Partial Thromboplastin Time: Accurate Measurement Through Evidence-Based Practice.

At the University of Pittsburgh Medical Center's Hillman Cancer Center, multiple occurrences of critically elevated partial thromboplastin time (PTT) levels drawn by central venous access devices (implantable ports) were determined to be inaccurate. Root cause analysis revealed the institutional policy and staff education for collection did not support peripheral venipuncture for coagulation panels. Peer-reviewed literature and case studies were evaluated by the evidence-based practice council, and the data revealed that PTT levels yielded incorrect results when drawn through an implantable port. This suggested that peripheral venipuncture might be preferable.

Behavioral responses during the forced swim test are not affected by anti-inflammatory agents or acute illness induced by lipopolysaccharide.

Pro-inflammatory cytokines and other molecules traditionally associated with immune function have been implicated in mediating behavioral and physiological consequences of stressor exposure. There is also evidence that cytokines are aberrantly expressed in depressive populations, suggesting they may play an etiological role in the development of depression/despair-related processes. Thus, we conducted a series of experiments to determine whether agents known to suppress cytokine activity or inflammatory responses in the CNS would alter the normal progression of behavioral responses during the forced swim test (FST, an animal model of depression/behavioral despair). Adult male Sprague-Dawley rats were injected with indomethacin (1 or 10 mg/kg intraperitoneally (i.p.)), alpha-MSH (0.25 or 0.5 microg icv), or minocycline (20 or 40 mg/kg i.p.) prior to each day of the FST and behavioral assessments were performed. Injection of indomethacin, alpha-MSH, or minocycline had no effect on the development of the immobility response during the FST on either day of testing. In a second series of experiments, we examined whether behavioral responses during forced swim would be affected by acute illness induced by a single injection of lipopolysaccharide (LPS). Acute injection of LPS (10 or 100 microg/kg i.p.) had no effect on behavioral responding during the FST irrespective of when it was injected, despite pronounced reductions in social behavior following these same doses of LPS. From these studies, we conclude that (a) endogenous inflammatory mediators do not appear to be involved in the normal progression of behavioral responses during the FST, and (b) behavioral responses during the FST are not affected by acute systemic injection of LPS.

Exposure to forced swim stress does not alter central production of IL-1.

In recent years, there has been increasing recognition that pro-inflammatory cytokines play a role in behavioral and physiological alterations produced by exposure to psychological stressors. Indeed, increases in central IL-1 production have been observed following stressors such as inescapable tailshock and social isolation, while no changes in IL-1 have been observed following other stressors (e.g., exposure to a predator). The goal of the following work was to establish whether exposure to the forced swim test (FST), a commonly used animal model of behavioral despair/depression, leads to an increase in central or peripheral production of IL-1. Briefly, adult male Sprague-Dawley rats (n=8 per group) were forced to swim for 15-30 min (25 degrees C) and killed at various intervals (ranging from immediately to 24 h) following stressor termination. Brains (hippocampus, hypothalamus, posterior cortex) and multiple peripheral tissues (pituitary, adrenals, spleen, plasma) were then dissected and frozen for subsequent measurement of IL-1 using a commercially available enzyme-linked immunosorbent assay. No observable increases in IL-1 were found in rats that were forced to swim acutely, or in rats that were re-exposed to the forced swim stressor 24 h later. These data suggest that exposure to forced swim does not lead to an increase in central production of IL-1, suggesting that the central IL-1 system is unlikely to play a role in mediating behavioral consequences of this stressor. However, these data do not exclude the possibility that other pro-inflammatory cytokines (such as IL-6 and TNF-alpha) might be produced in response to forced swim exposure.