scholarly journals Evaluation of cardiopulmonary parameters and recovery from anesthesia in cougars (Puma concolor) anesthetized with detomidine/ketamine and isoflurane or sevoflurane

2016 ◽  
Vol 36 (1) ◽  
pp. 33-38
Author(s):  
Verônica B. Albuquerque ◽  
Marcelo A. Araújo ◽  
Alice R. Oliveira ◽  
Guilherme Cavalcanti ◽  
Rodrigo C. Leal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Puma Concolor ◽  
Venous Pressure ◽  
Onset Time ◽  
Abdominal Ultrasound ◽  
Anesthesia Induction ◽  
Arterial Blood ◽  
Significant Difference ◽  
Recovery From Anesthesia

Abstract: The aim of this study was to assess the cardiopulmonary effects, the onset time after the administration of a detomidine/ketamine combination, and the recovery from anesthesia of cougars (Puma concolor) anesthetized with detomidine/ketamine and isoflurane or sevoflurane for abdominal ultrasound imaging. Fourteen animals were randomly allocated into two experimental groups: GISO (n=7) and GSEVO (n=7). Chemical restraint was performed using 0.15mg/kg detomidine combined with 5mg/kg ketamine intramuscularly; anesthesia induction was achieved using 2mg/kg propofol intravenously and maintenance with isoflurane (GISO) or sevoflurane (GSEVO). The following parameters were assessed: heart rate, respiratory rate, systolic and diastolic arterial blood pressure, mean arterial blood pressure, oxyhemoglobin saturation, rectal temperature, central venous pressure, and end-tidal carbon dioxide. The time to sternal recumbency (TSR) and time to standing position (TSP) were also determined. There was not statistically significant difference for the cardiopulmonary variables or TSP whereas TSR was significantly shorter in GSEVO. The time to onset of anesthesia was 11.1±1.2 minutes and 11.3±1.8 minutes for GISO and GSEVO, respectively. The anesthesia of cougars with detomidine/ketamine and isoflurane or sevoflurane was conducted with safety, cardiopulmonary stability, and increased time to sternal recumbency in the GISO group.

Some Cardiorespiratory Effects of Histamine, 5-Hydroxytryptamine, and Compound 48/80 in the Calf

1972 ◽  
Vol 50 (6) ◽  
pp. 545-553 ◽  
Author(s):  
A. J. Lewis ◽  
P. Eyre
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Toxic Response ◽  
Arterial Blood ◽  
Initial Rise ◽  
Significant Difference ◽  
Blood Histamine ◽  
Pulmonary Arterial ◽  
Cell Changes

The cardiorespiratory responses to histamine, 5-hydroxytryptamine, and compound 48/80 have been examined in the calf. The simultaneous measurement of whole blood histamine and plasma 5-hydroxytryptamine during compound 48/80 infusion showed significantly elevated levels that followed a biphasic pattern. However, mast cell changes in the sites examined were minimal and there was no significant difference in histamine concentrations in tissues examined. Marked systemic effects were observed and included an initial rise in femoral arterial blood pressure which was later followed by a terminal hypotension and death. Pulmonary arterial blood pressure and venous pressure were both elevated and dyspnoeic respiration was also evident. A combination of mepyramine and methysergide inhibited the toxicity of compound 48/80 which suggested that histamine and 5-hydroxytryptamine played a major role in the toxic response to this substance in the calf.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Cardiopulmonary baroreceptor control of muscle sympathetic nerve activity in heat-stressed humans

1999 ◽  
Vol 277 (6) ◽  
pp. H2348-H2352 ◽  
Author(s):  
C. G. Crandall ◽  
R. A. Etzel ◽  
D. B. Farr
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Whole Body ◽  
Nerve Activity ◽  
Arterial Blood

Whole body heating decreases central venous pressure (CVP) while increasing muscle sympathetic nerve activity (MSNA). In normothermia, similar decreases in CVP elevate MSNA, presumably via cardiopulmonary baroreceptor unloading. The purpose of this project was to identify whether increases in MSNA during whole body heating could be attributed to cardiopulmonary baroreceptor unloading coincident with the thermal challenge. Seven subjects were exposed to whole body heating while sublingual temperature, skin blood flow, heart rate, arterial blood pressure, and MSNA were monitored. During the heat stress, 15 ml/kg warmed saline was infused intravenously over 7–10 min to increase CVP and load the cardiopulmonary baroreceptors. We reported previously that this amount of saline was sufficient to return CVP to pre-heat stress levels. Whole body heating increased MSNA from 25 ± 3 to 39 ± 3 bursts/min ( P < 0.05). Central blood volume expansion via rapid saline infusion did not significantly decrease MSNA (44 ± 4 bursts/min, P > 0.05 relative to heat stress period) and did not alter mean arterial blood pressure (MAP) or pulse pressure. To identify whether arterial baroreceptor loading decreases MSNA during heat stress, in a separate protocol MAP was elevated via steady-state infusion of phenylephrine during whole body heating. Increasing MAP from 82 ± 3 to 93 ± 4 mmHg ( P < 0.05) caused MSNA to decrease from 36 ± 3 to 15 ± 4 bursts/min ( P < 0.05). These data suggest that cardiopulmonary baroreceptor unloading during passive heating is not the primary mechanism resulting in elevations in MSNA. Moreover, arterial baroreceptors remain capable of modulating MSNA during heat stress.

Functional Interaction between Angiotensin and Sympathetic Reflexes in Cats

1982 ◽  
Vol 62 (1) ◽  
pp. 51-56 ◽  
Author(s):  
R. Hatton ◽  
D. P. Clough ◽  
S. A. Adigun ◽  
J. Conway
Keyword(s):  
Blood Pressure ◽  
Central Venous Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Partial Recovery ◽  
Ang Ii ◽  
Central Venous ◽  
Efferent Nerve ◽  
Arterial Blood ◽  
Sympathetic Reflexes

1. Lower-body negative pressure (LBNP) was used to stimulate sympathetic reflexes in anaesthetized cats. At −50 mmHg for 10 min it caused transient reduction in central venous pressure and systemic arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. Central venous pressure showed only partial recovery. The resting level of plasma renin activity (PRA; 2.9–3.2 ng h−1 ml−1) did not change until approximately 5 min into the manoeuvre. 2. When converting-enzyme inhibitor (CEI) was given 75 s after the onset of suction it caused a greater and more sustained fall in arterial blood pressure than when administered alone. The angiotensin II (ANG II) antagonist [Sar1,Ala8]ANG II produced similar effects after a short-lived pressor response. 3. This prolonged fall in arterial blood pressure produced by CEI was not associated with reduced sympathetic efferent nerve activity. This indicates that the inhibitor affects one of the peripheral actions of angiotensin and in so doing produces vasodilatation of neurogenic origin. 4. These findings suggest that angiotensin, at a level which does not exert a direct vasoconstrictor action, interacts with the sympathetic nervous system to maintain arterial blood pressure when homeostatic reflexes are activated. A reduction in the efficiency of these reflexes by CEI may contribute to its hypotensive effect.

Measurement Of Bradykinin-Induced Venous Dilation By Ultrasound And Correlation With Heart Rate, Arterial And Venous Pressure And Endothelial Damage

1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Endothelial Damage ◽  
Whole Body ◽  
Arterial Blood

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.

scholarly journals Comparison of Use of Isoflurane or Sevoflurane for Anaesthesia Induced by Mask in Calves

2020 ◽  
Vol 48 ◽  
Author(s):  
Selvinaz Yakan ◽  
Ozgur Aksoy ◽  
Celal Sahin Ermutlu
Keyword(s):  
Blood Pressure ◽  
General Anaesthesia ◽  
Arterial Blood Pressure ◽  
Head Movements ◽  
Anaesthesia Induction ◽  
Sevoflurane Group ◽  
Arterial Blood ◽  
Isoflurane Group ◽  
Significant Difference ◽  
Swallowing Reflex

Background: Inhalation anaesthesia is an effective and reliable general anaesthesia method for inactivity, analgesia, and unconsciousness in extensive surgical procedures. Although widely used, especially in small animals, there are very few studies investigated the reliability and superiority of inhalation anaesthesia in surgical procedures for ruminants. This study intended to evaluate the anaesthetic effects of isoflurane and sevoflurane in different surgical cases with endotracheal intubation following the induction of anaesthesia using a calve-specific facemask, which is not yet a routine option in cattle.Materials, Methods & Results: The study was conducted on 14 calves, from new-born up to 3 months-old, that undergoing various surgical operations. The animals were divided into isoflurane and sevoflurane groups, and each group contained 7 animals. In all cases, atropine (0.04 mg/kg was administered intramusculer as premedication before 15 min from anaesthesia induction. For induction, the anaesthetic agent was given at an inspiratory concentration of 3-5% in the isoflurane group and at an inspiratory concentration of 5 - 7% in the sevoflurane group during 5 min via mask at 15min after atropine administration. In both groups, endotracheal intubation was performed (about 1-3 min) after of general anaesthesia symptoms starting. At 5min after induction, anaesthesia was continued at 1.5 - 3% in the isoflurane group and at 2.5 - 4% in the sevoflurane group during operation. The animals were monitored during anaesthesia and,  anaesthetic effect, reaction of the calve, pronounced side effects, Heart Rate (HR), Systolic Arterial Blood Pressure (SABP), Diastolic Arterial Blood Pressure (DABP), Mean Arterial Blood Pressure (MABP), Respiration Rate (RR), Pulse Rate (PR), Arterial Oxygen Saturation (SpO2) were recorded at before anaesthesia, the premedication period, 5, 15, 30, 45, 60, 75 and 90min of anaesthesia. During anaesthesia, from the clinical parameters, mucosal capillary refilling time was evaluated by applying finger pressure to the oral mucosa. Mucous membrane color was determined by observing the oral mucosa. The time for palpebral reflex and swallowing reflex disappearance was measured and processed into individual forms. Anaesthesia induction and reanimation times were determined and recorded in the forms. After the operation, the return of the swallowing reflex and the time to stand up were recorded. During the operation, urination, defecation, salivation, vomiting, animal reactions, the shape and duration of the reamination period were recorded. In the isoflurane group anaesthesia induction was 3.71 ± 0.28 min, head movements started and came to the sterno- abdominal position at 4.57 ± 0.36 min, got up at 8.71 ± 0.42 min without assistance, meanwhile. In sevoflurane group, anaesthesia induction was 2.57 ± 0.20 min, head movements started and came to the sterno- abdominal position at 3.86 ± 0.40 min, the time to stand up was determined as 6.43 ± 0.29 min. During anaesthesia, HR, SABP, DABP, MABP, RR, PR, SpO2 findings were within physiological acceptable limits in 2 groups. In terms of indicators, there were no obvious differences in either group. The results revealed no significant difference between groups during anaesthesia.Discussion: The isoflurane and sevoflurane anaesthesia used in this study provided an adequate anaesthetic effect in calves characterized by adequate analgesia and muscle relaxation without any complications. The results of our study revealed that there was no significant difference between isoflurane and sevoflurane in calves. Both anaesthetic agents can be used safely for general anaesthesia in calves.

Muscle chemoreflex causes renal vascular constriction

1996 ◽  
Vol 270 (3) ◽  
pp. H951-H956 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
J. E. Sulentic ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Sympathetic Nerve Activity ◽  
Vascular Conductance ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Blood ◽  
Significant Difference ◽  
Renal Vascular ◽  
Muscle Chemoreflex ◽  
Renal Sympathetic

The purpose of this study was to investigate the effects of the muscle chemoreflex on vascular conductance in innervated and denervated kidneys. During each experiment, six dogs ran at 10 km/h for 8-16 min, and the muscle chemoreflex was stimulated by reducing hindlimb blood flow (HLBF) (0%-74%) at 4-min intervals. Small reductions in HLBF did not cause changes in arterial blood pressure or renal vascular conductance. However, further reductions of HLBF caused increases in arterial blood pressure and decreases in renal vascular conductance. Decreases in renal vascular conductance occurred in the denervated kidneys when the HLBF was reduced below 1,500 +/- 215 ml/min and occurred in the innervated kidneys when HLBF was reduced below 1,402 +/- 161 ml/min. There was not a significant difference between the reductions in HLBF required to cause a decrease in vascular conductance in the innervated and denervated kidneys. These results demonstrate that reductions in HLBF cause decreases in renal vascular conductance, which are not dependent on renal sympathetic nerve activity.

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