No abstract

Renal blood flow is reduced in patients with chronic respiratory failure caused by chronic obstructive pulmonary disease (COPD), and changes in renal hemodynamics are likely to be important in the pathogenesis of the edematous state of cor pulmonale. We therefore examined the hypothesis that this renal vasoconstriction is reversible by comparing the effects of oxygen therapy and the renal vasodilator dopamine on renal hemodynamics in both hypoxemic patients with COPD and those who were also hypercapnic. We assessed renal hemodynamics noninvasively with color-flow Doppler ultrasound. In order to validate the technique we recorded renal hemodynamics in a group of healthy volunteers before and during a dopamine infusion, and in a subgroup we simultaneously measured effective renal plasma flow (ERPF) with para-aminohippurate clearance. In the healthy volunteers there was a 22.5% rise in time-adjusted mean arterial velocity (Tamx) measured by Doppler compared with a 22% rise in ERPF with dopamine. This rise was significant (p < 0.05). In hypoxemic, normocapnic subjects Tamx rose by 25% with oxygen (p < 0.005), 20% with dopamine (p < 0.005), and 24% with both therapies. There was no significant change in aortic flow whether the subjects received air, oxygen, or dopamine (p = 0.77). In the hypercapnic patients there was no significant change in aortic or renal velocities while receiving oxygen or dopamine (p = 0.85 and 0.86). We conclude that color-flow Doppler velocity measurements can accurately detect changes in renal blood flow. Oxygen and dopamine are equipotent renal vasodilators in hypoxic COPD, but the effect is not additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Background -L-arginine is the precursor of endothelium derived nitric oxide (NO) and increasing the available substrate may increase the production of NO. This has been shown by local infusion in peripheral vascular beds but there are few studies of the effects during systemic infusion. Renal vasoconstriction is known to be important in the pathogenesis of cor pulmonale in patients with hypoxic chronic obstructive pulmonary disease (COPD). The effects of a systemic infusion of L-arginine on renal and aortic haemodynamics were therefore investigated in normal subjects and in patients with hypoxic COPD. Methods -Ten normal volunteers were recruited from the research staff of King's College Hospital. Six patients with COPD and hypoxia (arterial oxygen tension (Pao2) <8 5 kPa) were recruited from the thoracic medicine outpatient clinic at King's College Hospital and five age and sex matched normal subjects were recruited from a group of normal subjects recruited from the database of the Department of Health Care for the Elderly as volunteers for medical research. There was no history ofrenal, cardiac, or hepatic disease. Baseline values of time averaged mean of the maximum instantaneous velocity (Tamx) and maximum velocity (Vmax) ofblood flow in intrarenal arteries were obtained using colour flow Doppler ultrasound. Using the same technique, Vmax was obtained from the abdominal aorta just distal to the xiphisternum before and after infusion of L-arginine via a large peripheral vein (20 g in 100 ml sterile water over 30 minutes). Results -In normal subjects L-arginine increased blood velocity in the intrarenal vessels from a mean of0*22 mis to 0*26 mis, an increase of 19-8%. There was no effect on arterial blood pressure, heart rate, or aortic blood velocity. L-arginine had no effect on intrarenal or aortic blood velocity in patients with hypoxic COPD. In age matched controls L-arginine increased blood velocity in the intrarenal vessels from a mean of 0 20 m/s to 0 26 mis, an increase of 36-8%. There was no effect on arterial blood pressure, heart rate, or aortic blood velocity. Conclusions -L-arginine, at the doses administered, increased renal blood flow, as assessed by renal arterial velocity. This effect was not seen in patients with hypoxic COPD but was present in age matched controls. This suggests that the abnormal renal vascular control seen in hypoxic patients with COPD may reflect a disturbance of the L-arginine/nitric oxide pathway.

Study Objectives: To look for an association between the vertical position of the hyoid, as measured by the sella-hyoid (S-H) distance and the severity of obstructive sleep apnea (OSA). A previously published study on this subject showed a significant correlation between S-H distances more than 120 mm and severe OSA. Design and Setting: A retrospective study of patients who were treated with a mandibular advancement splint (MAS) for sleep disordered breathing during June 2000 to May 2005 at the orthodontic department of Colchester University Hospital. Patients and Participants: One hundred and six consecutive patients who were treated with MAS during the period. Measurements and Results: Lateral cephalograms were taken and traced prior to the provision of MAS therapy, and the distance S-H was measured. The mean S-H distance was 125.5 mm (103-148 mm) with a median of 126 mm. Four out of 8 patients (50%) with severe OSA had a S-H distance more than 120 mm, as did 38 out of 50 (76%) with mild to moderate OSA (AHI 5-30), and 17 out of 22 patients (77.27%) with an AHI of 0 to 4. No significant correlations between the S-H distance and the severity of OSA were found (Pearson correlation coefficient -0.034 and 95% confidence interval: -0.25, 0.18). Conclusion:There was no correlation between patients' OSA severity and their cephalometric S-H distance. The utility of the latter as a screening test cannot therefore be recommended as a substitute for existing diagnostic tests.

MF-DPI 400 microg BID was therapeutically equivalent to FP-DPI 500 microg BID in patients with moderate-to-severe persistent asthma.