Anaphylactic shock during hyperbaric oxygen therapy.

A case of a 38-year-old woman is reported who was treated with hyperbaric oxygen therapy to cure a dehiscent wound. She suffered from "oral-allergy syndrome" (OAS) while eating certain fruits, and from itching when wearing latex gloves to handle hair dyes. Fifteen minutes after the start of compression, malaise, anxiety, dyspnoea, tachycardia, cold sweating and laryngeal stridor occurred. Despite intensive care treatment, face angioedema persisted for several days. On the basis of history, radioallergosorbent test (RAST) and prick tests, latex was assumed to be responsible for the anaphylactic reaction. To our knowledge, this is the first extensive report of an anaphylactic reaction to latex in a hyperbaric chamber. The lesson drawn from this case record can be summarized as follows: 1) never fail to collect a thorough history; 2) set up a latex-safe hyperbaric chamber when needed; 3) have an emergency kit always near at hand.

Effects of enzyme-replacement therapy in patients with Anderson-Fabry disease: a prospective long-term cardiac magnetic resonance imaging study.

BACKGROUND: Anderson-Fabry disease is a multisystem X linked disorder of lipid metabolism frequently associated with cardiac symptoms, including left ventricular (LV) hypertrophy gradually impairing cardiac function. Evidence showing that enzyme-replacement therapy (ERT) can be effective in reducing LV hypertrophy and improving myocardial function in the long term is limited. OBJECTIVE: This study aimed to assess the long-term effects of ERT with recombinant alpha-galactosidase A (agalsidase beta, Fabrazyme) on LV function and myocardial signal intensity in 11 patients with Anderson-Fabry disease. PATIENTS: Eleven patients (eight males, three females) with varying stages of genetically confirmed Anderson-Fabry disease were examined by means of physical examination and magnetic resonance imaging before ERT with agalsidase beta at 1 mg/kg every other week (study 1) and after a mean treatment duration of 45 months (study 2). RESULTS: At 45 months of treatment, LV mass and LV wall thickness had significantly reduced: 188 (SD 60) g versus 153 (47) g, and 16 (4) mm versus 14 (4) mm, respectively. Furthermore, a significant reduction in myocardial T2 relaxation times was noted in all myocardial regions, that is, interventricular septum 80 (5) ms versus 66 (8) ms, apex 79 (10) ms versus 64 (10) ms, and lateral wall 80 (8) ms versus 65 (16) ms. Changes in LV ejection fraction were not significant. Amelioration of clinical symptoms was observed in all patients. CONCLUSIONS: Long-term therapy with agalsidase beta at 1 mg/kg every 2 weeks was effective in significantly reducing LV hypertrophy, improving overall cardiac performance and ameliorating clinical symptoms in patients with Anderson-Fabry disease.

Effect of hyperbaric oxygen therapy in experimental subcutaneous and pulmonary infections due to Pseudomonas aeruginosa.

About 80% of nosocomial infections are caused by aerobic bacteria. Pseudomonas aeruginosa is a Gram-negative bacterium belonging to the Pseudomonadaceae family; P. aeruginosa is responsible for 6-22% of all hospital infections. The aim of this study was to evaluate the efficacy of hyperbaric oxygen (HBO2) therapy (2 atm abs x 55 min.day-1) alone for 8 days and combined with antibiotic chemotherapy (amikacin 15 mg.kg-1.day-1 for 8 days by intraperitoneal route) in rats infected subcutaneously and via the pulmonary route. In the rats infected by P. aeruginosa, HBO2 induced a reduction in mortality and morbidity with bacteria eradication in blood culture, bronchial aspirate, and skin biopsies when compared to control. These effects were increased by the use of amikacin, an antibiotic used for the treatment of sensitive Gram-negative bacteria.

[Effects of hyperbaric oxygenation in skin and pulmonary infections caused by Pseudomonas aeruginosa]. / Effetti dell'ossigenoterapia iperbarica nelle infezioni sperimentali cutanee e polmonari da Pseudomonas aeruginosa.

About 80% of nosocomial infections are caused by aerobic bacteria. The Pseudomonas aeruginosa is a Gram-negative bacterium pertaining to the Pseudomonadaceae family. P. aeruginosa is responsible for 6-22% of all hospital infections. The aim of this paper is to evaluate the efficacy of both hyperbaric oxygen-therapy (HBO 2 Atm x 35 min/day) alone for 8 days and when associated to the chemoantibiotic therapy (amikacine 15 mg/kg/day for 8 days intraperitoneal), in rats infected through pulmonary and subcutaneous intake. In rats affected by P. aeruginosa, HBO induces a significant reduction in mortality and morbility with bacteria eradication in blood culture findings, bronchial aspirate and skin biopsies. These effects were increased by the use of amikacine which is an antibiotic used for the treatment of Gram-negative bacteria.

Neonatal monosodium glutamate treatment increases epididymal adipose tissue sensitivity to insulin in three-month old rats.

We determined the response of glucose transport to insulin in isolated adipocytes and the lipogenic activity of insulin in fragments of epididymal adipose tissue obtained from male MSG-obese rats. Basal glucose transport rates (pmol 3 min-1 10(5) cells-1) were 100% higher in MSG than in control cells (3-month old male Wistar rats) pre-incubated for 30 min (P < 0.01). Nevertheless, when expressed as fmol 3 min-1 microns 2 cell surface area-1, transport rates were similar for the two groups (31.2 +/- 2.6 for MSG and 26.5 +/- 3.2 for controls, N = 7). No differences were observed in maximally insulin-stimulated glucose transport rates between groups (72.6 +/- 10.6 for MSG and 101.0 +/- 12.0 for controls, N = 7). In contrast, for adipocytes pre-incubated for 2 h, the basal uptake rates were 3.7 times higher and the maximal response to insulin was 103% higher in cells from MSG rats compared to control cells. These alterations in MSG rat adipocytes were accompanied by changes in cell sensitivity to insulin (EC50, 0.13 +/- 0.02 ng/ml for MSG vs 0.46 +/- 0.10 ng/ml for controls, P < 0.01). The rates of incorporation of labelled substrates (3H2O and 14C-glucose) into total lipids showed that in vitro lipogenesis was also 79% (3H2O) and 250% (14C-glucose) higher in MSG adipose tissue fragments. The MSG animals were consistently hyperinsulinemic. These data suggest that the obesity of 3-month old MSG rats is a metabolic alteration characterized by an enhanced adipocyte capacity to transport glucose and to synthetize lipids resulting in increased insulin sensitivity.

Neonatal monosodium glutamate treatment increases epididymal adipose tissue sensitivity to insulin in three-month old rats

We determined the response of glucose transport to insulin in isolated adipocytes and the lipogenic activity of insulin in fragments of epididymal adipose tissue obtained from male MSG-obese rats. Basal glucose transport rates (pmol 3 min-1 10(5) cells-1) were 100 higher in MSG than in control cells (3-month old male Wistar rats) pre-incubated for 30 min (P < 0.01). Nevertheless, when expressed as fmol 3 min-1 microns 2 cell surface area-1, transport rates were similar for the two groups (31.2 +/- 2.6 for MSG and 26.5 +/- 3.2 for controls, N = 7). No differences were observed in maximally insulin-stimulated glucose transport rates between groups (72.6 +/- 10.6 for MSG and 101.0 +/- 12.0 for controls, N = 7). In contrast, for adipocytes pre-incubated for 2 h, the basal uptake rates were 3.7 times higher and the maximal response to insulin was 103 higher in cells from MSG rats compared to control cells. These alterations in MSG rat adipocytes were accompanied by changes in cell sensitivity to insulin (EC50, 0.13 +/- 0.02 ng/ml for MSG vs 0.46 +/- 0.10 ng/ml for controls, P < 0.01). The rates of incorporation of labelled substrates (3H2O and 14C-glucose) into total lipids showed that in vitro lipogenesis was also 79 (3H2O) and 250 (14C-glucose) higher in MSG adipose tissue fragments. The MSG animals were consistently hyperinsulinemic. These data suggest that the obesity of 3-month old MSG rats is a metabolic alteration characterized by an enhanced adipocyte capacity to transport glucose and to synthetize lipids resulting in increased insulin sensitivity.

Vasomotor responses in rats "intoxicated" with doxorubicin.

In rats intoxicated with doxorubicin, vasomotor responses were evaluated 12 hr after the last dosage. In rats pretreated with doxorubicin, hypertensive responses to L-norepinephrine and L-epinephrine, and hypertension by occlusion of both common carotid arteries were significantly (p < 0.05) reduced when compared with controls. Doxorubicin pretreatment also significantly reduced the arterial hypotension due to L-isoprenaline. In rats intoxicated with doxorubicin, pretreatment with L-sulpiride (12.5 to 50 mg/Kg/day for 30 days in drinking water ad libitum) did not modify the effects of doxorubicin on vasomotor reactivity. In contrast, pretreatment with amitriptyline (12.5 to 50 mg/Kg/day in drinking water ad libitum for 30 days) potentiated the inhibitory effects of doxorubicin on vasomotor responses. In conclusion, our research shows that doxorubicin intoxication induces a significant reduction of alpha- and beta-adrenergic reactivity and of baroreceptor activity.

Effect of monosodium glutamate treatment during neonatal development on lipogenesis rate and lipoprotein lipase activity in adult rats.

Monosodium glutamate (MSG) has been shown to alter several neuroendocrine functions in neonatally treated rats. To evaluate possible alterations in lipogenesis rate and lipoprotein lipase (LPL) activity, male and female rats were injected during the neonatal period with MSG or saline (controls). In male MSG rats, an increase in lipogenesis of liver and retroperitoneal adipose tissues was observed. Triton WR 1339 (an LPL inhibitor) administration decreased retroperitoneal lipogenesis in these animals. In female rats, MSG-treatment increased lipogenesis only in gonadal and retroperitoneal adipose tissues. No change was observed in hepatic lipogenesis and the Triton administration did not change retroperitoneal lipogenesis. LPL activity was increased in the gonadal and retroperitoneal adipose tissues in male and female MSG-treated rats. These data suggest that there is a specific sex-dependent response in the development of MSG-induced obesity.

Effect of fasting on monosodium glutamate-obese rats.

The effect of fasting was studied in lean and monosodium glutamate (MSG)-obese rats. Daily urinary urea excretion and body weight loss were studied before and during 21 days of fasting. MSG-obese rats showed reduced weight loss, higher total liver lipid content, and lower urea excretion during fasting, thus suggesting a higher capacity to spare body protein in comparison to controls. A significant decrease in retroperitoneal fat pad content was observed in both groups after 6 days of fasting (83% in the controls vs 35% in MSG-obese rats). These data suggest that the larger lipid stores of MSG-obese rats can explain their greater mean survival time after fasting.

Effect of fasting on monosodium glutamate-obese rats

The effect of fasting was studied in lean an monosodium glutamate (MSG)-obese rats. Daily urinary urea excretion and body weitht loss were studied before and during 21 days of fasting. MSG-obese rats showed reduced weight loss, higher total liver lipid content, and lower urea exretion during fasting, thus suggesting a higher capacity to spare body protein in comparison to controls. A significant decrease in retroperitoneal fat pad content was observed in both groups after 6 days of fasting (83% in the controls vs 35% in MSG-obese rats). These data suggest that the larger lipid stores of MSG-obese rats can explain their greater mean survival time after fasting

Neonatal treatment with monosodium glutamate increases plasma corticosterone in the rat.

Monosodium glutamate (MSG) has been shown to alter several neuroendocrine functions in neonatally treated rats. To evaluate for possible alterations in the hypothalamic-pituitary-adrenal axis, we injected rats during the neonatal period with MSG or saline (controls). An increase in basal plasma corticosterone levels associated with a blunted circadian variation was observed. Ether exposure produced a significant elevation in plasma corticosterone concentration in both groups of animals. However, while the increase in controls was 181.3% for male and 193.9% for female rats, in the MSG-treated rats it was only 60.7 and 31.6%, respectively. The intraperitoneal administration of high dexamethasone doses blocked corticosterone secretion in both groups. However, whereas the lowest dose (0.10 microgram/kg) suppressed corticosterone secretion in control animals, it was ineffective in MSG-treated rats. The morphological study of adrenals revealed signs of a hyperfunctional state in MSG-treated rats. These data suggest that the central lesions produced by MSG treatment disrupt the regulation of the hypothalamic-pituitary-adrenal axis.