Blood sugar, serum insulin and serum non-esterified fatty acid levels during thiopentone anaesthesia in dogs

Toso, Carlos E Reyes; Rodríguez, Rosalía; Renauld, A; Sverdlik, Rita C.; Linares, Laura

doi:10.1007/bf03009316

Cited by 10 publications

(7 citation statements)

References 28 publications

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“…Decreased TG concentrations from 3 to 32 hr after the operation in control dogs were supposed to be the influence of anesthesia and/or operation. Decreased NEFA concentrations in two groups at 3 hr might be due to anesthesia [25] and increased concentration at 16 hr might be associated with the influence of operation.…”

Section: Discussionmentioning

confidence: 95%

Lipoprotein Profile in Canine Pancreatitis Induced with Oleic Acid.

Chikamune

Katamoto

Nomura

et al. 1998

The Journal of Veterinary Medical Science

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ABSTRACT. Lipid and lipoprotein concentrations and apolipoprotein profile were investigated in canine pancreatitis induced by infusion with oleic acid (OA) into the accessory pancreatic duct. Pancreatitis was diagnosed by physical, hematological, biochemical and pathological examinations. In OA-treated dogs, serum triglyceride (TG) concentration was increased; however, there were no changes in serum total cholesterol (TC) and phospholipid (PL) concentrations. Serum concentrations of TG, TC, PL and total lipids (TL) in beta lipoprotein and those of TC, PL and TL in pre-beta lipoprotein were increased and those of TC, PL and TL in alpha 1 lipoprotein were decreased. In apolipoprotein profile, the proportions of apolipoprotein B100 in low density lipoprotein fraction and apolipoprotein A-IV in high density lipoprotein fraction were increased. In addition, decreased proportion of apolipoprotein A-I and the appearance of serum amyloid A protein in high density lipoprotein fraction were observed. These results suggest that lipoprotein profiles observed in canine acute pancreatitis are attributed to the alterations in apolipoprotein compositions. -KEY WORDS: apolipoprotein, canine, lipid, lipoprotein, pancreatitis.J. Vet. Med. Sci. 60(4): 413-421, 1998 in clinical pancreatitis [15,27], increase of TG are not observed in these experimentally induced pancreatitis [4,27]. Therefore, hyperlipidemia in acute pancreatitis might not be reproduced by ligation of pancreatic duct and infusion with mixture of bile and trypsin. In this study, induction of canine acute pancreatitis was attempted by the infusion with oleic acid (OA) into pancreatic duct. Hyperlipidemia is brought by changes of lipoprotein metabolism. Apolipoproteins are structural proteins and participate in lipoprotein metabolism. Changes of apolipoprotein composition bring about abnormality in lipoprotein metabolism. Analysis of apolipoprotein is important to understand the changes of lipoprotein metabolism; however, there is no report on serum apolipoprotein profile in canine pancreatitis. The purpose of this study is to examine the effects of acute pancreatitis induced with OA on serum lipid and lipoprotein concentrations and apolipoprotein profile in dogs. MATERIALS AND METHODSExperimental animals: Eight male beagle dogs, weighing 10.5 to 14.5 kg and aged over one year were used. These dogs were divided into two groups. OA-treated dogs were injected with OA (Sigma Chemical Co., U.S.A.) and control dogs were injected with physiological saline (PS; Otsuka Seiyaku Co., Ltd., Tokyo).Surgical manipulation and inducing pancreatitis: Operative procedures were performed on the dogs after premedication with atropine sulfate (Tanabe Seiyaku Co., Ltd., Osaka) and xylazine hydrochloride (Bayer Japan Co., Ltd., Tokyo) and induction with sodium thiamylal (Yoshitomi Seiyaku Co., Ltd., Osaka) and under inhalation anesthesia with isoflurane (Dainabot Co., Ltd., Tokyo). Laparotomy through a midline approach and duodenotomy was done. A flexible 22-gauge needle was inserted via...

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Section: Discussionmentioning

confidence: 95%

Lipoprotein Profile in Canine Pancreatitis Induced with Oleic Acid.

Chikamune

Katamoto

Nomura

et al. 1998

The Journal of Veterinary Medical Science

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“…Barbiturates are known to induce hyperglycemia and produce disturbances of glucose and FFA metabolism. [11][12][13][14] Benzodiazepines and xylazine have hyperglycemic effects as well. 15,16 Hyperglycemia can be induced in mice 17 and rats 18 by administration of chlorpromazine, which is a phenothiazine that is structurally related to acepromazine and used as an antipsychotic agent.…”

Section: Discussionmentioning

confidence: 99%

Investigation of the effect of acepromazine on intravenous glucose tolerance tests in dogs

Ionut

Kirkman²,

Bergman³

2004

ajvr

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“…These differences may be due to differences in the experimental set up, including the use of anesthesia, sampling route, vehicle, dose range, and in the kinetics. According to Kanaris et al (1975), Renauld and Sverdlik (1975) and Reyes Toso et al (1993) the metabolism of NEFA may be perturbed by barbiturate anesthesia, so it is noteworthy that CarballoJane et al (2007) used conscious rats while our rats were anaesthetized with Na-thiobutabarbital. Furthermore, venous blood samples were used by Carballo-Jane et al (2007) whereas we collected arterial blood samples.…”

Section: Isaksson and Othersmentioning

confidence: 96%

Turnover Modeling of Non-Esterified Fatty Acids in Rats after Multiple Intravenous Infusions of Nicotinic Acid

et al. 2009

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The objective of this investigation was to use a pharmacokinetic (PK)/pharmacodynamic (PD) approach to describe and evaluate a PK model of nicotinic acid (NiAc) in guinea pigs and a PD feedback model of changes in non-esterified fatty acid (NEFA) concentrations in rats following multiple intravenous infusions of NiAc at different rates and durations of inhouse and literature (NEFA after extravascular NiAc dosing) data. Serial arterial blood samples were taken for evaluation of NiAc exposure in guinea pigs and NEFA in rats. The biophase kinetics of NiAc was assumed to impact on NEFA turnover with feedback incorporated via an inhibitory moderator compartment. The response acted linearly on the production of moderator, which then acted inversely on the turnover rate of response. The potency, expressed as the amount of NiAc in the biophase causing a 50 % inhibitory effect (ID(50)), was 6.5 nmol +/- 31 % and the half-life of response (t(1/2, kout)) 2 min +/- 18 %. The half-life of tolerance (t(1/2, ktol)) was 9 min +/- 27 %. The model can be used to provide information about factors that determine the time course of NEFA response following different rates and routes of administration of NiAc or NiAc analogues.

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Blood sugar, serum insulin and serum non-esterified fatty acid levels during thiopentone anaesthesia in dogs

Cited by 10 publications

References 28 publications

Lipoprotein Profile in Canine Pancreatitis Induced with Oleic Acid.

Lipoprotein Profile in Canine Pancreatitis Induced with Oleic Acid.

Investigation of the effect of acepromazine on intravenous glucose tolerance tests in dogs

Turnover Modeling of Non-Esterified Fatty Acids in Rats after Multiple Intravenous Infusions of Nicotinic Acid

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