Comparative study of epidural xylazine or clonidine in horses

Objective To evaluate the cardiorespiratory and behavioural effects of epidural xylazine (XYL) or clonidine (CLO) in horses.Study design Blinded, randomized experimental study.Twelve healthy Arabian yearling horses weighing 117-204 kg were randomly allocated into two groups: XYL (n = 6) and CLO (n = 6).Methods An epidural catheter was inserted and a facial arterial catheter was placed and the next day the horses were restrained in stocks. Baseline values for heart (HR) and respiratory (RR) rates, arterial pressure and behavioural responses were evaluated before (TO) and 10, 20, 30, 45, 60, 90 and 120 minutes after epidural injection (T10-T120). The horses received 0.2 mg kg(-1) of XYL or 5 mu g kg(-1) CLO; adjusted to (3.4 + (body weight in kg x 0.013) mL with saline. Data were analysed by the Kolmogorov-Smirnov test, one-way ANOVA with repeated measures, and one-way ANOVA followed by a Student-Newman-Keuls test or Fisher's exact test, as necessary. Significance was set at p <= 0.05.Results Sedation and ataxia were seen at T10, persisting until T120 in four and three horses, respectively, in XYL and all horses in CLO respectively. Two XYL and one CLO horses became recumbent at T45 and T25 respectively. Penile prolapse occurred in four of five males at T30 and T45, in the XYL and CLO groups, respectively, resolving by T120. Tail relaxation was present from T10 to T120 in all horses in XYL and in four horses in CLO. Head drop was observed from T20 to T60 and from T10 to T120 in XYL and CLO respectively. Respiratory rate decreased significantly only at T45 in the CLO group. Heart rate and arterial blood pressure remained stable.Conclusions and clinical relevance Epidural CLO and XYL produce similar cardiorespiratory and behavioural changes but neither would be safe to use clinically at the doses used in this study.

Evaluation of Vmax as an index of myocardial contractility during afterload and preload elevations

In order to test if the maximal velocity of shortening (V(max)TP) reflects the level of inotropism and is affected by preload and afterload, the behavior of this index was compared in two groups of anesthetized, atropinized dogs when preload and afterload were raised with an angiotensin II infusion. In seven dogs (group I), the arterial pressure elevation was allowed to inhibit reflectively the sympathetic tone and depress contractility. In eleven dogs (group II), the adrenergic activity was abolished by previous administration of reserpine. In group I, there was a significant decrease in V(max)TP during the angiotensin infusion. In group II, there was no significant change in the value of this index when the drug was infused. In six animals of this group, a further increase of arterial pressure was induced, but the values of V(max)TP remained similar to control. These results suggest that this index reflects the inotropic state of the myocardium and does not suffer significantly from the influence of preload and afterload elevations within our experimental limits.

Efeitos do pentobarbital sódico e do enfluorano sobre a circulação sanguínea hepática: fluxometria eletromagnética e manometria (estudo experimental no cão)

In 18 dogs, previously anesthetized with sodium pentobarbital for the surgical preparation, catheterism and monitoring, the action of sodium pentobarbital (7.5 mg/kg) and enflurane (1.5 - 2%) in the liver circulation was studied. Measurements of the following parameters were made in four different times, before and 15, 30 and 60 min after the drug administration. By direct determination: hepatic artery flow, portal vein flow, mean pressure of the abdominal aorta, peripheral arterial pressure (mean), pressure in the caudal cava vein, portal pressure; and by indirect determination: total flow, arterial-cava gradient, portal-cava gradient, resistance in the hepatic artery territory, resistance in the territory of the portal vein, and total resistance. Based on the results, it is concluded that in the experiment's conditions: sodium pentobarbital doesn't change significantly the hepatic circulation, and enflurance produces a fall in the total hepatic flow, by reducing the portal flow, without alterations of the hepatic arterial flow. It diminishes the total hepatic resistance by diminishing the arterial resistance without alterations of the portal resistance; it diminishes the arterial-cava gradient in consequence of the reduction of the abdominal aorta pressure and of the portal pressure, but it seems that the caudal cava pressure is not altered. It also occurs a fall in the peripheral mean pressure.

Efeitos do pentobarbital sódico sobre o fluxo sanguíneo renal. Estudo experimental no cão

In six dogs, previously anesthetized with sodium pentobarbital (30 mg/kg) for surgical preparation, catheterism and monitoring, the action of sodium pentobarbital (7,5 mg/kg) on renal flow was studied. Determinations of mean arterial pressure, venous pressure, cardiac rate, arterio-cava pressure gradient and renal arterial resistance were made. Pentobarbital doesn't change significantly the renal blood flow or any of the other parameters studied, with the exception of venous pressure in the inferior caval vein where the drug produces a significant fall.

Pressor, dipsogenic, natriuretic and kaliuretic responses to central carbachol in rats with lesion of the medial septal area

In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the dipsogenic, natriuretic, kaliuretic and pressor responses elicited by intracerebroventricular (i.c.v.) injection of the cholinergic agonist carbachol. Freely moving rats with sham or MSA lesion (1-7 days and 14-18 days) and a stainless steel cannula implanted into the lateral ventricle were studied. In sham rats, i.c.v. injection of carbachol (7.5 nmol) produced an increase in water intake (10.2 ± 1.5 ml/h), mean arterial pressure (MAP) (35 ± 5 mmHg) and urinary Na+ and K+ excretion (551 ± 83 and 170 ± 17 μEq 120 min, resp.). The pressor (18 ± 3 and 14 ± 4 mmHg, resp.) and natriuretic responses (178 ± 58 and 172 ± 38 μEq 120 min) produced by i.c.v. carbachol in acute or chronic MSA-lesioned rats were reduced. No change was observed in urinary K+ excretion and a reduced water intake (5 ± 1.3 ml/h) was observed only in acute MSA-lesioned rats. These results suggest that the MSA plays an important role for the pressor and natriuretic responses induced by central cholinergic activation in rats. A small influence of this structure on water intake may also be suggested. © 1991.

Effect of AV3V lesion on the cardiovascular, fluid, and electrolytic changes induced by activation of the lateral preoptic area

In this study we investigated the effect of the anteroventral third ventricle (AV3V) lesion on the pressor, bradycardic, natriuretic, kaliuretic, and dipsogenic responses induced by the injection of the cholinergic agonist carbachol into the lateral preoptic area (LPOA) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with stainless steel cannula directly into the LPOA. Injection of carbachol (7.5 nmol) into the LPOA of sham rats induced natriuresis (405 ± 66 μEq/120 min), kaliuresis (234 ± 44 μEq/120 min), water intake (9.5 ± 1.7 ml/60 min), bradycardia (-47 ± 11 bpm), and increase in mean arterial pressure (28 ± 3 mmHg). Acute AV3V lesion (1-5 days) reduced the natriuresis (12 ± 4 μEq/120 min), kaliuresis (128 ± 27 μEq/120 min), water intake (1.7 ± 0.9 ml/60 min), and pressor responses (14 ± 4 mmHg) produced by carbachol into the LPOA. Tachycardia instead of bradycardia was also observed. Chronic (14-18 days) AV3V lesion reduced only the pressor response (10 ± 2 mmHg) induced by carbachol. These results showed that acute, but not chronic, AV3V lesion reduced the natriuretic, kaliuretic, and dipsogenic responses to carbachol injection into the LPOA. The pressor response was reduced in acute or chronic AV3V-lesioned rats. The results suggest that the lateral areas may control the fluid and electrolyte balance independently from the AV3V region in chronic AV3V-lesioned rats. © 1992.

EFEITOS DA INFUSAO CONTINUA DO PROPOFOL SOBRE A FUNCAO RENAL DO CAO. ESTUDO COMPARATIVO COM O PENTOBARBITAL SODICO

Little research has been done with propofol in relation to renal function. The aim of this study was to evaluate the effects of the continuous infusion of propofol on renal function in dogs. Sixteen dogs, previously anesthetized with pentobarbital sodium (30 mg.kg-1) for surgical preparation, catheterism and monitoring, were studied. The dogs were mechanically ventilated with air and received alcuronium (0.2 mg.kg-1 in bolus and 0.06 mg.kg-1 - maintenance). The following parameters were studied: heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP), aortic blood flow (A(o)BF - by electromagnetic flowmeter installed in the ascending aortic), aortic vascular resistance index (A(o)VRI), renal plasma flow (ERPF - by para-aminohipurate clearance), glomerular filtration rate (GFR - by creatinine clearance), effective renal blood flow (ERBF = ERPF/1 - hematocrit), urinary volume (UV), renal vascular resistance (RVR = MAP.80/ERBF.10-3), urinary sodium excretion (UE(Na)), fractionated sodium excretion (FE(Na)), osmolar clearance (C(osm)) and free water clearance (C(H2O)). These parameters were studied at 15 (M1), 30 (M2), 45 (M3) and 60 (M4) min after beginning pentobarbital sodium infusion (5 mg.kg-1.h-1). The dogs were allocated into two groups of eight animals each: G1 (control-pentobarbital sodium) and G2 (propofol). In G1, pentobarbital was given at the four times studied. G2 dogs received the same treatment as G1 dogs at M1 and M2; infusion of pentobarbital was substituted by propofol (3 mg.kg-1 bolus, followed by 12 mg.kg-1.h-1 continuous infusion) at M3 and M4. Profile Analysis was used to analyze the results statistically. In G1 (pentobarbital), there was a significant increase in RVR (M1 < M4) and a decrease in ERPF and ERBF (M1 > M4). In G2 (propofol) there was only a significant increase in A(o)BF (M1 < M2 = M3). In comparison among groups, these was a significant alteration of FE(Na) at M3 (pentobarbital > propofol). It was observed that the continuous infusion of propofol in dogs, at the given doses, did not alter the basic variables of renal function and hemodynamics studied. We concluded that propofol can be one of the drugs of choice to provide base anesthesia in studies of renal function in dogs.

INFLUENCIA DO ACRESCIMO DE MANITOL A SOLUCAO NUTRIENTE NO DESEMPENHO MECANICO E NO GRAU DE EDEMA MIOCARDICO DE CORACOES ISOLADOS DE RATOS

Purpose - To analyse the influence of mannitol added to Krebs-Henseleit (KH) solution on the myocardium edema and myocardial function. Methods - Isolated rat heart under isovolumetric contractions studied according to Langendorff's technique were perfused with KH solution at constant flow during 90 min. The coronary perfusion pressure, diastolic and systolic pressures were recorded at every 15 min. At the end of the experiment, myocardium water content was measured in hearts perfused with KH solution (group I, n = 9) and in hearts perfused with KH solution plus 8 mM mannitol (group II, n = 8). These results were compared to non-perfused control heart (n = 9). Results - Myocardial water content was statistically higher in group I (80.8 ± 1.3%) compared to group II (78.1 ± 0.7%) and control group (75.5 ± 0.5%). Systolic arterial pressure was statistically higher in group I (86.2 ± 11.5 mmHg) compared to group II (72.7 ± 21.1 mmHg). There was no difference in the diastolic pressure between the two groups. Coronary perfusion pressure (Pp) increased progressively during the experiment in both groups. However, Pp was lower in group II than in group I. Conclusion - Mannitol added to KH solution significantly attenuates the myocardium edema in the isolated perfused rat heart.

ESTUDO DA UMIDIFICACAO E DO AQUECIMENTO DOS GASES INSPIRADOS DURANTE A VENTILACAO MECANICA NO CAO

The authors studied the effect of temperature and humidity of inhaled gases on the respiratory tract of dogs submitted to mechanic ventilation. According to these two variables, fourty dogs were divided in five groups: -G1: 22-26°C and 17-20 mg H2O.l-1; G2: 27-31°C and 23-27 mg H2O.l-1; G3: 32-36°C and 30-36 mg H2O.l-1; G4: 37-41°C and 40-49 mg H2O.l-1; G5: 42-46°C and 59-65 mg H2O.l-1. The following parameters were evaluated: medial arterial pressure, cardiac frequency, venous pressure of inferior cava (CVP), endotracheal pressure, arterial pH, PaO2, PaCO2, rectal temperature, and the histology of the tracheobronchial tree. In the groups G1 and G5, the endotracheal pressure and CVP presented a slight raise. In the groups G1, G2 and G3, there was no histological modification or progressive hypothermia. The group G5 presented metabolic acidosis and great histological alteration; in this group the rectal temperature remained stable. The group G4 presented great histological alteration and hypothermia. In conclusion, the temperature and humidity of inhaled gases should not be higher than 36°C and 36 mm H2O.l-1, respectively. However, the stability of body temperature only is achieved when the temperature of the inhaled air is 42°C or higher.

Papel da regiao AV3V no choque septico experimental em ratos tratados com NaCl 7,5%

The effect of intravenous infusion of hypertonic saline (HS) on the recovery of mean arterial pressure (MAP) during septic shock was studied in sham-operated rats and in rats with electrolytic lesion in the anteroventral third ventricle (AV3V) region. Our results show that intravenous HS infusion in rats treated with endotoxin (Etx) partially restores MAP, but when we have a severe shock produced by Etx, HS was not able to reverse the hypotension. We also show that the integrity of the AV3V region is essential for the protective action of HS in endotoxin shock. It is possible that NO production contributes to the deleterious effect of endotoxin. So, the unraveling of the release of NO by the vascular endothelium and their role as regulators of vascular tone is increasing our understanding of the physiology and pathophysiology of the cardiovascular system and will therefore enhance the possibilities of preventing and treating endotoxin shock.

Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia

Six Welsh gelding ponies (weight 246 ± 6 kg) were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) followed by 0.02 mg/kg of detomidine i.v. Anaesthesia was induced with 2 mg/kg of ketamine i.v. Ponies were intubated and lay in left lateral recumbency. On one occasion anaesthesia was maintained for 2 h using 1.2% halothane in oxygen. The same group of ponies were anaesthetized 1 month later using the same induction regime and anaesthesia was maintained with a combination of detomidine, ketamine and guaiphenesin, while the ponies breathed oxygen-enriched air. Electrocardiogram, heart rate, mean arterial blood pressure, cardiac output, respiratory rate, blood gases, temperature, haematocrit, glucose, lactate and cortisol were measured and cardiac index and systemic vascular resistance were calculated in both groups. Beta-endorphin, met-enkephalin, dynorphin, arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH) and catecholamines were measured in the halothane anaesthesia group only and 11-deoxycortisol during total intravenous anaesthesia (TIVA) only. Cardiorespiratory depression was more marked during halothane anaesthesia. Hyperglycaemia developed in both groups. Lactate and AVP increased during halothane anaesthesia. Cortisol increased during halothane and decreased during TIVA. There were no changes in the other hormones during anaesthesia. Recovery was smooth in both groups. TIVA produced better cardiorespiratory performance and suppressed the endocrine stress response observed during halothane anaesthesia.

Functional evidence that the central renin-angiotensin system plays a role in the pressor response induced by central injection of carbachol

We investigated the effects of losartan, an AT 1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/l μl) into the LV blocked the pressor response induced by ANG II (12 ng/l μl) and carbachol (2 nmol/l μl). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 ± 1 and 28 ± 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 ± 1 and 5 ± 2 mmHg, respectively). The injection of ramipril (12 ng/l μl) prior to carbachol blocked the pressor effect of carbachol to 7 ± 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure.

Acute renal failure in renal allograft recipients and patients with native kidneys

In order to evaluate the role of underlying disease in the high mortality observed in acute renal failure (ARF) and risk factors related to the development of oliguric ARF in renal allograft recipients, two groups were selected: 34 patients with native kidneys, aged 16 and 57 years, and presenting ischemic ARF caused by cardiovascular collapse, with no signs of infection at the time of diagnosis; and 34 renal allograft recipients who developed ARF immediately after transplantation, without rejection. ARF was defined either as 30% increase of basal plasmatic creatinine in patients with native kidneys or non-normalization of plasmatic creatinine at day 5 after transplantation in renal allograft recipients; oliguria as diuresis ≤ 400 mL/24 h. There were no differences in age, male frequency, oliguria presence and duration, need for dialysis, and infection episodes for renal allograft recipients and patients with native kidneys. The development of sepsis (3% and 41%) and death rate (3% and 44%) were higher in patients with native kidneys (p < 0.01). The renal allograft recipients with both oliguric (n = 18) and nonoliguric (n = 16) ARF were evaluated and no difference was observed in the recipient's age, donor's age, cold ischemia time, time elapsed until plasmatic creatinine normalization, donor's plasmatic creatinine or urea, and mean arterial pressure. No differences were observed between the groups regarding frequency of infection episodes during ARF and frequency of death. In conclusion, renal allograft recipients presented a lower death rate and were less susceptible to sepsis. Cold ischemia time, age, and hemodynamic characteristics of the donor did not affect the development of oliguria.