Background/aim: Sonographic assessment of diaphragm structure and function would be a useful clinical tool in patients with chronic obstructive pulmonary disease (COPD). Our aim was to determine the muscle thickness of the diaphragm and the usefulness of clinical practice in patients with COPD. Materials and methods:The diaphragmatic thickness of 34 COPD patients and 34 healthy subjects was measured during tidal volume (Tmin) and deep inspiration (Tmax) on both sides using a B-mode ultrasound. The body mass index and the modified Medical Research Council (mMRC) index values were reported.Results: There was no correlation among TminR (P = 0.134), TminL (P = 0.647), TmaxR (P = 0.721), and TmaxL (P = 0.905) between the patients with COPD and the control group. There was also no significant difference between diaphragmatic thickness and COPD severity, respiratory function (P = 0.410), and frequency of exacerbations (P = 0.881) and mMRC (P = 0.667). Conclusion:Diaphragmatic dysfunction in COPD is related to mobility restriction rather than muscle thickness.

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A number of microvascular changes, such as the development of astrocyte lucency, increased endothelial pit/vesicle activity, development of crater like lesions, and endothelial microvilli have been reported after injury to the brain. Lateral head acceleration in the non-human primate, however, still provides the best experimental model for human diffuse axonal injury. No attempt has yet been made to document the spatial extent or time course of the microvascular response to acceleration injury to the head. We have examined the brains of baboons 1, 4, 6, and 12 h and 7 days after acceleration injury to the head to analyse the microvascular response. In the experimental animals there was a short-term rise in intracranial pressure followed by a long-term resolution, and a reduction in both mean arterial blood pressure and cerebral perfusion pressure which, however, never dropped below 75% of baseline for more than 5 min after injury in any animal. We found evidence for extravasation of blood in a small number of blood vessels in all parts of the brain. Interendothelial tight junctions are not disrupted. Pit/vesicle activity rises in the 1st h in the occipital cortex, but not until 4 h in the frontal cortex, and remains elevated for at least 7 days. There is little change in the thalamus. Development of microvilli is most rapid in the frontal cortex with peak values at 1 h, but slower in the thalamus and occipital cortex where peak values are only obtained at 6 h. Highest numbers of microvilli occur in parasagittal regions of the brain.(ABSTRACT TRUNCATED AT 250 WORDS)

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