André Schoutens

Effect of propofol on cerebral blood flow and metabolism in man.

Cerebral blood flow, cerebral oxygen consumption, lactate and glucose metabolism were measured in 13 patients during anaesthesia with nitrous oxide, oxygen and enflurane 0.5% and after 30 minutes infusion of propofol. The mean blood concentration of propofol was 4.06μg/ml. Cerebral blood flow decreased by 27.6% and cerebral vascular resistance by 51%. There were no changes in lactate and glucose metabolism. Cerebral oxygen consumption decreased by 18.25%. Changes in the electroencephalograph were related to the blood levels of propofol.

The number of fibroblastic colonies formed from bone marrow is decreased and the in vitro proliferation rate of trabecular bone cells increased in aged rats

Four- and 21-month old female Sprague-Dawley rats were sacrificed and their tibiae and femurs isolated for histology and initiation of bone marrow and trabecular bone cultures. The bone loss observed in 21-month old rats was associated with a markedly decreased osteoblastic index. The percentages of mineralizing trabecular surfaces were only slightly decreased in aged rats, whereas the percentages of mineralizing endocortical surfaces were strikingly decreased. Diaphyseal femoral marrows from 21-month old rats were less cellular than those from four-month old rats, and developed in culture fewer fibroblast colony forming units (FCFU) and fewer adherent cells with phenotypic characteristics of osteoblast-like cells. Trabecular bone cultures from 21-month old rats produced as many cells as cultures from four-month old rats, whereas the amount of trabeculae put into culture was much less in aged rats. Moreover, the proliferation rate in secondary culture was significantly increased in 21-month old rats. Similar responses to calcitriol were observed in bone marrow and trabecular bone cells from aged and younger mature rats, while cAMP responses to PTH were decreased in cells from aged rats. Our data confirm the age-related decrease in the FCFU efficiency of the bone marrow and show a stimulated proliferation of trabecular bone cultures from 21-month old rats that could be seen either as the result of the inhibition in vivo of the response to a signal to proliferate, or as a rebound response to factors present in the serum-enriched medium and lacking in vivo.

Selenium deficiency-induced growth retardation is associated with an impaired bone metabolism and osteopenia.

Although the importance of selenium for bone metabolism is unknown, some clinical conditions such as Kashin‐Beck osteoarthropathy have been associated with selenium deficiency. Although selenium deficiency induces growth retardation in rats, it has not been established whether this growth inhibition is associated with changes in bone metabolism. We investigated the effect of selenium deficiency on bone metabolism in growing male rats fed a selenium‐deficient diet for two generations (Se−). In Se− rats, erythrocyte glutathione peroxidase activity and plasma selenium concentration were strongly reduced compared with pair‐fed selenium‐adequate rats (Se+). Weight and tail length were reduced by 31% and 13% in the Se− rats, respectively (p < 0.001). The Se− diet was associated with a 68% reduction of pituitary growth hormone (GH; p = 0.01) and a 50% reduction of plasma insulin‐like growth factor I (IGF‐I; p < 0.001). Plasma calcium was lower and urinary calcium concentration was greater in Se− rats. This group had a 2‐fold increase in parathyroid hormone (PTH) and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3] in plasma. Plasma osteocalcin and urinary deoxypyridoline were reduced by 25% and 57% in the Se− rats (p < 0.001). Selenium deficiency resulted in a 23% and 21% reduction in bone mineral density (BMD) of the femur and tibia (p < 0.001) and this effect persisted after adjustment for weight in a linear regression model. A 43% reduction in trabecular bone volume of the femoral metaphysis (p < 0.001) was found in Se− rats. This experimental study shows that growth retardation induced by selenium deficiency is associated with impaired bone metabolism and osteopenia in second‐generation selenium‐deficient rats.

Longitudinal study of calcium and bone metabolism in paraplegic patients.

A longitudinal study of bone and calcium metabolism in 28 patients with spinal chord lesion shows an enhancement of bone calcium accretion, generalized to the whole skeleton. The bone calcium turnover rate is more increased in the non-paralysed area during the first 2 months.

Brain hypometabolism of glucose in anorexia nervosa: A PET scan study

Cerebral glucose metabolism was studied in 20 underweight anorectic girls and in 10 age- and sex-matched healthy volunteers using positron emission tomography with (18-F)-fluorodeoxy-glucose. Both groups were scanned during rest, with eye closed and with low ambient noise. Compared to controls, the underweight anorectic group showed a global hypometabolism (p = .002) and an absolute (p < .001) as well as relative (p < .01) hypometabolism of glucose in cortical regions, with the most significant differences found in the frontal and the parietal cortices. Within the underweight anorectic and the control groups, no correlations were found between absolute or relative rCMRGlu and BMI, anxiety scores, or Hamilton scores of depression. Different factors might explain this reduction of glucose metabolism in anorexia nervosa. It might be the consequence of neurophysiological or morphological aspects of anorexia nervosa and/or the result of some associated symptoms such as anxiety or depressed feelings. Supported by cognitive studies, we can also hypothesize a primary corticocerebral dysfunctioning in anorexia nervosa.

The effect of orchidectomy on bone metabolism in aging rats

SummaryWe have shown that orchidectomy in postpubertal 55-day-old rats led beyond 2 months to a decrease in bone growth and loss of weight. At 1 month postorchidectomy, we observed a threefold increase in bone blood flow, an increase in calcium accretion rate, and an increase in the number of osteoclasts in the metaphysis. In the present experimental study, orchidectomy was performed in 1-year-old rats when bone growth in length was no longer measurable. In the tibia and femur we observed a decrease in bone volume, a still more rapid decrease of bone calcium during the first postoperative month, a thinning of the cortical width, an initial increase in calcium accretion rate (+20% when compared to 31 days controls) followed by a decrease at 120 days (−22% and−11% when compared to controls for tibia and femur respectively), a 29% increase in bone blood flow, and an increase in the number of osteoclasts. We conclude that androgen deprivation in young and old animals leads to a modified bone architecture, independent of the androgen impact on bone growth.

Circannual Variations in the Density of Tritiated Imipramine Binding Sites on Blood Platelets in Man

We demonstrate a circannual variation in the density of binding sites of 3H-imipramine on human platelets of normal controls and depressed patients. These results imply further reassessment of previously published data on 3H-imipramine binding studies in affective disorders.

Effects of inactivity and exercise on bone

SummaryBone mass and muscular mass show a parallel evolution during growth, and parallel involution with age. However, the bone loss related to the withdrawal of oestrogens is independent of muscular waste. The extensive study of disuse osteoporosis shows that exercise without weightbearing cannot counteract the loss of bone mass provoked by bed rest or weightlessness. Physical training, even at low frequency (30 to 60 min/day, 2 or 3 days/week), can increase bone mass or reduce bone loss associated with age. This effect is even present when exercise is practised by very old people at a seemingly low level of muscular tension on bone. It is not known whether muscular exercise could be helpful in pathological osteopenia.Experiments in animals indicate a short-lived benefit of exercise practised during a definite growth period; the long term effect of physical training in humans, after cessation of such activity, has not been studied extensively. Equal distribution of tension on all parts of the skeleton is probably not mandatory to obtain a general effect of exercise on bone mass. It is assumed that muscular exercise acts through tension exerted on bone, but the exact mechanism is unknown, as are the specifications of effective exercise in terms of site of application, intensity, frequency and duration. Moreover, little is known about the expected synergy between exercise and occupational activity.

Bone blood flow and In vitro proliferation of bone marrow and trabecular bone osteoblast-like cells in ovariectomized rats

SummaryOvariectomy in the rat induces a rapid osteopenia associated with an elevated bone turnover. One hundred and twenty-day-old rats were ovariectomized (OVX) or sham-operated (n=6–8 per group and per time period studied). 45Ca accretion rate and bone blood flow (microspheres trapping technique) in the femurs were determined at 28, 42, 84, and 119 days after ovariectomy. Both parameters were markedly increased by 84 days and subsided thereafter. At the 42nd day, when bone turnover was maximal, bone marrow and trabecular bone cultures were obtained from shamoperated and ovariectomized animals (n=10/group). Proliferation rate of bone marrow cells and trabecular osteoblast-like cells estimated by fibroblast colony-forming units (FCFU) efficiency and cell counting was markedly increased in primary and secondary cultures in ovariectomy. These data fitted well with the enhanced number of osteoblasts observed in situ in the long bone metaphyses of estrogen-depleted animals. As estrogens were shown in the literature to inhibit proliferation of the red cell line and of other hemopoietic lines, it is possible that estrogens, through a general mechanism, inhibit hemopoietic and stromal lines and also the proliferation of bone marrow-derived trabecular bone cells.

Prostaglandins and bone

A workshop devoted to a discussion of the role of prostaglandins (PGs) in bone physiology and in bone disease was held in Brussels on April 8 and 9, 1994. It was organized by the Interdisciplinary Group of Bone Physiopathology and Locomotor System Biomechanics of Brussels Free University (GIPOB). Fifteen speakers were invited to present their data regarding this subject, and there were approximately 45 participants. of cAMP (EP3). The distribution of prostanoid receptors in different tissues is variable; it conditions the intensity and the direction of the response, which can thus change with ligand concentration. PG receptors of bone cells have yet to be characterized.