Lung re-expansion and urinary lipid peroxidation in neonatal pneumothorax.

AIM: Experiential studies suggest that re-expansion of a collapsed lung may result in pulmonary ischaemia-reperfusion injury. We aimed to evaluate the effect of lung re-expansion on urinary lipid peroxidation products in neonates with pneumothorax. METHODS: This study included 20 mechanically ventilated neonates with pneumothorax, and 18 healthy neonates (controls). A chest tube was inserted immediately following the diagnosis of pneumothorax. Urine samples were obtained just before tube thoracostomy (first period), after one hour (second period), every 12 hours by complete reexpansion (third period). Vital signs and ventilatory parameters were recorded. Urinary lipid peroxidation was evaluated by measurement of thiobarbituric acid-reacting substances (TBARS). RESULTS: No significant difference was found between urinary TBARS concentrations in the first, second and third periods (4.08 +/- 2.4 nmol/L, 2.8 +/- 2.3 nmol/L and 3.3 +/- 2.1 nmol/L, respectively). Control TBARS levels (4.1 +/- 2.1 nmol/L) did not significantly differ from those of the neonates with pneumothorax (p > 0.05). The neonates with pneumothorax had higher heart rates compared to the controls (p < 0.01). When compared with controls, the systolic pressure was lower in all periods (p < 0.01), and diastolic blood pressure was lower only in the first and second period (p < 0.05). Oxygen saturation significantly decreased in the first period compared to saturation of the second period and of controls (p < 0.01). Ventilatory parameters did not show any significant difference between the periods. CONCLUSIONS: This prospective study showed that re-expansion of the lung did not significantly affect urinary TBARS concentration in neonatal pneumothorax. Indirectly, short-term lung collapse followed by re-expansion might not cause a clinically significant reperfusion injury in newborns.     

Osseous destruction and rupture of the extensor tendon caused by sarcoidosis of the finger.

We describe a woman with osseous destruction and rupture of the extensor tendon as a result of sarcoidosis in the left third finger with no evidence of systemic involvement. The tendon was repaired and she was successfully treated with prednisone.     

Tissue repair processes in healing chronic pressure ulcers treated with recombinant platelet-derived growth factor BB.

Cellular and molecular mechanisms responsible for the observed vulnerary effects of recombinant human platelet-derived growth factor BB (rP-DGF-BB) in man have not been elucidated. In a double-blinded trial, patients having chronic pressure ulcers were treated topically with either rPDGF-BB or placebo for 28 days. To explore how rPDGF-BB may induce chronic wounds to heal, biopsies were taken from the ulcers of a cohort of 20 patients from the trial and evaluated in a blinded fashion by light microscopy for 1), fibroblast content, 2) neovessel formation, and 3), collagen deposition. Electron microscopy also was used to assess fibroblast activation and collagen deposition. Before initiation of therapy most wounds had few fibroblasts and most of those present were not activated. When mean scores for the total active treatment phase (days 8, 15, and 29) for rPDGF-BB-treated ulcers were compared with the scores for placebo-treated ulcers, fibroblast content was significantly higher for the rPDGF-BB-treated ulcers (P = 0.03, Kruskal-Wallis test). More significant differences in fibroblast and neovessel content were observed when six nonhealing wounds were eliminated from the analysis (three placebo, three treatment). Thus, in all healing wounds, rPDGF-BB therapy significantly increased fibroblast (P = 0.0007) and neovessel (P = 0.02) content. These results were correlated with increased collagen fibrillogenesis by fibroblasts from healing rPDGF-BB-treated wounds, as assessed by intracellular procollagen type I immunostaining, and by electron microscopy, and were concordant with clinical measurements (eg, area of ulcer opening and ulcer volume) which showed greater healing in rPDGF-BB-treated wounds. These results suggest induction of fibroblast proliferation and differentiation is one mechanism by which rPDGF-BB can accelerate wound healing and that rPDGF-BB can augment healing responses within a majority of, but not all, nonhealing chronic pressure ulcers in man.     

Effect of melatonin in the prevention of post-operative adhesion formation in a rat uterine horn adhesion model

BACKGROUND: Our main aim was to investigate the effects of melatonin (ME), possibly the most powerful free-radical scavenger, on the prevention of i.p. adhesion formation in rat uterine horn. Our secondary aim was to determine whether different methods of administration of ME were beneficial. METHODS: Animals were randomly assigned into seven groups, each consisting of 13 rats. Measured serosal injury was created using a standard technique. While control and two sham groups were not given ME, two of the remaining four groups were given a single dose of 10 mg/kg (2 mg) of ME i.p. immediately after injury and 30 min prior to injury respectively. In the two other groups, ME treatment was continued daily for 5 days. All animals were killed 2 weeks after surgery and adhesions were determined and scored by a examiner blinded to the test. RESULTS: The extent, severity and total scores of adhesion were found to be significantly reduced in all of the ME treatment groups when compared with control and sham groups. There were no statistically significant differences between the treatment groups. CONCLUSIONS: This study showed that even single dose ME therapy was effective in the prevention of post- operative i.p. adhesion formation.