Clinical physiology (Oxford, England)最新文献

A celery petiole phloem cDNA library was constructed and used to identify a cDNA that gives Saccharomyces cerevisiae cells the ability to grow on mannitol and transport radiolabeled mannitol in a manner consistent with a proton symport mechanism. This cDNA was named AgMaT1 (Apium graveolens mannitol transporter 1). The expression profile in source leaves and phloem was in agreement with a role for mannitol in phloem loading in celery. The identification in eukaryotes of a mannitol transporter is important because mannitol is not only a primary photosynthetic product in species such as celery but is also considered a compatible solute and antioxidant implicated in resistance to biotic and abiotic stress.

Although reflex sympathetic activation is a major determinant of the haemodynamic tolerability of ventricular tachycardia (VT), the methods for evaluating this aspect during on-going VT remain invasive and complicated. Palmar sweating as an indirect but non-invasive measure of sympathetic activity was estimated by means of a unique hygrometer under right ventricular (RV) rapid pacing (up to 150 beats min-1) replicating VT, and concurrent monitoring of aortic blood pressure in five patients with various kinds of cardiac arrhythmias in our electrophysiological laboratory. The peak palmar sweating rate in arbitrary units was augmented as the RV pacing rate increased and was proportional to the pacing-induced fall in systolic blood pressure (SBP), with a correlation coefficient of more than 0.903 (P<0.006). The slope of linearity between the sweating rate and the fall in SBP varied among individual patients, with greater sweating amplitude in the younger patients even with the same extent of fall in SBP. This preliminary study suggests sympathetic acceleration caused by haemodynamic deterioration under simulated VT, and therefore this protocol may be able to predict the haemodynamic tolerability of sustained monomorphic VT.

Seven patients with histologically verified small cell lung carcinoma were given an oral glucose load of 75 g on two occasions to examine the effect of glucose on whole body and forearm thermogenesis with and without acute beta-adrenergic inhibition with propranolol. Whole body energy expenditure was measured by the open circuit ventilated hood system. Forearm blood flow was measured by venous occlusion strain-gauge plethysmography. The uptake of oxygen in the forearm was calculated as the product of the forearm blood flow and the difference in arteriovenous oxygen concentration. The glucose-induced thermogenesis in the 120 min following the glucose load was significantly reduced by beta-adrenergic inhibition with approximately 50% from 63.9 +/- 5.8 kJ 120 min-1 (mean +/- SE) to 27.8 +/- 9.8 kJ 120 min-1 (P < 0.01). Almost the entire reduction took place from 60 to 120 min (P < 0.005). The integrated glucose-induced forearm oxygen uptake in the period 60-120 min following the glucose load was significantly reduced after beta-adrenergic inhibition from 103 +/- 28 mumol 100 g-1 60 min-1 to 29 +/- 29 mumol 100 g-1 60 min-1 (P < 0.05). The noreadrenaline concentration in the arterial blood was not increased in the baseline period compared to healthy elderly; it increased following the glucose load while there was no demonstrable increase in adrenaline concentration in the two experiments. It is suggested that these patients have increased sensitivity of the beta-adrenergic receptors and an early facultative component of the glucose-induced thermogenesis in part takes place in the forearm.

The effects of two different vasodilating agents (MgSO4 infusion and the calcium antagonist nifedipine) on circulating levels of calcitonin gene-related peptide (CGRP) were studied in 12 women with pronounced primary Raynaud's phenomenon (PRP) and in 12 healthy females. There were no significant differences with regard to basal levels of circulating CGRP between women with PRP and the control group; median 15.5 (range 10-48) vs. 14 (range 10-69) pmol l-1, respectively. However, treatment with MgSO4 infusion significantly decreased circulating CGRP in women with PRP only from median 15.5 (range 10-48) to 10 (range 10-110) pmol l-1) (P < 0.05). On the other hand 14 days of treatment with nifedipine did not affect circulating CGRP in either of the investigated groups. Erythrocyte magnesium (ery-Mg) levels increased significantly after MgSO4 infusion in women with PRP (2.43 +/- 0.13 vs. 2.52 +/- 0.15 mmol l-1, P < 0.05) but not in the controls (2.51 +/- 0.24 vs. 2.57 +/- 0.28 mmol l-1, ns). In conclusion, the decrease of circulating CGRP after MgSO4 infusion in women with PRP provides further evidence that magnesium plays a significant role in the pathophysiology of PRP.

To assess whether age modifies the effects of preload on the Doppler indexes of left ventricular filling, 10 younger (mean age 31 years) and 10 older (mean age 53 years) healthy subjects underwent transmitral flow velocity measurements following acute changes of venous return produced by head-up and head-down tilts. In the horizontal supine position, almost all Doppler indexes differed significantly between the groups. As venous return increased from the head-up to the head-down position, the peak early and late transmitral velocities, their ratio, and the acceleration and deceleration of the early flow increased while the relaxation time shortened. These changes did not differ significantly between the younger and older subjects. In conclusion, both age and preload have strong effects on the Doppler transmitral velocity indexes. The preload-induced changes are not modified by age.

The effects of 6 months of recombinant growth hormone (GH) treatment (0.5 IU kg-1 per week) on muscle size, strength and neural activation (EMG) was studied in eight adults with childhood onset GH deficiency (GHD). Before treatment, height, body mass (BM) and lean body mass (LBM) of the GHD subjects were significantly lower (P < 0.01) from those recorded in eight healthy controls, while no significant differences were found between the body mass index (BMI) of the two populations. Thigh muscle + bone cross-sectional area (CSAM+B) and lower limb muscle plus bone volume (LLVM+B) of the GHD patients were 66.1 +/- 13.7% and 47.6 +/- 6.8% of those recorded in the controls (P < 0.01), whereas no difference in CSA/height2 was found between the two groups. By contrast, LLVM+B/height3 was 82.0 +/- 19.0% that of the controls (P < 0.05). Similarly, quadriceps muscle strength (MVC) of the GHD patients was 63.2 +/- 12.4% that of controls (P < 0.01), while no significant differences in the force per unit area (F/CSA) and per body mass (F/BM) were found. After 6 months of GH treatment LBM increased by 6.0 +/- 4.2% (P < 0.02), CSAM+B by 14.5 +/- 12.7% (P < 0.01) and LLVM+B by 10.1 +/- 7.3% (P < 0.01), absolute differences from the normals still persisting. However, the LLVM+B/height3 of the GHD patients after treatment was no longer significantly different from that of the controls. Quadriceps MVC increased by 9.8 +/- 12.0% (P < 0.02), differences from the controls being still significant, whereas the F/CSA and F/BM did not change. A right shift of the integrated EMG/Force relation, with no change in the maximal integrated EMG (iEMG) activity, was observed in the patients after treatment. In conclusion, the current study shows that adults with childhood onset GHD have a reduced skeletal muscle mass and strength which seem to be positively influenced by 6 months of GH treatment.

We measured the pulmonary clearance of 99mTc-labelled diethylene triamine penta-acetate (99mTc-DTPA) for 3 h in 17 non-smokers and in 16 healthy smokers. We found the clearance of 99mTc-DTPA to be well described by a mono-exponential equation in 14 non-smokers, the half-life being 66 +/- 17 min (mean +/- SD). In all smokers, a bi-exponential equation yielded a significantly better curve fit. The half-life of the slow and fast clearance components was 83 +/- 19 and 13 +/- 4 min, respectively. The relative amount of radioactivity cleared by the fast component was 57 +/- 15% and correlated significantly with cumulated tobacco consumption (r = 0.58, P < 0.02) and forced expiratory volume in 1 s in percentage of predicted value (r = -0.60, P < 0.02). We conclude that smoking induces a rapidly clearing pool of 99mTc-DTPA in the lung, the size of which may be related to smoking habits.