Publications by authors named "Laura Cagle"

6 Publications

  • Page 1 of 1

Role of Dual Oxidases in Ventilator-induced Lung Injury.

Am J Respir Cell Mol Biol 2021 02;64(2):208-215

University of California Lung Center, University of California, Davis, Davis, California.

Positive-pressure ventilation results in ventilator-induced lung injury, and few therapeutic modalities have been successful at limiting the degree of injury to the lungs. Understanding the primary drivers of ventilator-induced lung injury will aid in the development of specific treatments to ameliorate the progression of this syndrome. There are conflicting data for the role of neutrophils in acute respiratory distress syndrome pathogenesis. Here, we specifically examined the importance of neutrophils as a primary driver of ventilator-induced lung injury in a mouse model known to have impaired ability to recruit neutrophils in previous models of inflammation. We exposed and mice to low- or high-tidal volume ventilation with or without positive end-expiratory pressure (PEEP) and recruitment maneuvers for 4 hours. Absolute neutrophils in BAL fluid were significantly reduced in mice compared with mice (6.7 cells/μl; 16.4 cells/μl;  = 0.003), consistent with our hypothesis that neutrophil translocation across the capillary endothelium is reduced in the absence of DUOX1 or DUOX2 in response to ventilator-induced lung injury. Reduced lung neutrophilia was not associated with a reduction in overall lung injury in this study, suggesting that neutrophils do not play an important role in early features of acute lung injury. Surprisingly, mice exhibited significant hypoxemia, as measured by the arterial oxygen tension/fraction of inspired oxygen ratio and arterial oxygen content, which was out of proportion with that seen in the mice (141, 257,  = 0.012). These findings suggest a role for dual oxidases to limit physiologic impairment during early ventilator-induced lung injury.
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http://dx.doi.org/10.1165/rcmb.2020-0197OCDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7874397PMC
February 2021

Evaluation of pulse oximetry as a surrogate for PaO in awake dogs breathing room air and anesthetized dogs on mechanical ventilation.

J Vet Emerg Crit Care (San Antonio) 2019 Nov 18;29(6):622-629. Epub 2019 Oct 18.

Department of Veterinary Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA.

Objective: To evaluate the ability of arterial hemoglobin oxygen saturation measurement via pulse oximetry (SpO ) to serve as a surrogate for PaO in dogs.

Design: Two-part study: prospective observational and retrospective components.

Setting: University teaching hospital.

Animals: Ninety-two dogs breathing room air prospectively enrolled on a convenience basis. Retrospective evaluation of 1,033 paired SpO and PaO measurements from 62 dogs on mechanical ventilation.

Interventions: Dogs with concurrent SpO and PaO measured on room air had a data sheet completed with blood gas analysis. SpO , PaO , and FiO values were collected from medical records of dogs on mechanical ventilation.

Measurements And Main Results: Predicted PaO was calculated from SpO using the dog oxyhemoglobin dissociation curve. The correlation coefficient between measured and predicted PaO was 0.49 (P < 0.0001) in room air dogs and 0.74 (P < 0.0001) in ventilated dogs. In room air dogs, Bland-Altman analysis between measured minus predicted PaO versus the average showed a mean bias of -6.0 mm Hg (95% limit of agreement, -35 to 23 mm Hg). The correlation coefficient between PaO /FiO and SpO /FiO ratios was 0.76 (P < 0.0001). After combining data sets, receiver operating characteristic curve analysis showed the optimal cutoff value for detecting hypoxemia (PaO  < 80 mm Hg) was an SpO of 95%, with sensitivity and specificity of 77.8% and 89.5%, respectively. Using this cutoff, 6.9% of SpO readings failed to detect hypoxemia, whereas 7.2% predicted hypoxemia that was not present.

Conclusions: The SpO was not clinically suitable as a surrogate for PaO , though it performed better in mechanically ventilated dogs. As sensitivity for the detection of hypoxemia was poor, pulse oximetry does not appear to be an acceptable screening test. The SpO /FiO ratio may have value for evaluation of anesthetized dogs on supplemental oxygen. Arterial blood gas analysis remains ideal for assessment of oxygenation.
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http://dx.doi.org/10.1111/vec.12898DOI Listing
November 2019

Severe hypernatremia and transient azotemia in a cat following inadvertent intravenous administration of a commercial polyethylene glycol solution.

J Vet Emerg Crit Care (San Antonio) 2019 Nov 31;29(6):690-695. Epub 2019 Aug 31.

Department of Veterinary Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA.

Objective: To describe the clinical signs, clinicopathologic abnormalities, treatment, and outcome after IV administration of polyethylene glycol 3350 (PEG3350) in a cat.

Case Summary: A cat was inadvertently administered 6 g/kg of PEG3350 in electrolyte solution, IV, resulting in severe hypernatremia (203 mmol/L), diffuse encephalopathy, hemolysis, and moderate azotemia. The hemolysis and acute kidney injury observed immediately following PEG3350 administration resolved with supportive care. Administration of IV and oral electrolyte-free water slowly corrected the hypernatremia and the neurologic signs subsequently improved. Complete resolution of clinical signs was documented one month following hospital discharge. The PEG3350 concentrations in serum, plasma, and urine samples confirmed toxic exposure to PEG3350. Efficacy of treatment was evident by decreasing concentrations of PEG3350 in serum after the first 24 hours of treatment. Renal elimination of PEG3350 was significant and PEG3350 was still detected in the urine 17 days after exposure.

New Information Provided: This is the first report to describe the clinical signs and clinicopathologic abnormalities in a cat intoxicated with IV PEG3350. Potential pathophysiologic mechanisms are discussed, and the successful supportive medical treatment is outlined.
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http://dx.doi.org/10.1111/vec.12888DOI Listing
November 2019

Effects of positive end-expiratory pressure and recruitment maneuvers in a ventilator-induced injury mouse model.

PLoS One 2017 7;12(11):e0187419. Epub 2017 Nov 7.

Center for Comparative Respiratory Biology and Medicine, University of California, Davis, Davis, CA, United States of America.

Background: Positive-pressure mechanical ventilation is an essential therapeutic intervention, yet it causes the clinical syndrome known as ventilator-induced lung injury. Various lung protective mechanical ventilation strategies have attempted to reduce or prevent ventilator-induced lung injury but few modalities have proven effective. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury.

Objectives: To evaluate the effects of positive end-expiratory pressure and recruitment maneuvers in reducing lung injury in a ventilator-induced lung injury murine model in short- and longer-term ventilation.

Methods: 5-12 week-old female BALB/c mice (n = 85) were anesthetized, placed on mechanical ventilation for either 2 hrs or 4 hrs with either low tidal volume (8 ml/kg) or high tidal volume (15 ml/kg) with or without positive end-expiratory pressure and recruitment maneuvers.

Results: Alteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation. Standardized histology scores, influx of bronchoalveolar lavage albumin, proinflammatory cytokines, and absolute neutrophils were significantly higher in the high-tidal volume ventilation group at 4 hours of ventilation. Application of positive end-expiratory pressure resulted in significantly decreased standardized histology scores and bronchoalveolar absolute neutrophil counts at low- and high-tidal volume ventilation, respectively. Recruitment maneuvers were essential to maintain pulmonary compliance at both 2 and 4 hrs of ventilation.

Conclusions: Signs of ventilator-induced lung injury are evident soon after high tidal volume ventilation (as early as 2 hours) and lung injury worsens with longer-term ventilation (4 hrs). Application of positive end-expiratory pressure and recruitment maneuvers are protective against worsening VILI across all time points. Dynamic compliance can be used guide the frequency of recruitment maneuvers to help ameloriate ventilator-induced lung injury.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0187419PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5675408PMC
November 2017

Injectable Anesthesia for Mice: Combined Effects of Dexmedetomidine, Tiletamine-Zolazepam, and Butorphanol.

Anesthesiol Res Pract 2017 22;2017:9161040. Epub 2017 Jan 22.

Division of Pulmonary, Critical Care, and Sleep Medicine, School of Medicine, University of California, Davis, CA, USA.

Anesthetic protocols for murine models are varied within the literature and medetomidine has been implicated in the development of urethral plugs in male mice. Our objective was to evaluate the combination of butorphanol, dexmedetomidine, and tiletamine-zolazepam. A secondary objective was to identify which class of agent was associated with urethral obstructions in male mice. BALB/c male ( = 13) and female ( = 23) mice were assigned to dexmedetomidine and tiletamine-zolazepam with or without butorphanol or to single agent dexmedetomidine or tiletamine-zolazepam. Anesthesia was achieved in 58% (14/24) of mice without butorphanol and in 100% (24/24) of mice with butorphanol. The combination of dexmedetomidine (0.2 mg/kg), tiletamine-zolazepam (40 mg/kg), and butorphanol (3 mg/kg) resulted in an induction and anesthetic duration of 12 and 143 minutes, respectively. Urethral obstructions occurred in 66% (25/38) of trials in male mice that received dexmedetomidine with a mortality rate of 38% (5/13). Tiletamine-zolazepam, when used alone, resulted in a 0% (0/21) incidence of urethral obstructions. Combination use of dexmedetomidine, tiletamine-zolazepam, and butorphanol results in a longer and more reliable duration of anesthesia than the use of dexmedetomidine and tiletamine-zolazepam alone. Dexmedetomidine is not recommended for use in nonterminal procedures in male mice due to the high incidence of urethral obstructions and resultant high mortality rate.
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http://dx.doi.org/10.1155/2017/9161040DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5292157PMC
January 2017

Concurrent occipital hypoplasia, occipital dysplasia, syringohydromyelia, and hydrocephalus in a Yorkshire terrier.

Authors:
Laura Cagle

Can Vet J 2010 Aug;51(8):904-8

Atlantic Veterinary Hospital, University of Prince Edward Island, 550 University Avenue, Charlottetown, Prince Edward Island C1A 4P3.

Magnetic resonance imaging of a 7.5-year-old neutered male Yorkshire terrier with mild generalized ataxia and intermittent neck scratching led to a diagnosis of caudal occipital malformation and syringohydromyelia. Surgical exploration led to a diagnosis of occipital dysplasia with concurrent occipital hypoplasia. Following a dorsal laminectomy of the first cervical vertebra there was no progression or improvement a month later.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905018PMC
August 2010
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