Effects of Ketamine/Xylazine and Pentobarbital Anesthesia on Cerebral Tissue Oxygen Tension, Blood Pressure, and Arterial Blood Gas in Rats

Author(s):  
Satoshi Taie ◽  
Steven B. Leichtweis ◽  
Ke Jian Liu ◽  
Minoru Miyake ◽  
Oleg Grinberg ◽  
...  
Author(s):  
M. Bush ◽  
J.P. Raath ◽  
D. Grobler ◽  
L. Klein

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (% O2Sa) = 49 % + 16 (mean + SD) and PaO2 = 4.666 + 1.200 kPa (35 + 9 mm Hg)), hypercapnic (PaCO2 = 8.265 + 1.600 kPa (62 + 12 mm Hg)) and acidaemic (pHa = 7.171 + 0.073 ). Base excess was -6.7 + 3.9 mmol/ℓ, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 + 5.465 kPa (164 + 41 mm Hg)) and tachycardic (HR = 107 + 31/min). Following nasal tracheal intubation and insufflation, the % O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged.Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the % O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.


2011 ◽  
Vol 15 (3) ◽  
pp. 585-592 ◽  
Author(s):  
Troels Halfeld Nielsen ◽  
Susanne I. Engell ◽  
Rikke Aagaard Johnsen ◽  
Mette K. Schulz ◽  
Oke Gerke ◽  
...  

2015 ◽  
Vol 3 ◽  
pp. 7-13
Author(s):  
Gareth Buckley ◽  
◽  
Daniela Bedenice ◽  
Katherine Holmes ◽  
Elizabeth Rozanski

1987 ◽  
Vol 252 (6) ◽  
pp. R1143-R1151
Author(s):  
H. J. Mangalam ◽  
D. R. Jones ◽  
A. M. Lacombe

The extreme elevation in plasma levels of free norepinephrine (NE) and free epinephrine (EP), which occurs during forced diving of ducks (Anas platyrhynchos), was studied before and after denervation of the adrenal glands. In intact animals both NE and EP concentration increased by up to two orders of magnitude in a 4-min dive but by a significantly lesser amount if the duck breathed O2 before the dive. Denervating the adrenal glands reduced the amounts of both catecholamines (CA) released during dives, plasma EP decreased to 10%, and NE to 50% of values obtained before denervation. Breathing O2 before a dive virtually eliminated CA release in denervates, indicating that hypoxia was the important non-neural releasing agent. Hypoxia was also the most important neural releasing agent compared with hypercapnia, acidosis, or hypoglycemia. Adrenal denervation did not cause significant changes in heart rate, blood pressure, arterial blood gas tensions, pH, or plasma glucose during dives, although denervation caused increased variation in some of these variables. In ducks CA release in dives is largely due to decreasing arterial O2 partial pressure, and full expression of the response is dependent on intact innervation of the adrenal gland.


2009 ◽  
Vol 111 (5) ◽  
pp. 988-1000 ◽  
Author(s):  
Tenille E. Ragoonanan ◽  
W Scott Beattie ◽  
C David Mazer ◽  
Albert K.Y. Tsui ◽  
Howard Leong-Poi ◽  
...  

Background Perioperative beta-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of beta-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). Methods Anesthetized rats were treated with metoprolol (3 mg x kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml x kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1alpha (HIF-1alpha) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. Results Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P < 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P < 0.05). Beta-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P < 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1alpha protein levels were increased in beta-blocked hemodiluted rats relative to hemodiluted controls (P < 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after beta-blockade and hemodilution. Conclusions Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute beta-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1alpha.


Author(s):  
Milad Shayan ◽  
Mohammad Sabouri ◽  
Leila Shayan ◽  
Shahram Paydar

ABSTRACTBackgroundTrauma is the third leading cause of death in the world and the first cause of death among people younger than 44 years. In traumatic patients, especially those who are injured early in the day, arterial blood gas (ABG) is considered a golden standard because it can provide physicians with important information such as detecting the extent of internal injury, especially in the lung. However, measuring these gases by laboratory methods is a time-consuming task in addition to the difficulty of sampling the patient. The equipment needed to measure these gases is also expensive, which is why most hospitals do not have this equipment. Therefore, estimating these gases without clinical trials can save the lives of traumatic patients and accelerate their recovery.MethodsIn this study, a method based on artificial neural networks for the aim of estimation and prediction of arterial blood gas is presented by collecting information about 2280 traumatic patients. In the proposed method, by training a feed-forward backpropagation neural network (FBPNN), the neural network can only predict the amount of these gases from the patient’s initial information. The proposed method has been implemented in MATLAB software, and the collected data have tested its accuracy, and its results are presented.ResultsThe results show 87.92% accuracy in predicting arterial blood gas. The predicted arterial blood gases included PH, PCO2, and HCO3, which reported accuracy of 99.06%, 80.27%, and 84.43%, respectively. Therefore, the proposed method has relatively good accuracy in predicting arterial blood gas.ConclusionsGiven that this is the first study to predict arterial blood gas using initial patient information(systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse rate (PR), respiratory rate (RR), and age), and based on the results, the proposed method could be a useful tool in assisting hospital and laboratory specialists, to be used.


2020 ◽  
Vol 47 (6) ◽  
pp. 849-851
Author(s):  
Tom Bleeser ◽  
Lennart Van Der Veeken ◽  
Sarah Devroe ◽  
Jan Deprest ◽  
Steffen Rex

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