
Luis Campoy
· Clinical Professor of Anesthesiology and Pain MedicineVerifiedCornell University · Clinical Sciences
Active 1999–2026
About
Luis Campoy, DVM (LV), ECVAA, MRCVS, is a Clinical Professor of Anesthesiology and Pain Medicine at Cornell University College of Veterinary Medicine. He specializes in developing and improving locoregional anesthetic techniques for all animal species, with a particular focus on dogs and horses. His research includes the development and application of anesthetic techniques aimed at ensuring safe and cost-effective outpatient surgery, as well as the creation of a Recovery Enhancing Device to assist horses during emergence from general anesthesia. Dr. Campoy earned his veterinary degree from Zaragoza University in Spain in 1995, followed by an internship in Veterinary Anaesthesia at Zaragoza University. He completed a residency in Veterinary Anaesthesia and Intensive Care at University College Dublin, Ireland, from 1998 to 2001, where he also served as a lecturer until 2005. He obtained his Certificate in Veterinary Anaesthesia from the Royal College of Veterinary Surgeons in 2000 and became a Diplomate of the European College of Veterinary Anaesthesia and Analgesia in 2004. Since 2005, he has been a faculty member at Cornell University, contributing extensively to the field through numerous publications in locoregional anaesthesia and analgesia across various species. Dr. Campoy has received multiple awards and honors, including the Association of Veterinary Anaesthetists Trust Award, the Langley Prize, and the AKORN ACVAA resident abstract award, and is actively involved in professional organizations such as the European College of Veterinary Anaesthesia and Analgesia, the Spanish Society of Veterinary Anaesthesia and Analgesia, and others.
Research topics
- Surgery
- Anesthesia
- Medicine
- Anatomy
Selected publications
American Journal of Veterinary Research · 2026-03-06
articleOpen accessObjective: To determine if sacrococcygeal epidural injection (SCEI) provides analgesia after feline ovariohysterectomy (OVH). Methods: Systemically healthy intact cats were randomly assigned to control or epidural groups (n = 29 each). After standard analgesic premedication IM, propofol induction, and OVH under isoflurane, the epidural group underwent SCEI [0.75 mL/kg total volume, 0.1 mg/kg preservative-free morphine, and 0.93 mg/kg preservative-free ropivacaine] using electrolocation. Extubation was 0 hours. A blinded anesthesiologist assessed pain using the Feline Grimace Scale and the short form of the Universidade Estadual Paulista-Botucatu multidimensional pain assessment scale (UFEPS-SF), as well as urination and pelvic limb neurological function, at 1, 2, 4, 6, 8, 12, and 20 hours. Rescue analgesia consisted of robenacoxib. Kaplan-Meier survival analyses estimated differences between groups in time to rescue analgesia, normal pelvic limb neurological function, and urination. The χ2-association test evaluated the need for robenacoxib. Linear mixed effects models with post hoc Tukey tests compared pain scores between groups and over time. Results: The SCEI had a significant effect on "survival" (robenacoxib unnecessary through 20 hours). Robenacoxib was required in 83% and 21% of cats in the control and epidural groups, respectively. Mean Feline Grimace Scale and (UFEPS-SF) scores were greater in the control group at 1 hour and 1 to 4 hours, respectively. Time to urination was significantly greater in the epidural group. Conclusions: The SCEI provides analgesia for up to 20 hours after OVH but delays urination. Clinical Relevance: The long duration of SCEI is similar to a single dose of an NSAID, providing a useful alternative if these are contraindicated.
Sacrococcygeal epidural injection provides analgesia after feline ovariohysterectomy (OVH)
Veterinary Anaesthesia and Analgesia · 2025-01-01
articlebioRxiv (Cold Spring Harbor Laboratory) · 2025-09-07
preprintOpen accessAbstract Background Polybrominated diphenyl ethers (PBDEs) are neuroendocrine disrupting chemicals that produce adverse neurodevelopmental effects. PBDEs have been implicated as risk factors for autism spectrum disorder (ASD), which is characterized by abnormal psychosocial functioning and is commonly accompanied by co-morbidities such as cognitive and attentional deficits. Here, we used a mouse model with translationally relevant exposure to establish direct causal evidence that maternal transfer of a commercial mixture of PBDEs, DE-71, produces ASD-relevant behavioral and neurochemical deficits in male offspring. Methods C57Bl6/N mouse dams were exposed to a commercial PBDE mixture, DE-71, via oral administration of 0 (vehicle control, VEH/CON), 0.1 (L-DE-71), or 0.4 (H-DE-71) mg/kg bw/d for 10 weeks, spanning three weeks prior to gestation through the end of lactation at postnatal day (PND) 21. Results Mass spectrometric analysis indicated dose-dependent transfer of PBDEs (in ppb) to brains of F1 male offspring at PND 30, with reduction in levels by PND 110. Adult F1 male offspring displayed ASD-relevant neurobehavioral phenotypes, including impaired short- and long-term social recognition memory (SRM), despite intact general sociability, and exaggerated repetitive behavior. Exposed mice also displayed altered olfactory discrimination of social odors, impaired novel object recognition memory, and reduced open field habituation. However, no changes were observed in anxiety-like, sensorimotor, or depressive-like behaviors relative to VEH/CON. At the molecular level, DE-71 exposed males displayed deregulated gene markers of prosocial neuropeptides. Oxt was upregulated in the paraventricular nucleus (PVN); Avp was upregulated in the PVN and bed nucleus of the stria terminalis (BNST) but downregulated in the lateral septum (LS); Avp1ar and Adcyap1 were upregulated in the BNST; and Adcyap1r1 was upregulated in the PVN, supraoptic nucleus (SON), and BNST. Conclusions These findings demonstrate that developmental PBDE exposure produces enduring behavioral and neurochemical phenotypes that resemble core domains of ASD, which may result from early neurodevelopmental reprogramming within central social and memory networks.
The Prevention and Management of Pain in Dogs
2025-07-25
otherOpen accessSenior authorThis chapter explores the fundamentals of acute and chronic pain management in dogs.The reader is directed to more comprehensive resources for discussions of pain neurobiology, neuropharmacology, and most drug doses.It is both the blessing and the curse of contemporary medicine that there exists an impressive array of tools in the pain management toolbox.What drug(s) should we use?In what order?In which combinations?For what type of pain?In which patients?At what dose?How often and S U M M A RYUndermanaged acute and chronic pain leads to a cascade of negative physiological, medical, and emotional consequences.Thus, the imperative for proper recognition, assessment, prevention, and treatment of pain is not only ethical but also physiological and medical.Fortunately, numerous pain management tools are available to the veterinarian to mitigate these effects and improve not only patient comfort but also overall recovery and quality (and often, length) of life.Unfortunately, it can be a challenge to know which treatment plan can best -and most safelymeet the needs of our patients.This chapter provides a succinct overview of the multimodal approach to the prevention and treatment of pain in dogs, using evidence-based veterinary medicine (EBVM) insofar as possible, and a consensus of expert opinion otherwise.Drug classes and modalities discussed include the following: nonsteroidal anti-inflammatory drugs (NSAID), opioids, alpha 2 agonists, locoregional anesthesia, subanesthetic ketamine, anti-nerve growth factor (NGF) monoclonal antibody, interventional modalities, and a variety of other pain-modifying analgesic drugs (PMADs) in common and emerging use.In addition, descriptions of other drugs possibly on the horizon for veterinary use (some based on use in human medicine) are included.Finally, evidence-based approaches to managing postsurgical and other varieties of chronic pain (osteoarthritis, osteosarcoma, and noninflammatory) are described, with sample cases to illustrate.
Veterinary Anaesthesia and Analgesia · 2025-03-11
articleSenior authorUltrasound-guided celiac plexus block increases intestinal motility in normal horses
American Journal of Veterinary Research · 2025-01-21 · 3 citations
articleOpen accessOBJECTIVE: To describe a technique for ultrasound-guided celiac plexus block in horses and characterize its effect on intestinal motility in healthy horses. METHODS: This study was conducted from January 2022 through June 2022. In phase 1 (dye study), an ultrasound-guided technique was optimized, and dye deposition around the celiac plexus branches was evaluated via postmortem dissection in 6 horses. In phase 2 (experimental study), 6 healthy horses were fasted and sedated with 0.6 mg/kg xylazine, IV (experiment 1). After a washout period, the ultrasound-guided celiac plexus block with lidocaine 1% (1.3 mg/kg) was performed after sedation (experiment 2). In both experiments, intestinal motility was recorded via transcutaneous ultrasound before sedation, after sedation (15, 30, and 45 minutes and 1, 2, 3, 4, and 6 hours), and 1 hour after refeeding. Ultrasound video recordings were blinded of horse identity, day, and time; randomly arranged; and scored using a specifically designed motility scoring system. RESULTS: Postmortem dissection confirmed dye deposition over the celiac plexus branches. In phase 2, a significant increase in intestinal motility was detected after the celiac plexus block compared to sedation alone, with a peak between 1 and 3 hours postblock (13.58 ± 2.8 vs 3.75 ± 2.4 at baseline); motility remained increased up to 6 hours. The only side effect observed was a transient hindlimb ataxia in 1 horse. CONCLUSIONS: Ultrasound-guided celiac plexus block is feasible and induces an increase in intestinal motility in healthy horses without significant complications. CLINICAL RELEVANCE: This technique can be considered in multimodal management of colic and paralytic ileus.
Physiology · 2025-05-01
articleThe prevalence of autism spectrum disorders (ASD) behaviors, marked by deficient social reciprocity and communication, has increased exponentially—now affecting 1 in 36 US children. Polybrominated diphenyl ethers (PBDEs) are flame retardants commonly detected in human tissues worldwide that have been associated with disrupted thyroid hormones (TH), hyperactivity, and lowered IQ in infants or toddlers. Our lab has previously shown that maternal transfer of PBDEs to female mice offspring produces deficits in social recognition memory, olfactory discrimination of social odors, and deregulated brain social neuropeptide genes. Our pilot data also show similar social behavioral deficits in exposed male offspring; however, the neuromolecular mechanisms are unknown. We tested the hypothesis that, in male mice, exposure to DE-71, a penta-PBDE mixture, alters olfactory discrimination, social stimuli signaling, and expression of prosocial neuropeptide gene markers for oxytocin (Oxt), vasopressin (Avp) and PACAP (Adcyap1) and/or their receptors Avp1ar, Oxtr, Adcyap1r1 in regions of the social brain network (SBN). Mouse dams were subjected to either 1) 0.1 mg/kg/d DE-71 (L-DE-71), 2) 0.4 mg/kg/d DE-71 (H-DE-71), or corn oil vehicle (VEH/CON) for 10 weeks with or without TH supplementation (T4, 5.7-9.9 ug/100g bw) administered from gestation day 12 to postnatal day 21. Adult male offspring were examined for their ability to discriminate social and non-social odors using the olfactory habituation/dishabituation test (OHT). Relative to VEH/CON, L-DE-71 males showed increased dishabituation for social odor 2. Using c-FOS immunohistochemistry, brain sections from VEH/CON male offspring exposed to 3 min of social stimulation showed increased c-Fos cell counts (normalized to ROI area) in the prelimbic (PrL) cortex, an area participating in social behavior. This number was reduced in socially activated L-DE-71 males and females but not L-DE-71+T4 females. Brain sections were micropunched to isolate RNA from specific anatomical regions. RT-qPCR was used to analyze expression of prosocial gene markers relative to ActB and group comparisons were made vs VEH/CON. Adcyap1r1 was upregulated in H-DE-71 of the supraoptic nucleus (SON) (p<.05, n=9-15) and paraventricular nucleus (PVN) (p<.05, n=9-12). Oxt was upregulated in L-DE-71 PVN (p<.05, n=9-13) and Oxtr was downregulated in L-DE-71 amygdala (AMG) (p<.05, n=12-16). Avp was upregulated in L-DE-71 in PVN (p<.05, n=10-13) and downregulated in both H-DE-71 AMG (p<.05, n=9-12) and L-DE-71 lateral septum (LS) (p<.05, n=9-10). These results suggest that developmental exposure to PBDEs reprogram circuits regulating olfactory discrimination and social cue signaling in a T4-dependent manner. Deregulated social neuropeptidergic systems resulting from environmentally-triggered neurodevelopmental reprogramming may contribute and serve as novel therapeutic targets for the mitigation of ASD. This work was supported by UCR Undergraduate Research Minigrant awards to NL and LC and RISE Fellowships to NL and NJ. This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-07-31 · 1 citations
preprintOpen accessAbstract Environmental toxicants that target the developing brain are suspected of contributing to autism spectrum disorder risk but causative evidence is lacking. We and others have shown that the indoor flame retardants, polybrominated diphenyl ethers (PBDEs), reduce prosocial behavior, however, few studies have assessed the central targets and underlying mechanisms. PBDEs are well established endocrine disruptors of the expanded thyroid system, which also regulates the prosocial neuropeptides oxytocin (OXT) and vasopressin (AVP) and their hypothalamic signaling. The potential role of PBDE-induced thyroid hormone (TH) deregulation in mediating disruption of central OXT and ASD-like social behavior deficits remains unmapped. To address this gap, we conducted a study in C57BL6/N mice that examined behavioral and neuromolecular reprogramming after developmental exposure to the commercial PBDE mixture, DE-71, and evaluated the therapeutic potential of TH supplementation. Dams were exposed daily during gestation and lactation to corn oil vehicle, low dose (0.1 mg/kg) and high dose (0.4 mg/kg) of DE-71 with or without concurrent L-thyroxine (+mT4). In offspring, dose-dependent ASD-relevant behavioral responses and central neuroendocrine OXT neuron depletion after developmental PBDE exposure was prevented with mT4. mRNA transcripts for the TH transporter Mct8 , deiodinase ( Dio3) and estrogen receptor beta ( Esr2 ) expressed on OXT neurons in PVH were upregulated in low dose females. In contrast, Mct8 and Dio3 were downregulated in low dose males. These findings uncover sex-specific mechanisms of PBDE-induced reprogramming of TH-regulated pathways in hypothalamic neuroendocrine cells leading to depleted central OXT signaling and ultimately ASD-relevant phenotypes. Importantly, we provide novel evidence of the therapeutic potential of maternal thyroid supplementation against toxicant-induced neurodevelopmental disorders.
Ultrasound‐Guided Saphenous Nerve Block
2024-02-09
otherOpen access1st authorCorrespondingUltrasound‐Guided (Distal) RUMM Block
2024-02-09
otherSenior author
Frequent coauthors
- 217 shared
Manuel Martin‐Flores
New York State College of Veterinary Medicine
- 179 shared
Robin D. Gleed
Cornell University
- 73 shared
Daniel M. Sakai
University of Georgia
- 48 shared
Jordyn M. Boesch
New York State College of Veterinary Medicine
- 32 shared
Joaquín Araos
- 26 shared
Chia T. Tseng
Carolina Veterinary Specialists
- 23 shared
Jonathan Cheetham
- 22 shared
Cheyenne J. Cannarozzo
Cornell University
Awards & honors
- Association of Veterinary Anaesthetists Trust Award (1998)
- Petsaver’s Resident in Veterinary Anaesthesia and Intensive…
- Certificate in Veterinary Anaesthesia from The Royal College…
- Diplomate, European College of Veterinary Anaesthesia and An…
- Recertified Diplomate, European College of Veterinary Anaest…
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