Avaliaram-se os efeitos do butorfanol e da buprenorfina sobre variáveis cardiovasculares e neuroendócrinas em cães anestesiados com desfluorano, utilizando-se 30 cães adultos, machos e fêmeas, distribuídos em três grupos denominados grupo butorfanol (GBT), grupo buprenorfina (GBP) e grupo-controle (GCO). A anestesia foi induzida com propofol (8mg/kgIV) e nos animais intubados administrou-se desfluorano (1,5CAM). Após 30 minutos, nos cães do GBT, aplicou-se butorfanol (0,4mg/kgIM); nos do GBP, buprenorfina (0,02mg/kgIM); e nos do GCO, solução de NaCl a 0,9% (0,05ml/kgIM). Avaliaram-se: freqüência cardíaca; pressões arteriais sistólica, diastólica e média; débito cardíaco; pressão venosa central; cortisol; hormônio adrenocorticotrópico; noradrenalina; e glicose. As colheitas dos dados foram feitas aos 30 minutos após o início da administração do desfluorano (M0), 15 minutos após a administração do opióide ou placebo (M15), e a cada 15 minutos após M15 (M30, M45, M60 e M75). Para a avaliação neuroendócrina utilizaram-se os momentos M-30 (antes da administração dos fármacos), M0, M15 e M45. Na freqüência cardíaca houve diferença entre M0 e M15 (129 e 111bat/min) em GBT, e entre M0 e M30 (131 e 112bat/min) em GBP. Na pressão arterial média, a diferença foi entre M0 (86mmHg) e todos os momentos que se seguiram (todos os valores foram menores que 72mmHg), em GBT. A pressão arterial diastólica foi menor em todos os momentos (<53mmHg) quando comparada com a do M0 (67mmHg), em GBT. Na pressão arterial sistólica, a diferença foi entre M0 e M15 e M30 (112 versus 93 e 94mmHg, respectivamente) em GBT. A inclusão dos opióides determinou discreta redução nos parâmetros cardiovasculares, enquanto o desfluorano interferiu na função neuroendócrina elevando os níveis plasmáticos de glicose.

The effects of butorphanol and buprenorphine on cardiovascular and neuroendocrine variables in dogs anesthetized with desflurane were studied. Thirty adult healthy, males and females, mongrel dogs were distributed in three groups denominated butorphanol group (BTG), buprenorphine group (BPG) and control group (COG). The anesthetic induction was done using propofol (8mg/kg, IV), and immediately, the dogs were intubated and submited to desflurane anaesthesia (1.5 MAC). After 30 minutes, the BTG animals received butorphanol (0.4mg/kg IM), the BPG animals buprenorphine (0.02mg/kg IM) and the COG animals saline solution at 0.9% (0.05 ml/kg IM). Heart rate; systolic, diastolic and mean arterial blood pressures; cardiac output; venous central pressure; cortisol; ACTH; noradrenalin; and glucose were measured. The measurements were recorded at 30 minutes after beginning the inhalatory anaesthesia (M0) and at 15 minutes after opioid or saline administration (M15). Also a serial measurements were carried out in 15-minute intervals after M15 (M30, M45, M60 and M75). For neuroendocrine evaluation measurements were recorded before desflurane administration (M-30), and at M0, M15 AND m45. For heart rate there were differences between M0 and M15 (129 and 111 beats/min) in BTG, and between M0 and M30 (131 and 112 beats/min), in BPG. For mean arterial blood pressure there were differences between M0 (86mmHg) and all the recorded measurements (all measurements were lower than 72mmHg), in BTG. All recorded diastolic arterial blood pressures were lower than 53mmHg and different of the recorded measure M0 (67mmHg), in BTG. For systolic arterial blood pressure there were differences between M0 and M15 and M30 (112 vs 93 and 94mmHg, respectively), in BTG. Opioids administration determined discrete reduction in cardiovascular parameters while desflurane caused alterations in neuroendocrine function, increasing plasmatic levels of glucose.

Rats fed a high-fructose diet represent an animal model for insulin resistance and hypertension. We recently showed that a high-fructose diet containing vegetable oil but a normal sodium/potassium ratio induced mild insulin resistance with decreased insulin receptor substrate-1 tyrosine phosphorylation in the liver and muscle of normal rats. In the present study, we examined the mean blood pressure, serum lipid levels and insulin sensitivity by estimating in vivo insulin activity using the 15-min intravenous insulin tolerance test (ITT, 0.5 ml of 6 µg insulin, iv) followed by calculation of the rate constant for plasma glucose disappearance (Kitt) in male Wistar-Hannover rats (110-130 g) randomly divided into four diet groups: control, 1:3 sodium/potassium ratio (R Na:K) diet (C 1:3 R Na:K); control, 1:1 sodium/potassium ratio diet (CNa 1:1 R Na:K); high-fructose, 1:3 sodium/potassium ratio diet (F 1:3 R Na:K), and high-fructose, 1:1 sodium/potassium ratio diet (FNa 1:1 R Na:K) for 28 days. The change in R Na:K for the control and high-fructose diets had no effect on insulin sensitivity measured by ITT. In contrast, the 1:1 R Na:K increased blood pressure in rats receiving the control and high-fructose diets from 117 ± 3 and 118 ± 3 mmHg to 141 ± 4 and 132 ± 4 mmHg (P<0.05), respectively. Triacylglycerol levels were higher in both groups treated with a high-fructose diet when compared to controls (C 1:3 R Na:K: 1.2 ± 0.1 mmol/l vs F 1:3 R Na:K: 2.3 ± 0.4 mmol/l and CNa 1:1 R Na:K: 1.2 ± 0.2 mmol/l vs FNa 1:1 R Na:K: 2.6 ± 0.4 mmol/l, P<0.05). These data suggest that fructose alone does not induce hyperinsulinemia or hypertension in rats fed a normal R Na:K diet, whereas an elevation of sodium in the diet may contribute to the elevated blood pressure in this animal model.

Insulin stimulates the tyrosine kinase activity of its receptor resulting in the tyrosine phosphorylation of pp185, which contains insulin receptor substrates IRS-1 and IRS-2. These early steps in insulin action are essential for the metabolic effects of insulin. Feeding animals a high-fructose diet results in insulin resistance. However, the exact molecular mechanism underlying this effect is unknown. In the present study, we determined the levels and phosphorylation status of the insulin receptor and pp185 (IRS-1/2) in liver and muscle of rats submitted to a high-fructose diet evaluated by immunoblotting with specific antibodies. Feeding fructose (28 days) induced a discrete insulin resistance, as demonstrated by the insulin tolerance test. Plasma glucose and serum insulin and cholesterol levels of the two groups of rats, fructose-fed and control, were similar, whereas plasma triacylglycerol concentration was significantly increased in the rats submitted to the fructose diet (P<0.05). There were no changes in insulin receptor concentration in the liver or muscle of either group. However, insulin-stimulated receptor autophosphorylation was reduced to 72 ± 4% (P<0.05) in the liver of high-fructose rats. The IRS-1 protein levels were similar in both liver and muscle of the two groups of rats. In contrast, there was a significant decrease in insulin-induced pp185 (IRS-1/2) phosphorylation, to 83 ± 5% (P<0.05) in liver and to 77 ± 4% (P<0.05) in muscle of the high-fructose rats. These data suggest that changes in the early steps of insulin signal transduction may have an important role in the insulin resistance induced by high-fructose feeding.