Mean Arterial Pressure In Dogs Research Articles

Computer-controlled closed-loop norepinephrine infusion system for automated control of mean arterial pressure in dogs under isoflurane-induced hypotension: a feasibility study.

Intra-operative hypotension is a common complication of surgery under general anesthesia in dogs and humans. Computer-controlled closed-loop infusion systems of norepinephrine (NE) have been developed and clinically applied for automated optimization of arterial pressure (AP) and prevention of intra-operative hypotension in humans. This study aimed to develop a simple computer-controlled closed-loop infusion system of NE for the automated control of the mean arterial pressure (MAP) in dogs with isoflurane-induced hypotension and to validate the control of MAP by the developed system. NE was administered via the cephalic vein, whereas MAP was measured invasively by placing a catheter in the dorsal pedal artery. The proportional-integral-derivative (PID) controller in the negative feedback loop of the developed system titrated the infusion rate of NE to maintain the MAP at the target value of 60 mmHg. The titration was updated every 2 s. The performance of the developed system was evaluated in six laboratory Beagle dogs under general anesthesia with isoflurane. In the six dogs, when the concentration [median (interquartile range)] of inhaled isoflurane was increased from 1.5 (1.5-1.5)% to 4 (4-4)% without activating the system, the MAP was lowered from 95 (91-99) to 41 (37-42) mmHg. In contrast, when the concentration was increased from 1.5 (1.0-1.5)% to 4 (4-4.8)% for a 30-min period and the system was simultaneously activated, the MAP was temporarily lowered from 92 (89-95) to 47 (43-49) mmHg but recovered to 58 (57-58) mmHg owing to the system-controlled infusion of NE. If the acceptable target range for MAP was defined as target MAP ±5 mmHg (55 ≤ MAP ≤65 mmHg), the percentage of time wherein the MAP was maintained within the acceptable range was 96 (89-100)% in the six dogs during the second half of the 30-min period (from 15 to 30 min after system activation). The median performance error, median absolute performance error, wobble, and divergence were - 2.9 (-4.7 to 1.9)%, 2.9 (2.0-4.7)%, 1.3 (0.8-1.8)%, and - 0.24 (-0.34 to -0.11)%·min-1, respectively. No adverse events were observed during the study period, and all dogs were extubated uneventfully. This system was able to titrate the NE infusion rates in an accurate and stable manner to maintain the MAP within the predetermined target range in dogs with isoflurane-induced hypotension. This system can be a potential tool in daily clinical practice for the care of companion dogs.

A Novel Etomidate Analog EL-0052 Retains Potent Hypnotic Effect and Stable Hemodynamics without Suppressing Adrenocortical Function.

Etomidate is a potent and rapidly acting anesthetic with high therapeutic index (TI) and superior hemodynamic stability. However, side effect of suppressing adrenocortical function limits its clinical use. To overcome this side effect, we designed a novel etomidate analog, EL-0052, aiming to retain beneficial properties of etomidate and avoid its disadvantage of suppressing adrenocortical steroid synthesis. Results exhibited that EL-0052 enhanced GABAA receptors currents with a concentration for EC50 of 0.98 ± 0.02 μM, which was about three times more potent than etomidate (3.07 ± 1.67 μM). Similar to hypnotic potency of etomidate, EL-0052 exhibited loss of righting reflex with ED50s of 1.02 (0.93-1.20) mg/kg in rats and 0.5 (0.45-0.56) mg/kg in dogs. The TI of EL-0052 in rats was 28, which was higher than 22 of etomidate. There was no significant difference in hypnotic onset time, recovery time, and walking time between EL-0052 and etomidate in rats. Both of them had minor effects on mean arterial pressure in dogs. EL-0052 had no significant effect on adrenocortical function in dogs even at a high dose (4.3 × ED50), whereas etomidate significantly inhibited corticosteroid secretion. The inhibition of cortisol synthesis assay showed that EL-0052 had a weak inhibition on cortisol biosynthesis in human H259 cells with an IC50 of 1050 ± 100 nM, which was 2.09 ± 0.27 nM for etomidate. EL-0052 retains the favorable properties of etomidate, including potent hypnotic effect, rapid onset and recovery, stable hemodynamics, and high therapeutic index without suppression of adrenocortical function. SIGNIFICANCE STATEMENT: The novel etomidate analog EL-0052 retains the favorable properties of etomidate without suppressing adrenocortical function and provides a new strategy to optimize the structure of etomidate.

Effect of oxygen supplementation on propofol anesthesia in acepromazine/tramadol premedicated dogs

Research in the area of injectable anesthetics in dogs requires mindfulness of ventilation, in order to supply artificial oxygen, which is often achieved with special equipment which may be unaffordable for veterinarians in developing countries. This study evaluated the effect of oxygen supplementation in dogs anesthetized with acepromazine-tramadol-propofol. Six Nigerian indigenous dogs were premedicated with intramuscular injection of acepromazine (0.03 mg/kg) and tramadol (5 mg/kg), followed by induction of anesthesia with propofol (4 mg/kg) IV 20 min later. Maintenance of anesthesia for 2 h was achieved with repeated bolus injections of propofol (2 mg/kg) at 10 min interval and anesthetized dogs breathed oxygen. This experimental trial was repeated a week later without oxygen supply as a control. Anesthetic indices, cardiopulmonary parameters, and rectal temperature were recorded at 10 min intervals for 2 h. Duration of anesthesia, duration of recumbency, time to extubation, and time to standing were not significantly (P > .05) different from their respective control values. Mean heart rate progressively decreased from the 60 min interval in both groups of anesthetized dogs. Mean arterial pressure in dogs with supplemented oxygen was similar to the control group. The mean oxygen-haemoglobin saturation was similar in both experimental trials. There was a progressive decrease in rectal temperature from the 60 min interval in both groups of anesthetized dogs. It was concluded that bolus injection of propofol, with and without supplemental oxygen, appeared to be efficacious and relatively safe in acepromazine-tramadol premedicated healthy dogs not undergoing any surgical or diagnostic procedures.

Dogs mean arterial pressure and heart rate responses during high propofol plasma concentrations estimated by a pharmacokinetic model

Propofol total intravenous anesthesia should provide stability of the cardiovascular system. In this study, mean arterial pressure and heart rate were evaluated in eight healthy dogs anesthetized with increasing rates of propofol. The cerebral state index (CSI) was studied as an additional parameter. Although the estimated propofol plasma concentration reached a maximal value of 15.3 μg ml −1, no hypotension or bradycardia were observed. Exploration of each animal’s data revealed high inter-individual variability regarding mean arterial pressure and heart rate. Considering the logarithmic of the concentration, a moderate depressant effect of propofol on mean arterial pressure was revealed in five dogs but the effect was not followed on heart rate.

Effects of SC-52458, an Angiotensin AT 1 Receptor Antagonist, in the Dog

We have previously reported on the basic pharmacologic properties of SC-52458 (5-[(3,5-dibutyl-1H-1,2,4-triazol-1-yl)methyl]-2-[2-(1H-tetrazol-5-ylphenyl)]pyridine), a novel angiotensin (AII) receptor antagonist that binds potently to AT 1 receptors in rat adrenal cortex and blocks AII-mediated contraction in isolated rabbit aorta. In the present study, the ability of SC-52458 to block AII pressor responses in conscious dogs was measured. In addition, we determined whether SC-52458 lowered mean arterial pressure in dogs with 2 kidney/1 clip renal hypertension when given daily for 4 days. In conscious, normotensive dogs, SC-52458 at 30 mg/kg orally, blocked the pressor response to AII (50 ng/kg, intravenously) with maximal inhibition (91%) observed 2 h after dosing. Plasma concentrations of SC-52458 measured by HPLC also were highest at the 2-h time point. After 24 h, the AII pressor response remained inhibited (by 35%) and SC-52458 was still measurable in plasma from treated dogs. In dogs made hypertensive by constriction of the left renal artery, SC-52458 lowered mean arterial pressure compared to vehicle treatment although heart rate was not different in the two groups. The maximal blood pressure lowering achieved with SC-52458 was similar to the maximal effect observed with the angiotensin converting enzyme inhibitor lisinopril. We conclude that SC-52458 blocks AII mediated pressor responses in normotensive, conscious dogs and SC-52458 is an efficacious antihypertensive agent in dogs with 2 kidney/1 clip renal hypertension.

Succinylcholine-Induced Increases in CSF Pressure Are Not Affected by PaCO2 or Mean Arterial Pressure in Dogs

The effects of PaCO2 and mean arterial pressure (MAP) on succinylcholine-induced changes in cerebrospinal fluid (CSF) pressure were examined in 31 dogs anesthetized with halothane (0.7% end-expired) and nitrous oxide (66% inspired) in oxygen. Group 1 (n = 9) received succinylcholine (1.5 mg/kg i.v.) without control of PaCO2 or MAP. Group 2 (n = 12) received succinylcholine with CO2 maintained at control, and no regulation of MAP. Group 3 (n = 10) received succinylcholine without regulation of PaCO2 and maintenance of MAP at control values with trimethaphan. Succinylcholine produced an increase in CSF pressure of 1.7 +/- 1.7-3.9 +/- 3.6 cm H2O (mean +/- SD). There were no differences in CSF pressure increase between groups. The increase in CSF pressure was compared to the variation in the uncontrolled physiological parameter (i.e., CSF pressure was compared to PaCO2 and MAP in group 1, MAP in group 2, and PaCO2 in group 3). The CSF pressure increase over time did not strictly parallel changes in PaCO2 and/or MAP, and the magnitude of increase of CSF pressure did not correlate significantly with PaCO2 and/or MAP. It is concluded that, in anesthetized dogs, succinylcholine produces relatively small increases in CSF pressure whether or not PaCO2 or MAP is controlled. These results do not support the hypothesis that a succinylcholine-induced increase in CSF pressure is due chiefly to an increase in PaCO2 and/or MAP and can be abolished by preventing those changes.

Circumferential External Counterpressure by Abdominal Wrapping and Its Effect on Simulated Intra‐abdominal Hemorrhage

Intra-abdominal hemorrhage was simulated by abdominal aortic cannulation through the femoral artery with shunting of blood into the peritoneal cavity via a transabdominal Foley catheter. Intravenous isotonic crystalloid fluid was administered to replace the blood lost. Hemorrhage was allowed to proceed to homeostasis with a compressive abdominal bandage in five dogs and without a bandage in three dogs. Placement of the compressive bandage decreased the fall in mean arterial pressure, slowed or stopped hemorrhage, slowed the rate of hemodilution, and increased survival time compared with unbandaged control dogs. Increases in pulmonary artery pressure and pulmonary capillary wedge pressure were not observed. Total peripheral resistance was elevated following wrapping. Cardiac index decreased in the bandaged group over time, but the change was not statistically significant. Cardiac index was significantly higher in the wrapped dogs. No gross abdominal organ damage was found. Compressive abdominal wraps composed of common bandaging materials were found to be effective in limiting blood loss and supporting mean arterial pressure in dogs with massive intra-abdominal hemorrhage. LTHOUGH FIRST investigated in 1903,' pneumatic

Dopamine reverses cardiovascular depression of toxic doses of pentobarbitone in dogs.

Pentobarbitone, 20 mg X kg-1 IV followed by infusion of 25 mg X kg-1 X hr-1, produced a progressive decrease in mean arterial pressure in dogs from 113 +/- 17 mmHg (SD) after one hour of infusion to 82 +/- 21 mmHg after 3.5 hours and to 49 +/- 22 mmHg after 5.5 hours. EEG silence occurred at 3.6 +/- 0.6 hours. In dogs similarly treated with pentobarbitone, a two hour infusion of dopamine 5 micrograms X kg-1 X min-1 beginning at the time of EEG silence prevented the further decrease in pressure and restored pressure to 87 +/- 18 mmHg. The mechanism for this effect of dopamine was an increase in cardiac output as systemic vascular resistance was unaffected by dopamine. The cardiac output increase was mainly the result of an increase in stroke volume as heart rate increased only slightly. Since reduced stroke volume was the main reason why pentobarbitone lowered blood pressure, the effect of dopamine on stroke volume and thus on blood pressure makes it an appropriate antagonist to the cardiovascular effects of toxic doses of pentobarbitone.

Reversal by acupuncture of cardiovascular depression induced with morphine during halothane anaesthesia in dogs.

The cardiovascular effects of morphine sulphate and/or acupuncture by means of electrocautery at Jen Chung (Go-26) were studied in 35 dogs. All animals were maintained under anaesthesia with halothane 0.75 per cent supplemented by the intravenous administration of succinylcholine to allow controlled ventilation during a two hour period of monitoring. Cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, [H+] (pH) PaCO2, PaO2 and base deficit were measured in each dog. Morphine 0.5 mg . kg-1, administered alone as a single bolus, significantly (P less than 0.05) decreased cardiac output, heart rate, mean arterial pressure, and significantly increased stroke volume and pulse pressure in dogs under halothane anaesthesia. Acupuncture by electrocautery alone induced a significant increase in cardiac output, stroke volume, heart rate, mean arterial pressure and pulse pressure with a significant decrease in total peripheral resistance following halothane. Acupuncture at Jen Chung (Go-26) for 10 minutes following the intravenous administration of morphine caused a significant increase in cardiac output, heart rate and mean arterial pressure with a significant decrease in central venous pressure and total peripheral resistance during halothane anaesthesia. The depressant effect of morphine on cardiac output, heart rate and mean arterial pressure in dogs under halothane anaesthesia appears to be reversed by acupuncture by electrocautery at Jen Chung (Go-26). Stimulation of this acupuncture locus could be helpful in resuscitating patients whose cardiovascular system is depressed by morphine and/or halothane anaesthesia.

Reduction of mean arterial pressure in dogs with chronic hypertension by pentobarbital.

Reduction of mean arterial pressure in dogs with chronic hypertension by pentobarbital.