53-56
TECHNICAL NOTE
Evaluation of vagal nerve blockade with epineural lignocaine application
by Wai Yeung Chung & Shi Ping Zhang

The effect of vagal nerve blockade by epineural application of lignocaine was studied in the rat. Vagal nerve conduction was assessed by subdiaphragmatic esophageal electromyogram (EMG) response evoked by stimulation of the cervical vagus nerve. It was found that epineural application of lignocaine completely blocked the evoked EMG response within one minute. After washing away the anesthetic, recovery of nerve conduction was gradual, taking approximately 60 min. Our results have implications for the use of local anesthetic blockade to interrupt of vagal transmission in experimental designs.

57-64
On the carbohydrate metabolic response to an experimental infection with Brachyspira hyodysenteriae (swine dysentery) in pigs
by Anongnart Somchit, Marianne Jensen-Waern, Magdalena Jacobson & Birgitta Essén-Gustavsson

The carbohydrate metabolic response to experimentally induced swine dysentery was studied in crossbreed pigs. Twelve pigs, with a mean weight of ~20 kg, were orally inoculated with Brachyspira hyodysenteriae strain B204. After an incubation period of 6-20 days, five animals developed swine dysentery with haemorrhagic diarrhoea and two animals developed non-haemorrhagic diarrhoea. Five animals remained healthy throughout the study. Blood samples from the animals with clinical signs of disease were collected before inoculation, several times during the course of the dysentery and finally after recovery. Blood samples from animals that remained healthy were obtained before inoculation and at slaughter four weeks later. Glucose, lactate and cortisol concentrations did not differ between sampling occasions in the healthy animals. In the sick animals, higher concentrations were observed when haemorrhagic diarrhoea occurred (mean peak value ± SD: glucose 7.6 ± 0.7 mmol/L; lactate 4.5 ± 1.7 mmol/L; cortisol 278 ± 86 nmol/L) compared to before inoculation (mean value ± SD: glucose 5.1 ± 1.2 mmol/L; lactate 1.3 ± 0.5 mmol/L; cortisol 24 ± 11 nmol/L). At slaughter, tissue samples from m. biceps femoris, m. longissimus dorsi, myocardium and liver were collected from 10 pigs and glycogen analysis was performed. Glycogen concentrations did not differ between the healthy pigs and those that developed swine dysentery: concentrations were highest in the liver and lowest in the heart. In conclusion, experimental infection with B. hyodysenteriae results in alteration of the carbohydrate metabolism, which is characterised by a transient increase in blood glucose and lactate concentrations during the initial phase of the haemorrhagic period of the disease.

65-72
Propranolol does not affect the oxidative burst of rat neutrophils or complement serum opsonizing capacity in in vivo and in vitro experiments
by Russo-Carbolante, EMS; Marasca, TS; Polizello, ACM; Azzolini, AECS; Lucisano-Valim YM

Propranolol is a ß-adrenergic antagonist used for the treatment of a variety of cardiac conditions and has a palliative value when used in situations in which adrenergic signals and symptoms are involved. It is used as a co-adjuvant in hyperthyroidism to decrease heart rate and output, as well as the tremor. The aim of this work was to study the effect of propranolol treatment on the oxidative burst of rat peripheral blood neutrophils and on the complement system. In the in vivo study, Wistar male rats were treated with propranolol by gavage for 16 days with 220 or 440 µg/animal/day. These doses are equivalent to 80 or 160 mg/adult human (~70 day/kg), respectively. Neutrophils were obtained and stimulated with opsonized immune complexes (opIC). The oxidative burst of control (from water treated rats) or propranolol-treated rat cells was measured by luminol- and lucigenin-dependent chemiluminescence (CL). The CL of treated rat neutrophils was not affected by any of the propranolol doses studied when compared to the control responses. In the in vitro study whole blood and serum from Wistar male rats were incubated for 1 h at 37C° with propranolol at three different concentrations (17.5, 35 and 70 µg/mL). After incubation, neutrophils were isolated from whole blood and stimulated with opIC while treated sera were used to opsonize IC. IC opsonized with treated sera were used to stimulate neutrophils from normal rats. In both cases oxidative burst was measured by luminol- and lucigenin-dependent CL. No differences in responses or activities were detected between in vitro treated neutrophils or sera and their respective controls. These results suggest that this drug, at the concentrations studied and with the experimental approach used, had no effect on the oxidative burst during phagocytosis of opIC or on the complement opsonization capacity of the sera.