Associação de cetamina S(+) e midazolam pelo método convencional de cálculo e pela extrapolação alométrica em bugios-ruivo (Alouatta guariba clamitans): resposta clínica e cardiorrespiratória

O objetivo deste estudo foi avaliar o protocolo de contenção química com cetamina S(+) e midazolam em bugios-ruivos, comparando o cálculo de doses pelo método convencional e o método de extrapolação alométrica. Foram utilizados 12 macacos bugios (Alouatta guariba clamitans) hígidos, com peso médio de 4,84±0,97kg, de ambos os sexos. Após jejum alimentar de 12 horas e hídrico de seis horas, realizou-se contenção física manual e aferiram-se os seguintes parâmetros: frequência cardíaca (FC), frequência respiratória (f), tempo de preenchimento capilar (TPC), temperatura retal (TR), pressão arterial sistólica não invasiva (PANI) e valores de hemogasometria arterial. Posteriormente, os animais foram alocados em dois grupos: GC (Grupo Convencional, n=06), os quais receberam cetamina S(+) (5mg kg-1) e midazolam (0,5mg kg-1), pela via intramuscular, com doses calculadas pelo método convencional; e GA (Grupo Alometria, n=06), os quais receberam o mesmo protocolo, pela mesma via, utilizando-se as doses calculadas pelo método de extrapolação alométrica. Os parâmetros descritos foram mensurados novamente nos seguintes momentos: M5, M10, M20 e M30 (cinco, 10, 20 e 30 minutos após a administração dos fármacos, respectivamente). Também foram avaliados: qualidade de miorrelaxamento, reflexo podal e caudal, pinçamento interdigital, tempo para indução de decúbito, tempo hábil de sedação, qualidade de sedação, e tempo e qualidade de recuperação. O GA apresentou menor tempo para indução ao decúbito, maior grau e tempo de sedação, bem como redução significativa da FC e PANI de M5 até M30, quando comparado ao GC. Conclui-se que o grupo no qual o cálculo de dose foi realizado por meio da alometria (GA) apresentou melhor grau de relaxamento muscular e sedação, sem produzir depressão cardiorrespiratória significativa.

Efeitos colaterais da ranitidina aplicada em dose terapêutica em cães saudáveis

O objetivo deste trabalho foi verificar se a dose de ranitidina 2mg kg-1, aplicada via intravenosa, causa êmese ou hipotensão em cães saudáveis. Foram selecionados 10 cães da raça Retriever do Labrador, 10 da raça Beagle e 10 cães sem raça definida, sendo cinco animais de cada sexo. Os animais foram submetidos ao exame clínico e à avaliação da pressão sanguínea antes da aplicação do fármaco e também 10 minutos e quatro horas após a administração deste. Após a aplicação, observou-se que 13,3% dos animais apresentaram-se normais; 6,7% dos cães apresentaram apatia; 50% dos animais apresentaram salivação e 30% apresentaram apatia, salivação, mímica de vômito ou êmese. Não houve diminuição significativa da pressão arterial após a administração do fármaco. Conclui-se que o uso de ranitidina na dose terapêutica, aplicada via intravenosa, pode provocar apatia, salivação, mímica de vômito e êmese.

Ocupação e hipertensão

Com base em revisão bibliográfica discute-se a literatura produzida nas décadas de 70 e 80, no campo da epidemiologia da hipertensão arterial sistêmica entre trabalhadores. Analisa-se não apenas o ponto de vista do conhecimento gerado, mas também os aspectos relacionados ao instrumental teórico-metodológico empregado.

Dynamics of follicle populations and gonadotropin concentrations in fillies age two to ten months

Follicle populations and concentrations of circulating gonadotropins were studied during age 2-10 months in 10 spring-born pony fillies. Blood sampling and ultrasound scanning were done every 4 days and daily for four 30 day periods. During 5-12 weeks, FSH concentrations were lower in 6 fillies with follicles greater than or equal to 6 mm (mean +/- s.e. 1.4 +/- 0.1 ng/ml) than in 4 fillies with follicles <6 mm (2.8 + 0.3 ng/ml). The diameters and numbers of follicles and gonadotropin concentrations increased progressively during age 2-4 months. A plateau in follicle activity and reduced levels of gonadotropins occurred during 5-7 months. During 8-10 months, follicles grew to >10 mm and gonadotropin concentrations increased. Waves of follicular growth were identified during the 30 day periods by significant increases in the diameter of the 10 largest follicles. The waves did not partition into dominant and subordinate follicles. Results indicated an initial postnatal period of negative ovarian feedback, temporally related changes in gonadotropins and follicles for months 3-10, and development of follicles in waves.

Midazolam and ketamine induction before halothane anaesthesia in ponies: cardiorespiratory, endocrine and metabolic changes

Six Welsh gelding ponies were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) prior to induction of anaesthesia with midazolam at 0.2 mg/kg and ketamine at 2 mg/kg i.v.. Anaesthesia was maintained for 2 h using 1.2% halothane concentration in oxygen. Heart rate, electrocardiograph (EGG), arterial blood pressure, respiratory rate, blood gases, temperature, haematocrit, plasma arginine vasopressin (AVP), dynorphin, beta-endorphin, adrenocorticotropic hormone (ACTH), cortisol, dopamine, noradrenaline, adrenaline, glucose and lactate concentrations were measured before and after premedication, immediately after induction, every 20 min during anaesthesia, and at 20 and 120 min after disconnection. Induction was rapid, excitement-free and good muscle relaxation was observed. There were no changes in heart and respiratory rates, Decrease in temperature, hyperoxia and respiratory acidosis developed during anaesthesia and slight hypotension was observed (minimum value 76 +/- 10 mm Hg at 40 mins), No changes were observed in dynorphin, beta-endorphin, ACTH, catecholamines and glucose, Plasma cortisol concentration increased from 220 +/- 17 basal to 354 +/- 22 nmol/L at 120 min during anaesthesia; plasma AVP concentration increased from 3 +/- 1 basal to 346 +/- 64 pmol/L at 100 min during anaesthesia and plasma lactate concentration increased from 1.22 +/- 0.08 basal to 1.76 +/- 0.13 mmol/L at 80 min during anaesthesia, Recovery was rapid and uneventful with ponies taking 46 +/- 6 min to stand. When midazolam/ketamine was compared with thiopentone or detomidine/ketamine for induction before halothane anaesthesia using an otherwise similar protocol in the same ponies, it caused slightly more respiratory depression, but less hypotension. Additionally, midazolam reduced the hormonal stress response commonly observed during halothane anaesthesia and appears to have a good potential for use in horses.

Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats

We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and presser responses induced by the concomitant angiotensinergic, alpha(2) and beta adrenergic activation of the MnPO, whereas alpha(1) activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.

Níveis séricos de cortisol e 17-& estradiol durante o ciclo estral em marrãs (Sus domestica - Linnaeus 1758)

In the present study 21 young swine females, sexually mature, reared and kept under an industrial management system were assessed for cortisol and oestradiol-17 beta serum prolifes during the oestrus cycle. Blood sampling was performed always at the same interval, from 8:00 to 10:00 a.m. Each animal was submitted to 14 venal punctions at days 0, 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 21, 22 and 23 of the oestrous cycle. The first day of the oestrous phase was assumed to be day 0 and the 23(rd) as the first of the next cycle. Hormone determinations were performed using a solid phase radioimmunoassay (RIA). Regarding to cortisol concentrations, there was a variation from 3.5 to 8.0 mu g/dl and for oestradiol-17 beta the mean values detected varied from 3.5 to 14.9pg/ml.

Control of breathing in anuran amphibians

The primary role of the respiratory system is to ensure adequate tissue oxygenation, eliminate carbon dioxide and help to regulate acid-base status. To maintain this homeostasis, amphibians possess an array of receptors located at peripheral and central chemoreceptive sites that sense respiration-related variables in both internal and external environments. As in mammals, input from these receptors is integrated at central rhythmogenic and pattern-forming elements in the medulla in a manner that meets the demands determined by the environment within the constraints of the behavior and breathing pattern of the animal. Also as in mammals, while outputs from areas in the midbrain may modulate respiration directly, they do not play a significant role in the production of the normal respiratory rhythm. However, despite these similarities, the breathing patterns of the two classes are different: mammals maintain homeostasis of arterial blood gases through rhythmic and continuous breathing, whereas amphibians display an intermittent pattern of aerial respiration. While the latter is also often rhythmic, it allows a degree of fluctuation in key respiratory variables that has led some to suggest that control is not as tight in these animals. In this review we will focus specifically on recent advances in studies of the control of ventilation in anuran amphibians. This is the group of amphibians that has attracted the most recent attention from respiratory physiologists. (c) 2006 Elsevier B.V. All rights reserved.

Vascular effects of long-term propranolol administration after chronic nitric oxide blockade

Long-term propranolol treatment reduces arterial blood pressure in hypertensive individuals mainly by reducing peripheral vascular resistance, but mechanisms underlying their vasodilatory effect remain poorly investigated. This study aimed to investigate whether long-term propranolol administration ameliorates the impairment of relaxing responses of aorta and mesenteric artery from rats made hypertensive by chronic nitric oxide (NO) deficiency, and underlying mechanisms mediating this phenomenon. Male Wistar rats were treated with N-omega-Nitro-L-arginine methyl ester (L-NAME; 20 mg/rat/day) for four weeks. DL-Propranolol (30 mg/rat/day) was given concomitantly to L-NAME in the drinking water. Treatment with L-NAME markedly increased blood pressure, an effect largely attenuated by DL-propranolol. In phenylephrine-precontracted aortic rings, the reduction of relaxing responses for acetylcholine (0.001-10 mu M) in L-NAME group was not modified by DL-propranolol, whereas in mesenteric rings the impairment of acetylcholine-induced relaxation by L-NAME was significantly attenuated by DL-propranolol. In mesenteric rings precontracted with KCl (80 MM), DL-propranolol failed to attenuate the impairment of acetylcholine-induced relaxation by L-NAME. The contractile responses to extracellular CaCl2 (1-10 mM) were increased in L-NAME group, and co-treatment with DL-propranolol reduced this response in both preparations in most Ca2+ concentrations used. The NO2/NO3 plasma levels and superoxide dismutase (SOD) activity were reduced in L-NAME-treated rats, both of which were significantly prevented by DL-propranolol. In conclusion, propranolol-induced amplification of the relaxation to acetylcholine in mesenteric arteries from L-NAME-treated rats is sensitive to depolarization. Additional mechanisms involving blockade of Ca2+ entry in the vascular smooth muscle and increase in NO bioavailability contributes to beneficial effects of long-term propranolol treatment. (C) 2007 Elsevier B.V. All rights reserved.

Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs

To evaluate the effects of acepromazine maleate on the cardiovascular changes induced by dopamine in isoflurane-anesthetized dogs.Prospective, randomized cross-over experimental design.Six healthy adult spayed female dogs weighing 16.4 +/- 3.5 kg (mean +/- SD).Each dog received two treatments, at least 1 week apart. Acepromazine (0.03 mg kg(-1), IV) was administered 15 minutes before anesthesia was induced with propofol (7 mg kg(-1), IV) and maintained with isoflurane (1.8% end-tidal). Acepromazine was not administered in the control treatment. Baseline cardiopulmonary parameters were measured 90 minutes after induction. Thereafter, dopamine was administered intravenously at 5, 10, and 15 mu g kg(-1) minute(-1), with each infusion rate lasting 30 minutes. Cardiopulmonary data were obtained at the end of each infusion rate.Dopamine induced dose-related increases in cardiac index (CI), stroke index, arterial blood pressure, mean pulmonary arterial pressure, oxygen delivery index (DO2I) and oxygen consumption index. In the control treatment, systemic vascular resistance index (SVRI) decreased during administration of 5 and 10 mu g kg(-1) minute(-1) of dopamine and returned to baseline with the highest dose (15 mu g kg (-1) minute(-1)). After acepromazine treatment, SVRI decreased from baseline during dopamine administration, regardless of the infusion rate, and this resulted in a smaller increase in blood pressure at 15 mu g kg (-1) minute(-1). During dopamine infusion hemoglobin concentrations were lower following acepromazine and this contributed to significantly lower arterial O-2 content.Acepromazine prevented the return in SVRI to baseline and reduced the magnitude of the increase in arterial pressure induced by higher doses of dopamine. However, reduced SRVI associated with lower doses of dopamine and the ability of dopamine to increase CI and DO2I were not modified by acepromazine premedication.Previous acepromazine administration reduces the efficacy of dopamine as a vasopressor agent in isoflurane anesthetized dogs. Other beneficial effects of dopamine such as increased CO are not modified by acepromazine.

Maximal lactate steady state in running mice: Effect of exercise training

1. Maximal lactate steady state (MLSS) corresponds to the highest blood lactate concentration (MLSSc) and workload (MLSSw) that can be maintained over time without continual blood lactate accumulation and is considered an important marker of endurance exercise capacity. The present study was undertaken to determine MLSSw and MLSSc in running mice. In addition, we provide an exercise training protocol for mice based on MLSSw.2. Maximal lactate steady state was determined by blood sampling during multiple sessions of constant-load exercise varying from 9 to 21 m/min in adult male C57BL/6J mice. The constant-load test lasted at least 21 min. The blood lactate concentration was analysed at rest and then at 7 min intervals during exercise.3. The MLSSw was found to be 15.1 +/- 0.7 m/min and corresponded to 60 +/- 2% of maximal speed achieved during the incremental exercise testing. Intra- and interobserver variability of MLSSc showed reproducible findings. Exercise training was performed at MLSSw over a period of 8 weeks for 1 h/day and 5 days/week. Exercise training led to resting bradycardia (21%) and increased running performance (28%). of interest, the MLSSw of trained mice was significantly higher than that in sedentary littermates (19.0 +/- 0.5 vs 14.2 +/- 0.5 m/min; P = 0.05), whereas MLSSc remained unchanged (3.0 mmol/L).4. Altogether, we provide a valid and reliable protocol to improve endurance exercise capacity in mice performed at highest workload with predominant aerobic metabolism based on MLSS assessment.

Nitric oxide and anglotensin II receptors mediate the pressor effect of angiotensin II: A study in conscious and zoletil-anesthetized rats

The circumventricular structures of the central nervous system and nitric oxide are involved in arterial blood pressure control, and general anesthesia may stimulate the central renin-angiotensin system. We therefore investigated the central role of angiotensin 11 and nitric oxide on the regulation of systemic arterial blood pressure in conscious and anesthetized rats. METHODS: Rats with stainless steel cannulae implanted into their lateral ventricle were studied. We injected the AT(1) and AT(2) angiotensin 11 receptor antagonists, losartan and PD123319, L-NAME, 7-nitroindazole (nitric oxide synthetase inhibitors), and FK409 (nitric oxide donor agent) into the lateral ventricles. Mean arterial blood pressure (MAP) was recorded in conscious and zoletil-anesthetized rats. RESULTS: Mean +/- (SEM) baseline MAP was 117.5 +/- 2 mm Hg. Angiotensin II injected into the brain lateral ventricle increased MAP from 136.5 +/- 2 min Hg to 138.5 +/- 4 mm Hg (Delta 16 +/- 3 mm Hg to Delta 21 +/- 3 mm Hg) for all experimental groups versus control from 116 +/- 2 mm Hg to 120 +/- 3 mm Hg (Delta 3 +/- 1 mm Hg to A5 +/- 2 mm Hg) (P < 0.05). L-NAME or 7-nitroindazole enhanced the angiotensin II pressor effect (P < 0.05). Prior injection of losartan and PD123319 decreased the angiotensin 11 pressor effect and the enhancement effect of L-NAME and 7-nitroindazole (P < 0.05). Zoletil anesthesia did not interfere with the effects of angiotensin 11, AT,, AT2 antagonists, or nitric oxide synthetase inhibitors. CONCLUSIONS: Endogenous nitric oxide functions tonically as a central inhibitory modulator of the angiotensinergic system. AT, and AT2 receptors influence the angiotensin 11 central control of arterial blood pressure. Zoletil anesthesia did not interfere with these effects. (Anesth Analg 2007;105:1293-7)

THE EFFECT OF ANALOGS OF ANGIOTENSIN-II ON DRINKING AND CARDIOVASCULAR-RESPONSES TO CENTRAL ANGIOTENSIN-II IN THE RAT

1. Intracerebroventricular (I.C.V.) infusion (60 ng h-1) of Isoleu5-angiotensin II (Isoleu5-AngII) and des-amine-angiotensin II (des-amine-AngII) in rats caused increased drinking behaviour and an increase in arterial blood pressure.2. Des-amine-AngII caused similar increases in heart rate and arterial blood pressure as AngII.3. Previous I.C.V. injection of the antagonists [Leu8]-AngII, des-amine-[Leu8]-AngII and octanoyl-[Leu8]-AngII prevented the increases in heart rate and blood pressure produced by I.C.V. infusion of AngII and caused partial reduction of the dipsogenic response.4. The three antagonists had no effect on the increase in arterial blood pressure and heart rate caused by des-amine-AngII. The drinking response was reduced by previous injection of [Leu8]-AngII and des-amine-[Leu8]-AngII but not by octanoyl-[Leu8]-AngII.5. In conclusion, Isoleu5-AngII and des-amine-AngII increase drinking behaviour, arterial blood pressure and heart rate when infused into the cerebral ventricle of rats. The study with the antagonists showed that des-amine-AngII probably binds more strongly to AngII-receptors.

LH and FSH concentration and follicular development in Nellore heifers submitted to fixed-time artificial insemination protocols with different progesterone concentrations

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha(2)-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 mu g/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha(2)-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the a2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.