Many people in diverse roles contribute to the success of animal welfare and research outcomes in laboratory animal research programs. These personnel include but are not limited to animal care and veterinary staff, researchers and their teams, facility management support, IACUC and compliance members, institutional officials, board members, vendors, security personnel, administrative staff, and all others involved in laboratory animal science programs. Any of these persons are potentially vulnerable to the moral stressors innate to working with animals in research, teaching, and testing. Moral stress occurs when one is aware of the ethical principles at stake, but external factors prevent action. 11 This situation can happen in any profession. 25 An example in our industry is the performance of euthanasia. This activity is considered moral stress and is regarded as one of the most significant contributors to the development of compassion fatigue. 11 Although it is difficult to identify a specific definition of compassion fatigue across professions, it can be described as "the reduced capacity in being empathetic and the consequent behaviors and emotions resulting from knowing about a traumatizing event experienced or suffered by a person" 20 and is characterized by deep physical and emotional exhaustion. 15 Compassion fatigue results in reduced empathy for others (coworkers and loved ones) and can diminish the quality of medical care delivered to animals. The term "compassion fatigue" has been used interchangeably with the terms 'burnout' and 'secondary traumatic stress,' but there are slight variations in their inherent meanings. Burnout is a cumulative process associated with increased workload and institutional stress 1 and is not necessarily due to trauma. 11,16 Secondary traumatic stress (also called vicarious trauma) can occur even when a traumatizing event is not directly experienced by a person, but simply by hearing about a traumatizing event

The appearance of oxidative products of NO (NO2- and NO3-) in peripheral blood of patients with acute MI is the result of their increased release from infarcted heart during the inflammatory phase of myocardial ischemia. Further studies are needed to define the clinical value of these observations.

U ndoubtedly, the veterinary medical field attracts individuals with high levels of compassion and empathy and the drive to care for others. With increased public recognition of the human-animal bond and the greater value placed on it, veterinarians and their staff members are increasingly expected to display high levels of consideration and compassion in the veterinary workplace. Individuals tend to enter and remain in the veterinary profession in part because of compassion satisfaction (the joy or sense of achievement found in helping others and providing high-quality patient care), 1,2 and overall, veterinarians and other animal caretakers report high levels of satisfaction in their work. 1,3,4 However, caring at such a high level can be associated with considerable personal and professional costs. Over time, repeated exposure to traumatic events in the lives of patients and their owners (eg, abuse, illness, trauma, and euthanasia), moral dilemmas, and occupational stressors can lead to compassion fatigue or burnout. Compassion fatigue, also known as vicarious trauma, secondary traumatic stress, or secondary victimization, is a result of medical caregivers' unique relationship with ill or dying patients and the empathy they feel. 2,5,6 Burnout, on the other hand, is related to interactions with the workplace environment and feelings of being ineffec-Taking stock and making strides toward wellness in the veterinary workplace

Nitric oxide (NO) is an endogenous vasodilator and modulator of inflammation. During endotoxemia, the beneficial effects of NO are overwhelmed by the inflammatory cascade, resulting in a functional depletion of NO. S-nitroso-albumin (S-NO-alb) exists as a novel and highly stable NO thiol complex that slowly releases NO into the vascular micro-environment. Using a porcine model, we examined the ability of intravenous S-NO-alb to modulate cardiopulmonary dysfunction characteristic of endotoxemia. Pigs were anesthetized, instrumented for standard cardiopulmonary function measurements, and randomly assigned to receive: (i) albumin + saline; (ii) albumin + LPS; or (iii) S-NO-alb + LPS. Cardiopulmonary parameters were evaluated every 30 min and ex vivo phorbol myristate acetate (PMA)-stimulated superoxide release was serially determined as a marker of in vivo neutrophil priming. Lung myeloperoxidase (MPO) activity was measured as a marker of neutrophil migration into the lung. LPS-induced cardiopulmonary dysfunction was characterized by a sustained elevation in mean pulmonary arterial pressure, pulmonary vascular resistance, and peak intratracheal pressure, as well as a reduction in cardiac index, stroke volume index and PaO(2) over 6 h. Pretreatment with S-NO-alb attenuated LPS-induced cardiopulmonary dysfunction without adversely affecting systemic hemodynamics. Moreover, S-NO-alb blunted the LPS-induced hypoxemic response and reduced neutrophil activation. S-NO-alb did not, however, attenuate LPS-induced increases in lung MPO. Our results suggest that S-NO-alb can selectively modulate endotoxin-induced pulmonary dysfunction, attenuate neutrophil priming and block the early mortality (40%) in this model.

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