Effects of temperature on lung and blood gases in the South American rattlesnake Crotalus durissus terrificus

The effects of temperature on lung and blood gases were measured in the South American rattlesnake (Crotalus durissus terrificus). Arterial blood and lung gas samples were obtained from chronically cannulated animals at 15, 25, and 35 degrees C. As expected for reptiles, arterial pH fell with increased temperature (0.018 U degrees C-1 between 15 and 25 degrees C and 0.011 U degrees C-1 between 25 and 35 degrees C) while lung gas PCO2 rose from 5.8 mmHg at 15 degrees C to 13.2 mmHg at 35 degrees C. Concurrently, lung gas PO2 declined from 132 mmHg at 15 degrees C to 120 mmHg at 35 degrees C, and arterial PO2 increased from 33 to 76 mmHg in that temperature range. Arterial haemoglobin O-2 saturation rose from 0.53 at 15 degrees C to 0.83 at 25 degrees C but became slightly reduced (0.77) with a further elevation of temperature to 35 degrees C. Arterial haemoglobin concentration increased from 1.96 to 2.53 mM between 15 and 35 degrees C, consistent with higher demands on oxygen delivery to tissues at elevated temperatures. Moreover, the substantial increase of haemoglobin O-2 saturation between 15 and 25 degrees C conforms to the idea that reduction of the central vascular right-to-left shunt (pulmonary bypass of systemic venous return) is associated with high metabolic demands. (C) 1998 Elsevier B.V. All rights reserved.

Cardiorespiratory responses to hypoxia in the African catfish, Clarias gariepinus (Burchell 1822), an air-breathing fish

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

Frequent respiratory pathogens of respiratory tract infections in children attending daycare centers

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Long-term inhibition of 5-alpha reductase and aromatase changes the cellular and extracellular compartments in gerbil ventral prostate at different postnatal ages

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

The role of the vagus nerve in the generation of cardiorespiratory interactions in a neotropical fish, the pacu, Piaractus mesopotamicus

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Efeitos cardiorrespiratórios do butorfanol em cães pré-tratados ou não pela levomepromazina

Objetivou-se com este experimento avaliar os efeitos do butorfanol precedido ou não pela levomepromazina sobre a freqüência cardíaca (FC), as pressões arteriais sistólica, diastólica e média (PAS, PAD e PAM, respectivamente), a freqüência respiratória (f), a concentração de dióxido de carbono ao final da expiração (ETCO2), a saturação da oxihemoglobina (SpO2), o volume corrente (VC) e o volume minuto (VM), em cães. Para tal, foram empregados vinte animais adultos, clinicamente saudáveis, distribuídos igualmente em dois grupos (GC e GL). Ao GC administrou-se solução salina a 0,9% (Controle), no volume de 0,2mL kg-1, pela via intravenosa (IV). Decorridos 15 minutos, administrou-se butorfanol na dose de 0,3mg kg-1 pela mesma via. Aos animais do GL foi adotada a mesma metodologia, porém substituindo-se a solução salina pela levomepromazina na dose de 1mg kg-1. As medidas das variáveis cardiorrespiratórias iniciaram-se imediatamente antes da aplicação dos fármacos (M1). Novas mensurações foram realizadas 15 minutos após a administração da solução salina a 0,9% ou levomepromazina (M2) e 10 minutos após a administração de butorfanol (M3). As demais colheitas foram realizadas a intervalos de 10 minutos, durante 30 minutos (M4, M5 e M6, respectivamente). Os dados numéricos colhidos foram submetidos à Análise de Variância (ANOVA), seguida pelo teste de Tukey (p<0,05) para as comparações das médias. O emprego do butorfanol promoveu diminuição significativa das freqüências cardíaca e respiratória e do volume minuto no grupo previamente tratado pela levomepromazina; entretanto, essas alterações foram discretas, não comprometendo os demais parâmetros circulatórios e respiratórios.

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

This study investigated the involvement of serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) in the control of sodium (Na+) excretion, potassium (K+) excretion, and urinary volume in unanesthetized rats subjected to acute isotonic blood volume expansion (0.15 M NaCl, 2 ml/100 g of body wt over 1 min) or control rats. Plasma oxytocin (OT), vasopressin (VP), and atrial natriuretic peptide (ANP) levels were also determined in the same protocol. Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In rats treated with vehicle in the LPBN, blood volume expansion increased urinary volume, Na+ and K+ excretion, and also plasma ANP and OT. Bilateral injections of serotonergic receptor antagonist methysergide (1 or 4 mu g/200 eta 1) into the LPBN reduced the effects of blood volume expansion on increased Na+ and K+ excretion and urinary volume, while LPBN injections of serotonergic 5-HT2a/HT2c receptor agonist, 2.5-dimetoxi-4-iodoamphetamine hydrobromide (DOI;1 or 5 mu g/200 eta 1) enhanced the effects of blood volume expansion on Na+ and K+ excretion and urinary volume. Methysergide (4 mu g) into the LPBN decreased the effects of blood volume expansion on plasma ANP and OT, while DOI (5 mu g) increased them. The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion.

Blood glucose responses in humans mirror lactate responses for individual anaerobic threshold and for lactate minimum in track tests

The equilibrium point between blood lactate production and removal (La-min(-)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-](b), catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc](b), this study investigated the [Glc] and [La-](b) responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum;(Glc(min)) in addition to IAT and La-min(-) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v(3km)); IAT and IGT- 8 x 800 m runs at velocities between 84% and 102% of v(3km); La-min(-) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 8 x 800 m at intensities between 87% and 97% of v(3km); endurance test (ET)- 30 min at the velocity of IAT. Capillary blood (25 mu l) was collected for [La-](b) and [Glc](b) measurements. The TAT and IGT were determined by [La-](b) and [Glc](b) kinetics during the second test. The La-min(-) and Glc(min) were determined considering the lowest [La-] and [Glc](b) during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21)m. min(-1); r = 0.096; P < 0.001] and between La,, [285 (SD 21)] and Glc(min) [287 (SD 20) m. min(-1) = 0.77; P < 0.05]. During ET, the [La-](b) reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol 1(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min), as well as by IAT and La-min(-).

Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats

This study investigated the effects of bilateral injections of serotonergic receptor agonist and antagonist into the lateral parabrachial nucleus (LPBN) on the ingestion of water and 0.3 M NaCl induced by intracerebroventricular angiotensin II (ANG II) or by combined subcutaneous injections of the diuretic furosemide (Furo) and the angiotensin-converting enzyme inhibitor captopril (Cap). Rats had stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle. Bilateral LPBN pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (4 mu g/200 nl each site) increased 0.3 M NaCl and water intakes induced by intracerebroventricular ANG II (50 ng/mu l) and 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with bilateral LPBN injections of a serotonergic 5-HT2A/2C receptor agonist DOI (5 mu g/200 nl) significantly reduced 0.3 M NaCl intake induced by subcutaneous Furo + Cap. Pretreatment with methysergide or DOI into the LPBN produced no significant changes in the water intake induced by subcutaneous Furo + Cap. These results suggest that serotonergic mechanisms associated with the LPBN may have inhibitory roles in water and sodium ingestion in rats.

Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite

Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst) and are ineffective in inducing the intake of hypertonic saline solutions (i.e., the operational definition of sodium appetite). Recent studies have indicated that bilateral injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic activation with carbachol (an experimental condition where only water is typically ingested) after the blockade of LPBN serotonergic mechanisms with methysergide treatment in rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4 nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of methysergide (4 mug), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by intracerebroventricular carbachol was not changed by LPBN methysergide injections. The results indicate that central cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the LPBN are attenuated.

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.

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Previous studies demonstrated the inhibitory participation of serotonergic ( 5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD- induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PD-induced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT- and Fos-OT-immunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD- induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5- HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD- induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals.

Cholecystokinin actions in the parabrachial nucleus: effects on thirst and salt appetite

The present study investigated the effects of bilateral injections of the nonselective CCK receptor antagonist proglumide or CCK-8 into the lateral parabrachial nuclei (LPBN) on the ingestion of 0.3 M NaCl and water induced by intracerebroventricular injection of ANG II or by a combined treatment with subcutaneous furosemide (Furo) + captopril (Cap). Compared with the injection of saline (vehicle), bilateral LPBN injections of proglumide (50 mu g . 200 nl(-1). site(-1)) increased the intake of 0.3 ill NaCl induced by intracerebroventricular ANG II (50 ng/1 mu l). Bilateral injections of proglumide into the LPBN also increased ANG II-induced water intake when NaCl was simultaneously available, but not when only water was present. Similarly, the ingestion of 0.3 M NaCl and water induced by the treatment with Furo (10 mg/kg) + Cap (5 mg/kg) was increased by bilateral LPBN proglumide pretreatment. Bilateral CCK-8 (0.5 mu g . 200 nl(-1). site(-1)) injections into the LPBN did not change Furo + Cap-induced 0.3 M NaCl intake but reduced water consumption. When only water was available after intracerebroventricular ANG II, bilateral LPBN injections of proglumide or CCK-8 had no effect or significantly reduced water intake compared with LPBN vehicle-treated rats. Taken together, these results suggest that CCK actions in the LPBN play a modulatory role on the control of NaCl and water intake induced by experimental treatments that induce hypovolemia and/or hypotension or that mimic those states.

LATERAL PARABRACHIAL SEROTONERGIC MECHANISMS - ANGIOTENSIN-INDUCED PRESSOR AND DRINKING RESPONSES

This study investigated the effects of bilateral injections of serotonergic receptor ligands into the lateral parabrachial nucleus (LPBN) on the presser and dipsogenic responses induced by intracerebroventricular (icv) injection of angiotensin II (ANG II). Rats with stainless steel cannulas implanted bilaterally into the LPBN and into the left lateral ventricle were used to study icy ANG II-induced water intake and presser responses. Pretreatment with the serotonergic 5-HT1/5-HT2 receptor antagonist methysergide (1-8 mu g/200 nl) bilaterally injected into the LPBN increased the water intake induced by icv ANG II (50 ng/mu l) administered via the lateral ventricle, but pretreatment with methysergide (4 mu g/200 nl) did not change the presser response produced by icy ANG II. After bilateral injection of either serotonin (5-HT, 5 mu g/200 nl) or the serotonergic 5-HT2a/5-HT2c receptor agonist (+/-)-2,5-dimetoxy-4-iodoamphetamine hydrochloride (DOI; 0.5-10 mu g/200 nl) into the LPBN, the water intake induced by ANG II was significantly reduced. These results are consistent with other observations indicating that the LPBN is associated with inhibitory mechanisms controlling water intake induced by ANG II treatment and suggest that serotonergic pathways may be involved in this effect.