Testing a virtual reality intervention for pain control.

BACKGROUND: This study aimed (1) to assess the validity of a virtual reality (VR) intervention designed specifically to gain control over pain, (2) to test whether the association between the virtual environment and pain can be potentiated using a differential conditioning procedure, and (3) to examine the effects of this VR intervention in a cold pressor experiment. METHODS: The VR intervention was based on a figure representing pain. This figure could be manipulated until reaching a no-pain state. Participants were 64 undergraduate students, who were asked to evaluate this environment in terms of arousal and valence. A differential conditioning procedure was then applied, in which the pain figure was paired with electric shock and the no-pain figure was presented without shock. Afterwards, participants performed a cold pressor task. RESULTS: In the initial testing, the pain figure was evaluated as more arousing and more unpleasant than the no-pain figure. After the conditioning procedure, these ratings significantly increased; with the pain figure being rated as more anxiety eliciting and a better predictor of shocks than the no-pain figure. During cold pressor, the interaction with the conditioned VR figure led to significant increases in pain threshold and tolerance, as well as a significantly greater underestimation of time, but it did not affect pain intensity. CONCLUSIONS: These results provide preliminary support for the use of our VR intervention to gain control over pain.

Pheochromocytoma in a pregnant woman with multiple endocrine neoplasia type 2a.

Pheochromocytoma is a rare cause of hypertension. Its coexistence with pregnancy is exceptional and laparoscopic removal has rarely been reported. We describe the case of a 34-year-old woman with multiple endocrine neoplasia type 2a (MEN 2a) with adrenal pheochromocytoma diagnosed in the 6th week of pregnancy. After pretreatment with phenoxybenzamine, a successful transperitoneal laparoscopic adrenalectomy was performed in the twentieth week of gestation. The management of pheochromocytoma in pregnancy and the indications for laparoscopic surgery in pregnant patients are discussed.

Pulmonary response to free fatty acid intravenous infusion in the rabbit: role of leukotrienes and the effect of prostacyclin.

Intravenous infusion of free fatty acid (FFA) 20 mg.kg-1.min-1 produces pulmonary edema, hypoxemia, hyperventilation and increase in the alveolar surfactant content in rabbits in less than 15 min. We tried to study the role of leukotrienes (LT) and the effects of PGI2 in pulmonary response to FFA. We used Piriprost an inhibitor of LT synthesis or Epoprostenol (Prostacyclin: PGI2) in 4 series of rabbits treated with FFA or its vehicle. Piriprost given as an aerosol (0.1% W/W in THAM) scarcely modified the morphofunctional changes induced by FFA. The only pulmonary effect prevented by Piriprost was the increase in surfactant content (disaturated phosphatidylcholine: DSPC) in broncho-alveolar lavage gluid (BAL). PGI2 administered in a dose of 0.1 micrograms.kg-1.min-1 5 minutes prior to a 15 min infusion of FFA was also unable to prevent most of the effects of FFA on the lung. Only the increase in DSPC in BAL was prevented by PGI2. Some animals received a smaller dose of FFA, because they died earlier. Piriprost, as well as PGI2, shortened the survival time of rabbits treated with FFA. This decrease in the survival rate of animals treated with FFA could account for the lack of increase in DSPC post-FFA. Since other morphofunctional changes induced by FFA were scarcely modified by both Piriprost or PGI2, our results suggest that it is unlikely that either leukotrienes on PGI2 may have a significant effect on pulmonary disturbances induced by FFA.

Role of hypocapnia in the alveolar surfactant increase induced by free fatty acid intravenous infusion in the rabbit.

Intravenous infusion of free fatty acid (FFA) produces an increase in the alveolar surfactant pool of the rabbit and pulmonary edema, hyperventilation, hypoxemia and hypocapnia. Previous studies suggested that alveolar PCO2 would be a regulator of intracellular storages of surfactant. In order to study the role of hypocapnia in the increase of lung surfactant in our experiments we administered 20 mg FFA X kg-1 X min-1 i.v. to rabbits breathing room air (n = 10) or 5% CO2, 21% O2, 74% N2 (n = 7). Disaturated phosphatidylcholine (DSPC) was determined in bronchial-alveolar lavage fluid as index of alveolar surfactant content, 5% CO2 in the inspired air prevented the hypocapnia and blocked the increase in DSPC induced by FFA (p less than 0.01). Pulmonary edema post-FFA was not changed by 5% CO2 administration. We conclude that hypocapnia produced by hyperventilation during FFA infusion would be an important factor in the increase of DSPC observed after FFA infusion.

Effects of free fatty acid infusion on rabbit pulmonary surfactant. Influence of corticosteroids.

We studied the effect of free fatty acids (FFA) i.v. on alveolar lung surfactant content of rabbits. A FFA mixture was given in doses from 0.1 to 20 mg X kg-1 X min-1 during 15 min in seven different experimental series (n = 45). Disaturated phosphatidylcholine (DSPC) content in lung airway lavage fluid was measured as an index of alveolar surfactant pool. DSPC was significantly increased (p less than 0.05) by 86% in the series receiving 20 mg FFA X kg-1 X min-1 as compared to control values (means +/- SD: 4.4 +/- 1.1 mg DSPC X kg-1 body weight). Smaller doses of FFA did not change DSPC, but induced a dose-related pulmonary oedema. All the rabbits receiving 20 mg FFA X kg-1 X min-1 died before completion of the 15 min infusion; they were hypoxaemic, hyperventilated and had a decrease in lung compliance. Hydrocortisone (20 mg X kg-1 i.v.) and methylprednisolone (30 mg X kg-1 i.v.) administered 2 h before FFA blocked the increase of DSPC induced by 20 mg FFA X kg-1 X min-1. Both drugs decreased pulmonary oedema and tended to normalize some of the pulmonary function indices, although they did not modify the lethality. In conclusion, acute i.v. infusion of FFA increased alveolar surfactant pool and produced pulmonary oedema; pretreatment with corticosteroids reduced these effects and protected the lung from some of the noxious effects of FFA.

Thromboxane mediates the increase in alveolar surfactant pool induced by free fatty acid infusion in the rabbit.

Intravenous infusion of free fatty acid (FFA) produces pulmonary edema and an increase in the alveolar surfactant content of the rabbit. In order to identify a likely mediator of this lung response to FFA, we used inhibitors of cyclo-oxygenase (indomethacin, 15 mg X kg-1 i.v., or meclofenamate, 5 mg X kg-1 i.v.) and thromboxane synthetase inhibitors (imidazole, 50 mg X kg-1 i.v. or dazoxiben, 2 mg X kg-1 i.v.) which were administered before FFA, 20 mg X kg-1 X min-1 i.v., in four different experimental series (n = 54). Lung surfactant was measured in bronchial-alveolar lavage fluid by determining disaturated phosphatidylcholine (DSPC). Both kinds of inhibitors blocked the increase in FFA-induced DSPC. They increased the survival rate but they only slightly changed the post-FFA morphofunctional pulmonary alterations. We conclude that the increase in alveolar surfactant induced by FFA is likely mediated by thromboxane. This mediator would seem to play a minor role in the FFA-induced pulmonary edema observed.