on the modulated rat brain protein concentration, acetylcholinesterase, Na+K+-ATPase and Mg2+-ATPase activities induced by forced swimming.

BACKGROUND: Forced exercise produces free radicals and L-carnitine (L-C) administration reduces oxidative stress. AIM: To investigate whether short (2 hours) or prolonged (3 hours) forced swimming could modulate total antioxidant status (TAS), protein concentration and activities of acetylcholinesterase (AChE), Na(+)K(+)-ATPase and Mg(2+)-ATPase in rat brain following intraperitonal administration of L-C (300 mg/kg). METHODS: TAS, protein and enzyme activities were measured spectrophotometrically. RESULTS: TAS, protein concentration and AChE activity were reduced, whereas Na(+)K(+)-ATPase and Mg(2+)-ATPase were significantly increased after either 2 or 3 hours of training. L-C administration resulted in a profound restoration of TAS and protein concentration whereas AChE and Na(+)K(+)-ATPase were increased before exercise, followed by AChE restoration and Na(+)K(+)-ATPase reduction after exercise. Mg(2+)-ATPase remained unchanged. An in vitro study using L-C incubation of brain homogenates previously treated with L-C resulted in complete restoration of the modulated enzymes, whereas the enzyme activities from untreated animals remained unaltered. CONCLUSIONS: Short or prolonged swimming in rats may result in a reduction of brain TAS, protein concentration and AChE activity, and an activation of Na(+)K(+)-ATPase and Mg(2+)-ATPase. L-C administration may prevent reduction in TAS and protein concentration, and a decrease in AChE and Na(+)K(+)-ATPase activity; the latter reached pre-exercise values after L-C incubation.

In vitro binding of lidocaine to liver tissue under the influence of propranolol: another mechanism of interaction?

The co-administration of lidocaine and propranolol leads to significant drug-drug interactions. Beta-blockers decrease liver perfusion and inhibit the activity of hepatic microsomal lidocaine metabolizing enzymes of the P450_2D subfamily. Hence, there is a resulting reduction in the hepatic breakdown of lidocaine and an increase in its serum concentrations. In this study the ability of propranolol to displace lidocaine from its binding sites in liver tissue has been examined through an in vitro model. Rat liver slices were incubated together with propranolol and/or lidocaine in human serum and the percentage of the bound fraction of lidocaine in the experimental mixture was assessed. The present results indicate that propranolol significantly decreases the binding process of lidocaine in liver tissue. This effect develops only when blood is used as incubation medium and the incubation period lasts 60 min. In conclusion, propranolol can displace lidocaine from liver proteins and therefore the co-administration of the two drugs may increase the free fraction of lidocaine excreted by the liver. However, this result arises from an in virro model and thus further investigation is needed.

Injuries to the head and neck in Homer's Iliad.

We have found and reported on all injuries to the head and neck described in Homer's Iliad, and give several particularly graphic examples.

Impact of experimental trauma and niflumic acid administration on antimicrobials' concentration in serum and mandible of rats.

Administration of antibiotics and analgesics in surgery or trauma is of great importance for an effective treatment. Trauma, as stress stimulus, causes alterations in various functions of the organism as well as in drug pharmacokinetics. The aim of this study was to determine the effect of trauma upon the serum and bone levels of the antimicrobial ampicillin and cefapirin, with and without co-administration of a non-steroidal anti-inflammatory analgesic (NSAIDs). Fifty-six male Wistar rats were divided into two groups A (control) and B (experimental). Each group consisted of 4 subgroups (n=7) receiving ampicillin, ampicillin with niflunic acid, cefapirin, and cefapirin with niflunic acid. In group B traumatic injury was performed by incision (7 mm length) in the right cheek. The levels of the antibiotics were estimated by the inhibition zone of B. subtilis. An increase in antibiotic levels was observed in group B, being statistically significant only for cefapirin level in the mandible. Upon niflumic acid co-administration a statistically significant rise in serum ampicillin and mandible cefapirin levels was observed in both control and experimental groups (student t-test). It can be concluded that the combination of antibiotics and non-steroid antiinflammatory drugs (NSAIDs) may enhance the antibacterial drug concentration.

H3 Propranolol serum levels following lidocaine administration in rats with CCL4 induced liver damage.

Liver disease alters the pharmacokinetic and pharmacodynamic properties of hepatically eliminated drugs. The main factors influenced are plasma albumin levels, enzyme balance (induction & inhibition) and drug binding to tissue proteins. The influence of lidocaine on serum, heart and liver propranolol levels in Wistar rats after liver injury induced by carbon tetrachloride CCl4 0.4 ml/kg x 2/wkl, was investigated. 40 male Wistar rats were divided into four groups (I, II, III, IV; n=10), Group I animals received only propranolol (labelled + cold substance) 40 mg/kg/12 h p.o., group II propranolol plus lidocaine in a single dose of 4mg/kg s.c., group III was treated with CCl4 for 6 weeks and received propranolol x2 at the same dosage as group I, while group VI was treated with CCl4 and the same drug dosage as group II. The simultaneous administration of H3-propranolol and lidocaine increased propranolol levels in the serum and tissues. The liver in damaged animals showed an increase of propranolol level under lidocaine co-administration, probably due to CCl4 induced liver enzyme activity, resulting in a rapid propranolol metabolism or to competition between both drug protein binding sites. The increased propranolol levels in the heart after lidocaine administration were probably due to attributed to its high affinity for heart tissue. Consequently, as regards the therapeutic approach for patients with liver disease receiving propranolol their propranolol dosage should be reduced when lidocaine is co-administered.

Decreased vascular reactivity to alpha1 adrenergic stimulation in the presence of hypothyroid state: a part of an adaptive response?

AIM: A hypothyroid state frequently accompanies cardiac illnesses but its physiological significance for the cardiovascular hemodynamics remains largely unknown. Therefore, the present study investigated possible physiological consequences on vascular function in an experimental model of low thyroid hormone state. METHODS: Hypothyroidism was induced in rats by the administration of 6-n-propyl-2-thiouracil in drinking water (final concentration of 0.05%) for 3 weeks, HYPO rats, and untreated rats served as controls (Control). Isolated aortic rings with or without endothelium (E+, E-) were contracted with KCl (10 to 60 mM) and phenylephrine (PE) (10(-10) to 10(-5) M). Maximal tension (Tmax) in g and EC(50) in response to PE and KCl were measured. RESULTS: Tmax was significantly lower while EC(50) was significantly higher in response to PE in HYPO(E+) than in Control(E+). Upon endothelium removal, Tmax was not significantly different between the groups but EC(50) was still significantly higher in HYPO(E-) than in Control(E-). EC(50) in response to KCl was significantly higher in HYPO with or without endothelium and no difference was found in Tmax. CONCLUSIONS: Hypothyroid aortic rings respond less to a1 adrenergic stimulation probably due to the endothelium modulatory effect as well as to intrinsic smooth muscle defect. This seems to be of important clinical relevance.

Alterations in antioxidant status, protein concentration, acetylcholinesterase, Na+, K+-ATPase, and Mg2+-ATPase activities in rat brain after forced swimming.

The aim of this study was to investigate whether exercise stress (short [2 h] or prolonged [5 h] forced swimming in rats) could modulate brain total antioxidant status (TAS), tissue protein concentration, and the activities of acetylcholinesterase (AChE), Na +, K +-ATPase, and Mg 2+-ATPase. Protein concentration, TAS and enzyme activities in homogenized rat brain were determined spectrophotometrically. Protein concentration was decreased by 15 % (p < 0.01) and by 30 % (p < 0.001) after 2 h and 5 h of forced swimming, respectively. TAS was decreased by 20 - 25 % after 2 h or 5 h of exercise. AChE was inhibited by 30 % (p < 0.001) and 45 % (p < 0.001) after 2 h and 5 h of forced swimming, respectively. In contrast, Na +, K +-ATPase and Mg 2+-ATPase were stimulated by 80 % (p < 0.001) and 40 % (p < 0.001), respectively, after 2 h of swimming and by 100 % (p < 0.001) and 60 % (p < 0.001), respectively, after 5 h of exercise. Control values in nontreated rats were unaltered (p > 0.05). In conclusion, short or prolonged forced swimming induces oxidative stress in rats, probably resulting in a reduction in brain protein concentration and AChE activity. In addition, a Na +, K +-ATPase and Mg 2+-ATPase activation was observed under the above mentioned experimental conditions. This stress condition may modulate brain intracellular Mg 2+ concentration, neural excitability, metabolic energy production, and neurotransmission.

Alterations in cefalosporin levels in the serum and mandible of hyperlipaedemic rats after co-administration of ibuprofen.

Several interactions between antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs) have been described in the literature, and it has been reported that hyperlipidaemia induces significant changes in cefalosporin levels. The aim of this study was to determine the changes in the levels of several cefalosporins in the serum and mandible after ibuprofen co-administration in hyperlipaedemic rats. One hundred and forty male Wistar rats were used and divided in 4 groups (A-D), each of which was further divided into 5 subgroups (1-5), either with placebo or with various treatment regimes. The co-administration of NSAIDs led to increased cefalosporin levels in both control and hyperlipidaemic animals. Hyperlipidaemia was also found to augment cefalosporin levels. These observed increases might be due to the displacement of the cephalosporins from their binding sites in serum albumin and tissue proteins in the presence of ibuprofen. NSAIDs showed a greater binding affinity for tissue proteins compared to the cephalosporins, and probably play an antagonistic role in protein binding, resulting in higher concentrations of antibiotics.

Ketamine-induced changes in metabolic and endocrine parameters of normal and 2-kidney 1-clip rats.

BACKGROUND AND OBJECTIVE: The aim of this study was to investigate the effect of ketamine on the endocrine and lipid metabolic status of the renal-banded animals. METHODS: Forty male rats were randomly divided into four groups. Group A served as control, Group B animals received ketamine intraperitoneally at a dose of 100 mg kg(-1), Group C was submitted to 2-kidney 1-clip experimental hypertension and Group D received ketamine as above, as well as being submitted to renal artery clipping. Atrial natriuretic peptide, angiotensin II and free fatty acid concentrations were measured in serum. In addition, adipose tissue lipoprotein lipase activity and angiotensin II content were determined, while the left ventricular weight relative to body weight was used as a cardiac hypertrophy index. RESULTS: In renal-banded rats (Groups C and D) serum atrial natriuretic peptide, free fatty acid and angiotensin II concentrations as well as ventricular weight were increased, while adipose tissue lipoprotein lipase activity was lower than in control animals (Groups A and B). Ketamine administration did not influence angiotensin II concentrations either in normal (Group B) or banded rats (Group D). Ketamine increased serum atrial natriuretic peptide and free fatty acid concentrations only in normal animals (Group B). It had no influence on adipose tissue lipoprotein lipase activity either in normal (Group B) or banded animals (Group D). Adipose angiotensin II content did not differ between the four groups. CONCLUSION: Ketamine increased the atrial natriuretic peptide and free fatty acid concentration in normal rats. In 2-kidney 1-clip animals, ketamine did not elicit an additional response of serum atrial natriuretic peptide or free fatty acids levels. Its contribution to these factors was not significant.

Mechanisms of ketamine action on lipid metabolism in rats.

BACKGROUND AND OBJECTIVE: This study was conducted to determine the effect of ketamine on metabolic homoeostasis and particularly in lipoprotein lipase (LPL) activity in adipose tissue. METHODS: Sixty male Wistar rats were divided into six groups of 10 each. Group A served as controls, while Groups B-F received, respectively, ketamine 60, 80, 100, 120 and 140 mg kg(-1) intraperitoneally. The animals were sacrificed 20 min after the administration of ketamine. Insulin concentrations in plasma and total cholesterol, triglyceride, high-density lipoprotein (HDL) and free fatty acid (FFA) concentrations in serum were measured. LPL activity in adipose tissue and medium-chain acyl-CoA dehydrogenase (MCAD) content in muscle were determined. RESULTS: FFA concentrations in serum significantly increased from the second lowest dose of ketamine. Insulin concentrations in plasma did not exhibit any significant difference between groups. MCAD levels were 0.5-fold more in Group F than in Group A, while there were no significant differences between control group and Groups B-E. Furthermore, high concentrations (120 and 140 mg kg(-1)) of ketamine interfered with in metabolic homoeostasis by significantly reducing LPL activity, thus elevating triglyceride concentrations in serum without affecting cholesterol and HDL metabolism. CONCLUSIONS: Ketamine induces various metabolic effects due to changes in adipose LPL activity and MCAD levels in muscles. These findings seem to be significant only at high doses.

Adjuvant arthritis-induced changes on ampicillin binding in serum and tissues under the influence of non-steroidal anti-inflammatory drugs in rats.

Adjuvant arthritis, as a model for investigating rheumatoid arthritis (RA), is characterized by reduced plasma albumin levels and interferes with drug binding in the plasma and tissues (liver and bone). Ampicillin interacts with non-steroidal anti-inflammatory drugs (NSAIDs) due to the acidic pk(a). The aim of this study was to investigate in vitro the concentrations of ampicillin in the serum, femur, mandible and liver proteins following the co-administration of ketoprofen, flurbiprofen, ibuprofen, oxyphenbutazone and ASA in adjuvant arthritis versus healthy control rats. Ampicillin binding was found to be reduced in the serum of arthritic rats, and ampicillin binding to serum proteins was also reduced under the influence of NSAIDs in the control animals. Differences in ampicillin binding were observed in the various tissues due to the effect of adjuvant arthritis as well as that due to the co-administration of NSAIDs. In conclusion, this in vitro study may provide a plausible explanation for the ampicillin-NSAIDs interaction and such a finding may be of therapeutic significance in the treatment of painful arthritic disease such as RA.

Lipid kinetics in obese patients undergoing laparoscopy. The impact of cortisol inhibition by etomidate.

The aim of this study was to investigate the response of cortisol, insulin and lipid parameters [serum Lipoprotein Lipase activity, choleseryl-ester transfer protein, triglycerides, total Cholesterol, High Density Lipoprotein, Free Fatty Acids] during the perioperative period in obese patients undergoing laparoscopic cholecystectomy. Twenty obese patients were included and divided in two groups. In group A (n=10) patients were anaesthetized with propofol and group B (n=10) with etomidate. Blood samples were collected before induction in anaesthesia, just after the end of the operation and at one, two and three hours postoperatively. According to our results, in both groups serum LPL activity showed a significant decrease whereas serum Free Fatty Acids a potent increase over time. Likewise, both groups did not demonstrate significant changes over time in choleseryl-ester transfer protein activity, total cholesterol, triglycerides, High Density Lipoprotein or insulin concentrations in serum. Furthermore, cortisol release was significantly inhibited in the etomidate group while substantially enhanced in propofol group. Additionally, apart of triglycerides, no difference was found between the two groups in all the lipid parameters and insulin concentrations. In conclusion, serum Free Fatty Acids levels and Lipoprotein Lipase activity demonstrated significant alterations in obese patients underwent laparoscopic cholecystectomy and this result did not seem to be related with the anaesthetic agent used for induction in anaesthesia.