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Jay Gladden - DVM, DACVECC

Jay Gladden
Assistant Professor

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Anaphylaxis is characterized as a serious, generalized, allergic reaction that can be life threatening or even fatal, leading to cardiopulmonary arrest within minutes.  Anaphylaxis reactions are often associated with severe systemic signs including upper airway edema, bronchoconstriction, cardiopulmonary dysfunction, marked vasodilation, hypotension, increased vascular permeability and secondary hypovolemia leading to progressive anaphylactic shock. 

Over the last 13 years, I have acquired expertise in the emergent management of patients presenting with a number of life-threatening complications including those with presumed anaphylaxis. As I have managed a wide variety of species, given my keen interest in both companion and exotic animal emergency and critical care medicine, I truly appreciate the concept of one-health in the emergency setting. As anaphylaxis has a serious and devastating impact on all species, developing successful, yet practical, prognostic biomarkers and emergent interventions for the management of anaphylaxis in veterinary patients, would have important and far-reaching implications for humans and animals alike.

Anaphylaxis is a great model for furthering our understanding of the innate immune system’s role in critical illness. One of the key mediators of anaphylaxis, platelet activating factor (PAF), is thought to be an important factor in a number of disease states contributing to critical illness in both human and likely veterinary patients alike. PAF exerts its effects via its second messenger signaling cascade pathways that lead to systemic vasodilation, hypotension, increased vascular permeability and pro-inflammatory/coagulant disease states that span the spectrum of systemic inflammatory response syndrome (SIRS). PAF exerts these affects via binding to its platelet activating factor receptor (PAFr) that initiates second messenger pathways with a variety of biochemical outcomes.

PAF mediated shock in anaphylaxis appears to be primarily due to increases in constitutive nitric oxide synthetase (eNOS) and increased nitric oxide (NO) production. NO appears critical to PAF induced shock.  NO induces alterations in vascular tone leading to marked, systemic vasodilation associated with anaphylactic shock.  PAF antagonists or PAFr deficiency prevents fatal anaphylaxis in animal models. It is likely that these mechanisms contribute to other shock states in critical illness as well.

PAF’s biologic half-life is primarily determined by its inactivation via PAF acetylhydrolase (PAF-AH). PAF-AH rapidly inactivates PAF. Since PAF-AH plays a crucial role in the tight regulation of PAF levels, its inverse correlation with the severity of anaphylaxis underscores the importance of PAF inactivation in the prevention of anaphylaxis. In humans, serum PAF levels are significantly higher in patients with anaphylaxis compared to control groups and appear to correlate with the severity of anaphylaxis.  There is an inverse correlation of PAF levels and PAF-AH levels in human anaphylaxis patients. Patients with fatal anaphylaxis had overall significantly lower PAF-AH levels compared to control patients.

My research efforts are focused on understanding PAF’s roles in anaphylaxis and critical illness. By gathering more insight into the common mechanisms behind anaphylactic shock syndromes, potential future management strategies can be developed.  Future veterinary studies elucidating canine and feline PAF and PAF-AH levels in patients with anaphylaxis and critical illness are desperately needed to start unwinding the complex pathways associated with PAF induced illness in veterinary species.


  • DVM – North Carolina State University, 2002
  • BS – New Mexico State University, 1995

Board Certification

  • Diplomate of the American College of Veterinary Emergency Critical Care
  1. Gladden, J. 2013. Iatrogenic pneumothorax associated with inadvertent intrapleural NGT misplacement in two dogs. Journal of the American Animal Hospital Association.
  2. Gladden, J.N., Brainard, B.M., Shelton, J.L., Camus, A.C., Divers, S.J. 2010. Evaluation of isoeugenol for anesthesia in koi carp (Cyprinus carpio). American Journal of Veterinary Research.
  3. Hernandez-Divers, S.J., Hensel, P., Gladden, J., Hernandez-Divers, S.M., Buhlmann, K.A., Hagen, C., Sanchez, S., Latimer, K.S., Ard, M., Camus, A.C. 2009. Investigation of shell disease in map turtles (Graptemys spp.). Journal of Wildlife Diseases.
  4. Gladden, J.N. 2006. Clinical Management of Potential Ibuprofen Toxicosis in a South American Red-Footed Tortoise (Geochelone carbonaria). Veterinary Clinics of North America - Exotic Animal Practice.

General Research Interests

  • Anaphylaxis
  • Systemic Inflammatory Response (SIRS)
  • Role of Innate Immune System in Critical Illness
  • Role of Platelet Activating Factor (PAF) in Critical Illness
  • Role of Lipid Mediators in Critical Illness
  • Exotic Animal Emergency Critical Care Medicine

Research and Clinical Interests

  • Anaphylaxis
  • Systemic Inflammatory Response Syndrome (SIRS)
  • Role of Innate Immune System in Critical Illness
  • Role of Platelet Activating Factor (PAF) in Critical Illness
  • Role of Lipid Mediators in Critical Illness
  • Exotic Animal Emergency Critical Care Medicine


  • Clinical Reasoning