Propofol-anesthetized Dogs Research Articles

Comparison of cardiorespiratory effects and perioperative analgesia efficacy of dexmedetomidine or fentanyl continuous infusion during ovariohysterectomy in propofol-anesthetized dogs

The present study aimed to compare the cardiorespiratory, perioperative analgesic and blood gas analysis of the constant rate infusion of dexmedetomidine or fentanyl in 16 female dogs undergoing to elective ovariohysterectomy. The dogs were premedicated with morphine (0.5 mg/kg) and dexmedetomidine (5 µg/kg) or acepromazine (0.05 mg/kg), both intramuscularly (IM), in GDEX or GFEN, respectively. After anesthesia induction with propofol intravenously (IV), animals of GFEN received bolus of fentanyl (2.5 µg/kg) IV followed by continuous rate infusion (CRI) (10 µg/kg/h) and the GDEX received bolus of saline solution 0.9% (corresponding volume of fentanyl) followed by CRI of dexmedetomidine (1 µg/kg/h) and anesthesia was maintained with propofol (0.22 mg/kg/min). In the end of surgery all animals were evaluated using the Glasgow composite measure pain scale (GCPS) and a visual analogue scale (VAS). Data was compared with a statistical p value > 0,05. The mean heart rate was statistically lower in GDEX when compared to GFEN (p = 0.0498): 54.25 ± 3.919 and 88.38 ± 8.766 beats per minute, respectively. Opposed, the average mean blood pressure was statistically higher in GDEX when compared to GFEN (p = 0.0021): 99.38 ± 8.551 and 80.75 ± 11.12 mmHg, respectively. The GDEX and GFEN, in the firsts 4 and 2 postoperative hours, respectively, presented values significantly higher than baseline in the GCPS, occurring analgesic rescues for both groups. It is concluded that both drugs in the proposed rates were safe and efficient for nociceptive control during intraoperative, however, failed to promote efficient postoperative analgesia.

Two levels of the inspired oxygen fraction in propofol-anesthetized dogs with high intracranial pressure: cardiopulmonary function

In the initial stage of traumatic brain injury, the use of 1.0 inspired oxygen fraction (FiO2) is indicated. However, high FiO2 has been correlated with atelectasis. Thus, the effects of FiO2= 1.0 and FiO2= 0.6 on the cardiopulmonary function in propofol-anesthetized dogs with high intracranial pressure (ICP) were evaluated. Eight dogs were anesthetized on two occasions, receiving, during controlled ventilation, an FiO2= 1 (G100) or an FiO2= 0.6 (G60). Propofol was used for induction (10mg.kg-1) followed by a continuous rate infusion (0.6mg.kg-1.minute-1). An increase in the ICP was induced by temporary obliteration of the right jugular vein (OJv) 50 minutes after induction of anesthesia. The measurement was taken twenty minutes after OJv (T0) and then at 15-minute intervals (T15 to T60). Alveolar oxygen partial pressure in G60 was lower than in G100 during the whole procedure. Alveolar-arterial oxygen gradient in G100 was greater than in G60 at T0 and at T60. No differences were observed for arterial oxygen partial pressure/inspired oxygen fraction ratio, arterial-to-alveolar oxygen pressure ratio, respiratory index, venous admixture, oxygen delivery, oxygen consumption, oxygen extraction, heart rate, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, stroke index and systemic vascular resistance index. In G100, mean arterial pressure at T0 was higher than at T45. In dogs with high ICP, the cardiopulmonary function was not influenced by the different FiO2 used.

Hematologic changes in propofol-anesthetized dogs with or without tramadol administration

Drugs commonly used in anesthesia practice may significantly alter the oxidative state of blood cells. This mechanism could contribute to the immune suppression that occurs transiently in the early postoperative period. Thus, we assessed the effects of continuous rate infusion (CRI) of propofol associated or not with tramadol on hematologic parameters in dogs. Eight adult mongrel dogs were anesthetized on 2 occasions, 15 d apart. Two groups were formed: control group (CG) and tramadol group (GT). Propofol was used for induction (10mg kg-1) followed by a CRI (0.7mg kg-1minute-1). The animals were positioned in lateral recumbency and mechanically ventilated with inspired oxygen fraction of 0.6. In TG, tramadol (2mg kg-1) followed by a CRI (0.5mg kg-1minute-1) was administered in dogs. In the CG the sodium chloride (NaCl) solution at 0.9% was administered followed by its CRI, in the same volume that was used in TG. The measurement was taken before anesthesia induction (Tbasal), 30 minutes after induction (T0) and then at 30-minute intervals (T30 to T60). Red blood cells, hematocrit, hemoblogin concentration and total leukocytes count decreased from T0 in both groups. In TG, lymphocytes count at Tbasal [1.86 (0.82) x103µl-1] was greater than at T0, T30 and T60 [0.96(0.50), 0.92(0.48) and 0.95(0.48) x103µl-1, respectively]. No significant differences were observed for platelets neutrophil, eosinophil, basophil and monocyte count. In dogs, propofol-anesthesia associated or not with tramadol promoted decrease in blood cell count and should be used with caution in immunossupressed patients.

Intracranial variables in propofol or sevoflurane-anesthestized dogs subjected to subarachnoid administration of iohexol

The effects of subarachnoid administration of iohexol on intracranial hemodynamic in dogs anesthetized with propofol or sevoflurane were evaluated. Thirty adult animals (10.9±2.9kg) were distributed into two groups: PG, where propofol was used for induction (10±0.5mg/kg), followed by a continuous rate infusion at 0.55±0.15mg/kg/hour, and SG, where sevoflurane was administered for induction (2.5 MAC) and for anesthetic maintenance (1.5 MAC). A fiberoptic catheter was implanted on the right superficial cerebral cortex to monitor intracranial pressure (ICP). After 30 minutes, cerebrospinal fluid (CSF) was collected at the cisterna magna and iohexol was injected. The measurements were performed before CSF collection (TA), after the iohexol injection (T0), and at 10-minute intervals (T10 to T60). Intracranial pressure decreased at T0 in SG. Cerebral perfusion pressure at T0 was higher than at TA, T50 and T60 in PG, but in SG, the mean value at T0 was higher than the ones from T20 to T60. Mean arterial pressure at T0 was higher than at TA in PG, while in SG, the values from T20 to T60 were lower than at T0. The heart rate at T60 was lower than at T0 in PG. Cardiac output at TA was lower than at T60 in SG. The cerebrospinal fluid collection and administration of iohexol promoted decrease in intracranial pressure in sevolflurane-anesthetized dogs and increase in cerebral perfusion pressure in propofol-anesthetized dogs.

Cough reflex in allergic dogs

This study investigated the effects of antigen challenge on the cough reflex in dogs that were neonatally sensitized to ragweed. Tidal volume (VT), respiratory rate (f), pulmonary resistance (RL), dynamic lung compliance (CDyn) and the number and amplitude (increase in mean peak expiratory pressure) of coughs induced by mechanical stimulation of the intrathoracic trachea were measured in propofol-anesthetized dogs. Aerosolized ragweed challenge had no effect to induce spontaneous cough but increased f and RL and reduced VT and CDyn. Mechanical stimulation of the intrathoracic trachea at this time produced 19±5 coughs with an average increase in cough amplitude of 11±1 cm H2O which differed significantly from the number (9±2 coughs) and amplitude (30±5.5 cm H2O) of mechanically induced coughs after treatment with aerosolized saline. Both the number and amplitude of mechanically induced coughs returned to baseline values by 24–48 h after the ragweed challenge. Similar results were obtained after challenge with aerosolized histamine (0.3–1% histamine) that did not induce spontaneous coughs but increased f, reduced VT and decreased CDyn and increased the number but reduced the amplitude of the mechanically induced coughs. In conclusion, both antigen and histamine bronchoprovocation changed the characteristics of the mechanically induced cough in dogs to a response of increased cough number but reduced mean expiratory cough amplitude.

A simple noninvasive method to measure the cough reflex in dogs

Introduction: This study describes a method to measure the cough reflex in dogs that is simple to perform, requires no surgical intervention, and can be used to profile efficacy and side effect liabilities of antitussive drugs. Methods: Experiments were performed in propofol-anesthetized dogs in which cardiopulmonary functions were noninvasively monitored before and after the induction of cough produced by spraying 0.75 ml of distilled water into the trachea. Results: The magnitude of the cough response, measured by the frequency and amplitude, was not different for individual dogs performed with repeated trials on different days. Treatment with the opioid antitussive drug, torbutrol (0.055–0.0055 mg/kg sc), inhibited the cough frequency but not the amplitude induced by the water challenge. Furthermore, side effects of torbutrol were identified as mild respiratory depression and an anesthetic-sparing effect with propofol. Discussion: This method offers many distinct advantages to evaluate efficacy of antitussive drugs including the fact that no surgery is required, it takes only 15–20 min to complete an experiment, and it can be used to simultaneously profile antitussive and side effect liabilities of drugs developed for the treatment of cough.

Pulmonary vascular effects of propofol at baseline, during elevated vasomotor tone, and in response to sympathetic alpha- and beta-adrenoreceptor activation.

This in vivo study had two primary objectives. The first goal was to determine whether the pulmonary vascular effects of propofol depend on the preexisting level of vasomotor tone, and the second was to investigate the effects of propofol on the pulmonary vascular responses to sympathetic alpha- and beta-adrenoreceptor activation. Thirty-one mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relation. Left lung autotransplantation (LLA) was also performed in eight additional dogs to induce a long-term increase in pulmonary vascular resistance. LPQ plots were measured on separate days in the conscious state and during propofol anesthesia. LPQ plots were measured at baseline and when vasomotor tone was acutely increased with the alpha agonist, phenylephrine, or the thromboxane mimetic, U46619. In separate experiments, cumulative dose-response curves to alpha- (phenylephrine) and beta- (isoproterenol) adrenoreceptor agonists were generated in conscious and propofol-anesthetized dogs. Compared with the conscious state, propofol had no effect on the baseline LPQ relation in normal or post-LLA dogs. However, propofol caused pulmonary vasoconstriction (P < 0.05) when vasomotor tone was acutely increased with either phenylephrine or U46619 in normal or post-LLA dogs. The pulmonary vasoconstrictor response to alpha-adrenoreceptor activation was potentiated (P < 0.05) during propofol anesthesia, whereas the pulmonary vasodilator response to beta-adrenoreceptor activation was not altered. These results indicate that the pulmonary vascular response to propofol anesthesia is tone-dependent. During sympathetic activation, propofol may favor alpha-adrenoreceptor-mediated vasoconstriction over beta-adrenoreceptor-mediated vasodilation.

The effects of thoracic epidural anesthesia on functional recovery from myocardial stunning in propofol-anesthetized dogs.

The purpose of this investigation was to examine the effects of thoracic epidural anesthesia (TEA) on myocardial stunning during propofol anesthesia. Six dogs were chronically instrumented for measurement of left atrial, aortic, and left ventricular pressure, maximal rate of increase of left ventricular pressure, and myocardial wall-thickening fraction (WTF). Myocardial blood flow was determined with colored microspheres. Experiments were performed on separate days with 1) 10 min of left anterior descending artery (LAD) ischemia during propofol anesthesia without TEA, and 2) 10 min of LAD ischemia during propofol anesthesia with TEA. WTF was measured as baseline (BL) prior to propofol anesthesia and at predetermined time points until complete recovery from stunning. Propofol anesthesia caused a significant decrease of WTF in the LAD-perfused myocardium (LAD-WTF) compared to BL in awake animals. LAD ischemia led to a further significant decrease of LAD-WTF. There were no significant differences in LAD-WTF between the two experimental conditions at any of the time points measured. TEA did not change subendocardial blood flow in nonischemic myocardium. During ischemia neither the subendocardial/subepicardial nor the occluded/normal zone blood flow ratio were affected by TEA. After myocardial ischemia during propofol anesthesia TEA does not affect functional recovery of stunned myocardium in dogs.

The Effects of Thoracic Epidural Anesthesia on Functional Recovery from Myocardial Stunning in Propofol-Anesthetized Dogs

The Effects of Thoracic Epidural Anesthesia on Functional Recovery from Myocardial Stunning in Propofol-Anesthetized Dogs