Gastric myoelectrical and neurohormonal changes associated with nausea during tilt-induced syncope.

BACKGROUND: Nausea is a common prodromal symptom of neurally mediated syncope, but the biological factors linking nausea with syncope have not been studied. We aimed to characterize nausea during tilt-induced syncope by exploring related changes in gastric myoelectrical activity and plasma epinephrine, norepinephrine, and vasopressin concentrations across study phases of recumbency, tilt, syncope, and recovery. METHODS: Electrogastrographic and plasma hormone changes were compared between patients with tilt-induced syncope and nausea (n = 18) and control subjects (n = 6) without symptoms or hemodynamic changes during tilt-table testing. KEY RESULTS: Over a 4-minute period preceding syncope, sequential electrogastrography epochs demonstrated an increase over time in bradygastria (P = .003) and tachygastria (P = .014) power ratios, while the dominant frequency (P < .001) and the percent normogastria (P = .004) decreased. Syncope led to significant differences between cases and controls in electrogastrographic power ratios in each frequency range: bradygastria (P = .001), tachygastria (P = .005), and normogastria (P = .03). Nausea always followed electrogastrographic changes, and nausea resolution always preceded electrogastrographic normalization. Plasma vasopressin (676.5 ± 122.8 vs 91.2 ± 15.3 pg/mL, P = .012) and epinephrine (434 ± 91.3 vs 48.7 ± 2.5 pg/mL, P = .03), but not norepinephrine (P > .05), also differed with syncope between cases and controls. CONCLUSIONS AND INFERENCES: The nausea related to tilt-induced syncope is temporally associated with changes in gastric myoelectrical activity and increases in plasma vasopressin and epinephrine. The biological mechanisms that induce syncope are physiologically distinct from other experimental models of nausea such as illusory self-motion, yet nausea with syncope appears to have similarly associated electrogastrographic and hormone changes. Thus, tilt-induced syncope could serve as an informative experimental model for nausea research.

Suppression of multiple sclerosis in the rat during infection with Trichinella pseudospiralis.

Injection of the rat with guinea pig myelin basic protein (MBP) induces an inflammatory demyelination that leads to development of a condition mimicking human multiple sclerosis (MS), including severe depressions in mobility, coordination, and strength in the affected animal. This model was used to observe and compare the antiinflammatory effects of the intestinal and late migratory phases of infection with Trichinella pseudospiralis on development of MBP-induced, MS-like debilitation in rats. Animal performance was measured in an activity monitor and in a series of physical tests designed to assess animal coordination and strength. Uninfected animals injected with MBP showed declines in mobility, coordination, and strength typical for this model. These changes were similar in rats infected so that the intestinal phase of infection coincided with the peak of MBP-induced debilitation. Rats infected so that the late migratory phase of infection occurred during the period of peak MBP-induced debilitation showed significantly higher performance scores in mobility, coordination and strength compared to the latter 2 groups. These finding demonstrate the potency of the anti-inflammatory effects of elevations in host corticosteroids seen during the migratory phase of infection with T. pseudospiralis.