Effects of bupivacaine used with sevoflurane on the rhythm and contractility in the isolated rat heart.

BACKGROUND AND OBJECTIVE: The effects of sevoflurane on bupivacaine cardiotoxicity are mainly attributed to systemic effects. The purpose of this study was to investigate the direct myocardial effects of sevoflurane on bupivacaine toxicity. METHODS: Hearts of 30 Wistar albino rats were isolated and mounted on a Langendorff apparatus perfused by modified Tyrode solution. Experimental groups were: a sevoflurane group (Group S, n = 10)--following baseline and 20 min (Stage 1) recordings, sevoflurane was added in doses of 1.4% (1 MAC) and 2.8% (2 MAC). In the two bupivacaine groups, bupivacaine 5 micromol (Group B5, n = 10) and bupivacaine 10 micromol (Group B10, n = 10) was added to the solution at Stage 1, and sevoflurane was added to the system as in Group S. Haemodynamic variables, i.e. heart rate, PR interval, QRS duration, left ventricular systolic pressure, contractility (+dp/dtmax), relaxation, time to reach peak systolic pressure, change in left ventricular diastolic pressure from baseline, and rate-pressure product were recorded. RESULTS: In Group S, there was no change in cardiac rhythm. In bupivacaine groups, severe rhythm disturbances occurred and both the PR intervals and QRS complexes were prolonged significantly. All contractility variables deteriorated and the rate-pressure product decreased by 67-90% with the addition of bupivacaine. In all groups, 2 MAC sevoflurane lowered +dp/dtmax further. CONCLUSIONS: Sevoflurane does not have any untoward effect on bupivacaine-induced cardiotoxicity in clinically relevant doses in the isolated rat heart.

An experimental study on the relationship of intra-abdominal pressure and renal ischemia.

This study was undertaken in order to determine whether or not the increased intra-abdominal pressure during laparoscopic procedures causes renal ischaemia and parenchymal pathology. Fifteen adult New Zealand rabbits were used in the study. Anaesthesia was maintained by 2% isoflurane, 50% O2 in air. Heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), end-tidal carbon dioxide (PETCO2), airway pressure (Paw) and blood gases were monitored. Rabbits in control group (group C, n = 7) and study group (group S, n = 8) had a Veress needle placed supraumbilically. Group S was insufflated with CO2 sequentially at 5, 10 and 15 mmHg of intra-abdominal pressures (IAP); each pressure level was maintained for 20 minutes. At the end of the study, laparotomy was performed and blood was withdrawn from renal vein for measurements of renin and angiotensin I levels, and the other kidney was removed simultaneously for pathological evaluation. Haemodynamic and respiratory measurements were stable in group C and were variable in group S. The renin level was 7.27 +/- 0.34 ng.mL-1 and angiotensin I was 5.01 +/- 0.32 ng.mL-1 in group C. In group S, levels of renin and angiotensin I were 26.2 +/- 5.9 ng.mL-1 and 39.4 +/- 12.1 ng.mL-1 respectively, being significantly higher than group C (p < 0.05). Pathological scores were 0.02 +/- 0.008 in group C and 0.82 +/- 0.124 in group S (p < 0.05). There were significant histological changes in group S compared with group C. During prolonged laparoscopic operations high intra-abdominal pressures may result in intra-abdominal organ ischaemia.

Systemic stress response during operations for acute abdominal pain performed via laparoscopy or laparotomy in children.

We compared the endocrine and metabolic changes during acute emergency abdominal surgery performed using either laparoscopy or laparotomy in children. Twenty-nine children aged 1.5-14 years were assigned to undergo laparoscopy (n = 15) or laparotomy (n = 14) with a standard anaesthesia technique. Arterial blood gases and blood prolactin, cortisol, interleukin-6, glucose, insulin, lactic acid and epinephrine levels were determined 5 min after the induction of anaesthesia, 30 min into surgery and at the end of surgery. Intra-operative heart rate and mean arterial pressure were stable in both groups. In the laparoscopy group, slight respiratory acidosis occurred during surgery (p < 0.01) but there were no changes in the laparotomy group. Insulin, cortisol, prolactin, epinephrine, lactate and blood glucose levels increased in both groups (p < 0.05) although there was no difference between the groups. The surgical stress and trauma imposed by laparoscopy seems similar to that caused by laparotomy in children undergoing emergency abdominal surgery.

Tubular markers in children with insulin-dependent diabetes mellitus.

The aim of the present study was to investigate the prevalence of tubular dysfunction and to assess the clinical significance of low-molecular-weight proteinuria and enzymuria in children with insulin-dependent diabetes mellitus (IDDM). N.acetyl-beta-D-glucosaminidase (NAG) and beta-microglobulin (beta 2 M) excretion was determined in 52 children with insulin-dependent diabetes mellitus and 28 controls. Patients were grouped according to the duration of diabetes: group 1 (n = 7): less than one year; group 2 (n = 27): one to five years; groups 3 (n = 18): greater than five years. Both parameters were significantly increased in groups 2 and 3 compared to controls. Urinary beta 2 M levels correlated significantly with albuminuria and HbA1C, while urinary NAG levels correlated only with HbA1C. Two to four samples were obtained from 35 of 52 diabetic patients in the study group at one-month intervals. Of these, 23 patients had elevated NAG levels, and 22 patients increased beta 2 M excretion. However, only six patients displayed persistent enzymuria, and nine low-molecular-weight proteinuria. The mean (SD) of coefficients of variation of each patient was 50.45 (+/-28.24) for NAG and 68.25 (+/-42.57) for beta 2 M excretion. We concluded that early tubular dysfunction and/or damage occurs in IDDM but is not established in the majority of children.

Lipid metabolism alterations in patients with gestational diabetes mellitus associated fetal macrosomia.

Fetal macrosomia is commonly associated with gestational diabetes mellitus (GDM) which may lead to various complications. It has been suggested that some other metabolites apart from maternal hyperglycemia are responsible for the genesis of macrosomia. Lipid metabolism changes in GDM patients having macrosomic fetuses were studied. A lipid tolerance test (10% Lipovenous solution) was performed in 14 GDM. Pre- and post-infusion plasma lipid levels and their elimination rates were measured and compared to the ones of 8 non diabetic control pregnant women. HbA1c, basal glucose and triglyceride levels were found to be higher in GDM group and significantly higher levels of triglycerides persisted throughout the infusion. FFA, glycerol and phospholipid levels increased following infusion in both groups without significant differences. Glucose, C-peptide and insulin levels remained unchanged after the infusion. Increased basal triglycerides with slowed triglyceride metabolism may be responsible for the fetal macrosomia in mild GDM patients whose fasting blood glucose are below 105 mg/dl. A better metabolic control that provides plasma lipid regulation as well as glucose control may forestall the occurrence of fetal macrosomia.

Urinary N-acetyl-beta-D-glucosaminidase and beta 2-microglobulin excretion in primary nephrotic children.

Enzymuria and low molecular weight proteinuria reflect tubular damage and dysfunction, respectively. We examined urinary N-acetyl-beta-D-glucosaminidase (U-NAG) and beta 2-microglobulin (U-beta 2M) excretion in 17 steroid-resistant and 39 steroid-sensitive children with nephrotic syndrome whose glomerular filtration rates were within the normal range. Fourteen healthy children were taken as controls. U-NAG and U-beta 2M levels did not show a difference between the steroid-resistant and steroid-sensitive groups but were significantly higher in the nephrotic groups compared to the controls (p < 0.0001 and p < 0.01, respectively). In the steroid-sensitive group, U-NAG levels were significantly higher in patients in the relapse phase than in those in remission (p < 0.0001). This finding was also valid for U-beta 2M excretion, but reached significance only for patients in remission who did not receive steroids (p < 0.01). There was a positive correlation between proteinuria and U-NAG and U-beta 2M excretion in all patients (rs = 0.69, p < 0.001 and rs = 0.39, p < 0.001, respectively). In conclusion, massive glomerular proteinuria may cause a marked U-NAG excretion and a moderate urinary U-beta 2M elevation independent of primary renal disease.

Biochemical assessment of nutritional status in pre- and post-natal Turkish women and outcome of pregnancy.

OBJECTIVE: To determine by biochemical methods the nutritional status of pre- and post-natal Turkish women and its relationship with offspring anthropometry. DESIGN: Longitudinal study. SETTING: Health centres in Istanbul and Izmit, research department and university hospital laboratories. SUBJECTS: Randomly selected group of women attending health centres at 13-17 weeks gestation (n = 130); same sample of women at 28-32 weeks gestation (n = 88) and 13-17 weeks post-partum (n = 95); offspring at 13-17 weeks post-partum (n = 90). INTERVENTIONS: Blood samples taken from mothers at all three stages and analysed for ferritin, iron, zinc, calcium, alkaline phosphatase, total protein, albumin, vitamins B2, B6, B12, A, E, beta-carotene and folate levels; questionnaire completed for recording medical and socio-demographic background. Anthropometric measurements taken from mothers and offspring. RESULTS: High percentages of subjects were at risk for deficiencies of vitamin B12 (48.8%) and folate (59.7%) in early pregnancy; ferritin (52.3%), zinc (72.3%), vitamin B2 (38.8%), vitamin B12 (80.9%), and folate (76.4%) during late pregnancy; and ferritin (39.0%), vitamins B2 (43.1%), B6 (36.4%), B12 (60.0%), and folate (73.3%) at the post-partum stage. Bone loss was indicated in 55.0% and 80.0% of the subjects in late pregnancy and post-partum respectively. Haematocrit in later pregnancy correlated strongly with prenatal body fat (P < 0.001). Infant anthropometry at 13-17 weeks post-partum was significantly affected by pre-natal weight gain and a number of maternal blood nutrients in pregnancy and post-partum. CONCLUSIONS: Nutrition education programmes and enrichment of the staple food with iron, zinc, calcium, and the B vitamins should be considered.

The role of plasma, erythrocyte and platelet myo-inositol levels in the development of diabetic microangiopathy.

UNLABELLED: In this study the plasma, erythrocyte, and platelet myo-inositol levels in 24 type I, 24 type II diabetics, and in 15 healthy controls were determined. The diabetics were devided into two groups with microangiopathy (n = 26) and without microangiopathy (n = 22). The plasma, erythrocyte, and platelet myo-inositol levels in the whole diabetic group and control subjects were as follows. Diabetic group: 46.5 +/- 39.8 mumol.l-1 23.3 +/- 19.8 nmol.ml-1, 2.6 +/- 2.8 nmol.ml-1 (10(5) cells)-1. CONTROL GROUP: 17.4 +/- 3.7 mumol.l-1, 12.2 +/- 5.2 nmol.ml-1, 1.5 +/- 0.9 nmol.ml-1 (10(5) cells)-1. The values of the diabetic group were significantly higher than the values of the control group (p < 0.01). In patients with HbA1c levels more than 9% plasma, erythrocyte, and platelet myo-inositol values were significantly higher than the values of the group with HbA1C levels less than 9% (p < 0.05, p < 0.05 and p < 0.01). In diabetics without complications plasma and erythrocyte myo-inositol levels were higher than the values of the control group (p < 0.01), whereas there was no significant difference between the platelet myo-inositol values. In diabetics with complication all these three values were higher than those of the control group (p < 0.01, p < 0.01, p < 0.01). The most profound increase in the plasma, erythrocyte, and platelet myo-inositol levels were seen in complicated diabetics with a diabetes duration of 6-10 years (p < 0.01). After 10 years duration the values declined. In the group without complication there was no difference according to the duration of diabetes.

Use of ornidazole in fractionated radiotherapy: dose tolerance, serum and tumour tissue concentration.

Sensitizing and neurotoxic effect of ornidazole, was tested in a double-blind randomized study in patients with carcinoma of the cervix and larynx. Ornidazole or placebo were given orally, two times weekly, for 3 weeks. Dose was 2.5 g/m2 for each administration. Total dose given was 15 g/m2. Radiation therapy was given 3 h after the drug administration. Ornidazole was well tolerated in the majority of the patients. No neurotoxic side effects, such as peripheral neuropathy or convulsion, were observed with a total dose of up to 30 g. Dizziness, somnolence and nausea were the prominent acute side effects, seen mostly (70%) in women. In the placebo group this rate was 17% (p less than 0.01). No important side effect was observed in men receiving ornidazole. Serum concentration of ornidazole reached the maximum level in 2-4 h after oral administration and ranged (23 patients) from 65.1 to 139.8 micrograms/ml. Mean half-life was 15.6 +/- 2.8 h. Peak concentration in tumour tissue was achieved 1-3 h after the administration, ranging from 13.0 to 78.0 micrograms/g. Tumour concentration of ornidazole ranged from 14 to 93% of the serum concentration at the time of irradiation.