Search Results
You are looking at 1 - 10 of 24 items for
- Author or Editor: Manuel Martin-Flores x
- Refine by Access: All Content x
Abstract
OBJECTIVE To evaluate effects of 2 levels of partial neuromuscular block on the ventilatory response to a hypercapnic challenge in anesthetized dogs and to evaluate effects of edrophonium for reversing partial neuromuscular block.
ANIMALS 6 healthy adult Beagles.
PROCEDURES Each dog was anesthetized twice with propofol and dexmedetomidine. End-tidal partial pressure of CO2 (Petco 2), tidal volume (Vt), and peak inspiratory flow (PIF) were measured during breathing at rest. Maximal Vt and PIF (Vt MAX and PIFMAX, respectively) in response to a hypercapnic challenge consisting of 10% CO2 inhaled for 1 minute were measured. Variables were measured before administration of atracurium (baseline), during moderate (train-of-four [TOF] ratio, 0.3 to 0.5) and mild (TOF ratio, 0.6 to 0.8) atracurium-induced neuromuscular block, and after neuromuscular block recovery (TOF ratio, ≥ 0.9) following administration of edrophonium or saline (0.9% NaCl) solution. Dogs for which any variable returned to < 80% of the baseline value were identified.
RESULTS Partial neuromuscular block increased Petco 2; it impaired Vt at rest and Vt MAX but not PIF at rest and PIFMAX. All variables except Petco 2 returned to baseline values when the TOF returned to ≥ 0.9. After recovery from neuromuscular block, significantly more dogs had a Vt MAX < 80% of the baseline value when edrophonium was not administered.
CONCLUSIONS AND CLINICAL RELEVANCE Partial neuromuscular block in anesthetized Beagles decreased spontaneous ventilation at rest and impaired the response to a hypercapnic challenge. Response to hypercapnic challenge might remain partially impaired after recovery of the TOF ratio to ≥ 0.9.
Abstract
OBJECTIVE To evaluate the potency of vecuronium and duration of vecuronium-induced neuromuscular blockade in dogs with centronuclear myopathy (CNM).
ANIMALS 6 Labrador Retrievers with autosomal-recessive CNM and 5 age- and weight-matched control dogs.
PROCEDURES Dogs were anesthetized on 2 occasions (1-week interval) with propofol, dexmedetomidine, and isoflurane. Neuromuscular function was monitored with acceleromyography and train-of-four (TOF) stimulation. In an initial experiment, potency of vecuronium was evaluated by a cumulative-dose method, where 2 submaximal doses of vecuronium (10 μg/kg each) were administered IV sequentially. For the TOF's first twitch (T1), baseline twitch amplitude and maximal posttreatment depression of twitch amplitude were measured. In the second experiment, dogs received vecuronium (50 μg/kg, IV) and the time of spontaneous recovery to a TOF ratio (ie, amplitude of TOF's fourth twitch divided by amplitude of T1) ≥ 0.9 and recovery index (interval between return of T1 amplitude to 25% and 75% of baseline) were measured.
RESULTS Depression of T1 after each submaximal dose of vecuronium was not different between groups. Median time to a TOF ratio ≥ 0.9 was 76.7 minutes (interquartile range [IQR; 25th to 75th percentile], 66.7 to 99.4 minutes) for dogs with CNM and 75.0 minutes (IQR, 47.8 to 96.5 minutes) for controls. Median recovery index was 18.0 minutes (IQR, 9.7 to 23.5 minutes) for dogs with CNM and 20.2 minutes (IQR, 8 to 25.1 minutes) for controls.
CONCLUSIONS AND CLINICAL RELEVANCE For the study dogs, neither potency nor duration of vecuronium-induced neuromuscular blockade was altered by CNM. Vecuronium can be used to induce neuromuscular blockade in dogs with autosomal-recessive CNM.
Abstract
OBJECTIVE
To evaluate the cardiovascular effects of atipamezole administered at half the volume or the same volume as dexmedetomidine to isoflurane-anesthetized cats.
ANIMALS
6 adult (1 to 2 years old) domestic shorthair cats (body weight, 3 to 6 kg).
PROCEDURES
Each cat was anesthetized with isoflurane and rocuronium 3 times; there was a 1-week washout period between successive anesthetic procedures. For each anesthetic procedure, dexmedetomidine (5 μg/kg) was administered IV. Five minutes after dexmedetomidine was administered, atipamezole (25 or 50 μg/kg) or saline (0.9% NaCl) solution was administered IM. Pulse rate, mean arterial blood pressure (MAP), cardiac output (CO), and systemic vascular resistance (SVR) were measured during anesthesia before dexmedetomidine administration (baseline), after dexmedetomidine administration, and 15, 30, 60, and 120 minutes after administration of atipamezole or saline solution. Pulse rate and MAP were also recorded when MAP was at its lowest value. Hemodynamic variables were compared among treatments at baseline, after dexmedetomidine administration, and after administration of atipamezole or saline solution. Effects of treatment and time on all variables were assessed with mixed-effects models.
RESULTS
Both doses of atipamezole resulted in a significantly lower MAP than did saline solution. Pulse rate, CO, and SVR were not significantly different among treatments after atipamezole or saline solution were administered.
CONCLUSIONS AND CLINICAL RELEVANCE
Atipamezole administered IM at half the volume or the same volume as dexmedetomidine was ineffective at increasing pulse rate or CO in anesthetized cats that received dexmedetomidine. However, atipamezole caused short-lasting but severe arterial hypotension.
Abstract
OBJECTIVE
To elucidate the cardiovascular effects of escalating doses of phenylephrine and norepinephrine in dogs receiving acepromazine and isoflurane.
ANIMALS
8 beagles aged 1 to 2 years (7.4 to 11.2 kg).
METHODS
All dogs received acepromazine 0.01 mg/kg, propofol 4 to 5 mg/kg, and isoflurane and were mechanically ventilated. Mean arterial pressure (MAP) from a femoral artery catheter and continuous electrocardiogram were recorded. Cardiac output (CO) was measured with transpulmonary thermodilution. Systemic vascular resistance (SVR), global end-diastolic volume (GEDV), and global ejection fraction (GEF) were subsequently calculated. Phenylephrine and norepinephrine were infused in random order at 0.07, 0.3, 0.7, and 1.0 μg/kg/min. All variables were measured after 15 minutes of each infusion rate. The effects of dose, agent, and their interaction on the change of each variable were evaluated with mixed-effect models. A P < .05 was used for significance.
RESULTS
Atrial premature complexes occurred in 3 dogs during norepinephrine infusion at doses of 0.3, 0.7, and 1 μg/kg/min; no dysrhythmias were seen with phenylephrine administration. MAP increased during dose escalation (P < .0001) within each agent and did not differ between agents (P = .6). The decrease in HR was greater for phenylephrine (P < .0001). Phenylephrine decreased CO and GEF and increased GEDV and SVR (all P < .03). Norepinephrine decreased the SVR and increased CO, GEDV, and GEF (all P < .03).
CLINICAL RELEVANCE
Our results confirm that phenylephrine increases arterial pressures mainly through vasoconstriction in acepromazine-premedicated dogs while norepinephrine, historically considered a vasopressor, does so primarily through an increase in inotropism.
Abstract
OBJECTIVE
To create a model of transient unilateral laryngeal paralysis (LP) that will allow the study of cricoarytenoideus dorsalis dysfunction and a method for quantification of varying degrees of LP in dogs.
ANIMALS
5 castrated male research Beagles.
PROCEDURES
Between January and February 2018, dogs were anesthetized and instrumented with a laryngeal mask airway and a flexible endoscope to record the rima glottidis. The left or right recurrent laryngeal nerve (RLn) was localized using ultrasonography and electrical stimulation, then conduction blockade was induced with perineural lidocaine. The normalized glottal gap area (NGGA) was measured before and every 15 minutes after the block. Inspired 10% carbon dioxide (CO2) was administered for 1 minute at each sampling time. The inspiratory increase in NGGA (total and each side) was measured at peak inspiration. The change in hemi-NGGA for the control side versus the anesthetized side was evaluated with a mixed-effect model.
RESULTS
During CO2 stimulation, the increase in inspiratory hemi-NGGA was consistently less (P < .001) for the treated side (–8% to 13%) versus the control side (49% to 82%). A compensatory increase (larger than at baseline) in the control hemi-NGGA was observed. The total NGGA remained unaffected.
CLINICAL RELEVANCE
Unilateral local anesthesia of the RLn produced transient unilateral LP with a compensatory increase in the hemi-NGGA for the contralateral side. This model could facilitate the evaluation of respiratory dynamics, establishment of a grading system, and collection of other important information that is otherwise difficult to obtain in dogs with LP.
Abstract
OBJECTIVE
To assess the performance of transpulmonary thermodilution (TPTD) using room-temperature saline (CORT) and waveform-derived continuous CO (CCO) compared with TPTD using iced saline (COICED) as the indicator for measurements of CO in isoflurane-anesthetized dogs.
METHODS
8 Beagles aged 1 to 2 years (7.4 to 11.2 kg) were enrolled in this experimental study from March 21 to 31, 2023. Dogs were anesthetized with 0.01 mg/kg acepromazine, 5 to 6 mg/kg propofol, and isoflurane and were mechanically ventilated. Dogs were instrumented with a central venous catheter and a femoral arterial catheter equipped with a thermistor. The COICED, CORT, and pulse wave-derived CCO values were obtained at baseline, during infusions of phenylephrine and norepinephrine, and during blood withdrawal and replacement. Data were analyzed with a mixed effect model, Bland-Altman plots, and concordance. Percent error was calculated. P < .05 was used for significance.
RESULTS
Data were collected from 8 dogs. Significant effects of time and the interaction of time and method were found. Bland-Altman plots showed negligible bias with limits of agreement between −0.35 and 0.25 L/min for CORT versus COICED and −1.23 and 1.15 L/min for CCO versus COICED. Percent errors were 17.7% and 66.6%, respectively. In the 4-quadrant plots, the concordance rate was 95% and 68% for measurements obtained with CORT and for CCO, respectively.
CONCLUSIONS
Transpulmonary thermodilution using room temperature saline was accurate and able to track changes in CO. Continuous CO had a large percent error and low tracking ability.
CLINICAL RELEVANCE
Transpulmonary thermodilution using room temperature saline is reliable for monitoring CO and obviates the need for iced preparations in clinical scenarios.
Abstract
Objective—To determine whether dogs that received eyedrops containing phenylephrine and scopolamine would have a higher mean arterial blood pressure (MAP) when anesthetized than would dogs that did not receive the eyedrops.
Animals—37 nondiabetic and 29 diabetic dogs anesthetized for phacoemulsification and 15 nondiabetic dogs anesthetized for corneal ulcer repair (control dogs).
Procedures—Medical records were reviewed to identify study dogs. Dogs undergoing phacoemulsification received 2 types of eyedrops (10% phenylephrine hydrochloride and 0.3% scopolamine hydrobromide) 4 times during a 2-hour period prior to the procedure. Control dogs did not receive these eyedrops. Heart rate and MAP were measured before surgery in all dogs 10 and 5 minutes before, at the time of (t0), and 5 (t5) and 10 (t10) minutes after atracurium administration.
Results—MAP was greater in the 2 groups that received the eyedrops than in the control group at t0 and t5; at t10, it was greater only for the nondiabetic dogs that received eyedrops. Nine nondiabetic dogs and 1 diabetic dog anesthetized for phacoemulsification had at least 1 MAP value > 131 mm Hg; 73% of MAP values > 131 mm Hg were detected within 10 minutes after atracurium administration. At no time did a control dog have an MAP value > 131 mm Hg.
Conclusions and Clinical Relevance—Anesthetized dogs pretreated with eyedrops containing phenylephrine and scopolamine had higher MAP values than dogs that did not receive the eyedrops, suggesting the drops caused hypertension. Atracurium may interact with the eyedrops and contribute to the hypertension.
Abstract
OBJECTIVE To evaluate whether the ultrashort-acting neuromuscular blocking agent gantacurium can be used to blunt evoked laryngospasm in anesthetized cats and to determine the duration of apnea without hemoglobin desaturation.
ANIMALS 8 healthy adult domestic shorthair cats.
PROCEDURES Each cat was anesthetized with dexmedetomidine and propofol, instrumented with a laryngeal mask, and allowed to breathe spontaneously (fraction of inspired oxygen, 1.0). The larynx was stimulated by spraying sterile water (0.3 mL) at the rima glottidis; a fiberscope placed in the laryngeal mask airway was used to detect evoked laryngospasm. Laryngeal stimulation was performed at baseline; after IV administration of gantacurium at doses of 0.1, 0.3, and 0.5 mg/kg; and after the effects of the last dose of gantacurium had terminated. Duration of apnea and hemoglobin oxygen saturation (measured by means of pulse oximetry) after each laryngeal stimulation were recorded. Neuromuscular block was monitored throughout the experiment by means of acceleromyography on a pelvic limb.
RESULTS Laryngospasm was elicited in all cats at baseline, after administration of 0.1mg of gantacurium/kg, and after the effects of the last dose of gantacurium had terminated. The 0.3 and 0.5 mg/kg doses of gantacurium abolished laryngospasm in 3 and 8 cats, respectively, and induced complete neuromuscular block measured at the pelvic limb; the mean ± SE duration of apnea was 2 ± 1 minutes and 3 ± 1.5 minutes, respectively. Hemoglobin oxygen saturation did not decrease significantly after administration of any dose of gantacurium.
CONCLUSIONS AND CLINICAL RELEVANCE Gantacurium may reduce tracheal intubation-associated morbidity in cats breathing oxygen.
Abstract
OBJECTIVE To evaluate the efficacy of each of 3 incremental doses of MK-467 for alleviation of dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats.
ANIMALS 6 healthy adult domestic shorthair cats.
PROCEDURES Each cat was anesthetized with isoflurane and received a target-controlled infusion of dexmedetomidine estimated to maintain the plasma dexmedetomidine concentration at 10 ng/mL throughout the experiment. Heart rate (HR) and direct arterial pressures were measured at baseline (isoflurane administration only), during dexmedetomidine infusion, and before and after IV administration of each of 3 serially increasing doses (15, 30, and 60 μg/kg) of MK-467. Cardiac index (CI) and systemic vascular resistance (SVR) were recorded at baseline, during dexmedetomidine infusion, and at the mean arterial pressure nadir after administration of the 30- and 60-μg/kg doses of MK-467.
RESULTS Compared with baseline values, the dexmedetomidine infusion significantly decreased HR and increased arterial pressures. Each dose of MK-467 caused a significant decrease in arterial pressures and a significant, albeit clinically irrelevant, increase in HR (≤ 10%). Following administration of the 30- and 60-μg/kg doses of MK-467, all cats developed clinical hypotension (mean arterial pressure, < 60 mm Hg) even though CI and SVR returned to baseline values.
CONCLUSIONS AND CLINICAL RELEVANCE Results indicated administration of small doses of MK-467 to isoflurane-anesthetized cats receiving dexmedetomidine restored CI and SVR, but caused a substantial decrease in arterial pressures and only a marginal increase in HR. Therefore, caution should be used when MK-467 is administered to alleviate dexmedetomidine-induced hemodynamic depression in isoflurane-anesthetized cats.
