Effect of truncal vagotomy on functional and morphological changes produced by duodenogastric reflux

The effects of truncal vagotomy on the functional and morphological changes produced by duodenogastric reflux have been studied in the dog. Duodenogastric reflux caused progressive damage to gastric mucosa, hypersecretion of acid to pentagastrin, and a hypergastrinemic response to a standard meal. Truncal vagotomy barely altered the mucosal changes produced by reflux, but it did prevent antral gland hyperplasia and reduced the acid gastrin secretory responses. These findings are clinically reassuring in that vagotomy effectively prevented the hypersecretory state produced by duodenogastric reflux.     

Quantification of morphological changes in pituitary corticotropes produced by in vivo corticotropin-releasing factor stimulation and adrenalectomy

Physiological and morphological changes produced by corticotropin-releasing factor (CRF) stimulation in vivo were studied in pituitaries immunocytochemically stained for ACTH. After 48-h ip minipump infusions of 10 or 50 ng/min CRF, serum ACTH levels were increased significantly over values in control groups that included both intact rats and rats exposed to sham abdominal surgery. Correlative morphological changes included a striking increase in corticotrope cell area. This was coupled with an apparent decrease in the percentage of stained cells, probably due to degranulation. The cellular responses were similar to those after adrenalectomy described previously by us and others. Therefore, in a parallel study, additional groups of rats were adrenalectomized and studied 24 and 48 h after the surgery. Even greater changes in serum ACTH, corticotrope cell area, and percentages were observed in the adrenalectomized rats. The difference between the CRF-infused and adrenalectomized groups was probably due to the lack of corticosterone feedback in the latter group. Among the control groups, there were no differences between intact rats and rats exposed to sham abdominal surgery. Rats subjected to sham adrenalectomy, however, showed corticotrope responses similar to those of CRF-infused rats, except that the cells were more densely stained. The present studies thus show dramatic changes in ACTH cell area, extent of staining, and percentages after in vivo CRF stimulation. In all of the experimental groups, an excellent correlation existed between serum ACTH levels and the degree of the morphological changes in the corticotropes.     

Kinetic and morphological changes induced in human blood leucocytes by cytochalasin D and E

Summary The effect of increasing concentrations of cytochalasin D and E, up to toxicity, on the velocity of blood leucocytes from normal subjects was measured in vitro using a high-resolution objective and phase-contrast time-lapse photography. The dose-response effect for the two different cytochalasins differed in accordance with the different cell specificity of their membrane binding. The average velocity of granulocytes was reduced at cytochalasin D concentrations above 5×10^–7M and cytochalasin E concentrations above 5×10^–5M. The effect on monocytes and eosinophils was similar. In contrast the velocity of lymphocytes was not affected until cytotoxic concentrations were reached.The concentration ranges which inhibited locomotion corresponded well with the concentration ranges of the cytochalasins which have an in vitro effect on microfilaments. The concentrations which induced additional morphological changes in lymphocytes also correlate well with the concentrations found to inhibit cross-linking in vitro, as well as those known to induce morphological changes in, for example, fibroblasts in vivo. Cytotoxic effects were first observed with ten-fold higher concentrations of cytochalasin E than of cytochalasin D.     

In vivo and in vitro production of inhibin by cryptorchid testes from adult rats

Adult male rats were made bilaterally cryptorchid for 3, 7, 10, and 14 days, and the peripheral serum, testicular vein serum, and interstitial fluid levels of inhibin were measured by RIA, and compared with values obtained in intact animals. The levels of inhibin in peripheral serum, testicular vein, and interstitial fluid were significantly elevated (P less than 0.01) after 3 days of cryptorchidism but declined significantly thereafter. The secretion of inhibin was also studied in vitro using isolated segments of seminiferous tubules from scrotal and abdominal testis in adult rats made unilaterally cryptorchid for 3, 6, and 12 days. The basal inhibin secretion by 3-day cryptorchid seminiferous tubules incubated at 37 C was significantly greater when compared with the scrotal seminiferous tubules at 32 C. If seminiferous tubules from scrotal testes were incubated at 37 C, the secretion of inhibin was greatly increased to similar levels observed by the 3-day abdominal seminiferous tubule cultures. In addition inhibin secretion was significantly higher when tubules from 5-week hypophysectomized rats were cultured at 37 C compared to 32 C. The inhibin secretion by seminiferous tubules from 6-day abdominal testes had returned to scrotal seminiferous tubule levels but then decreased below scrotal seminiferous tubule levels after 12 days of cryptorchidism. Seminiferous tubules from cryptorchid testes remain responsive to FSH stimulation (500 ng/ml) up to 12 days of cryptorchidism. FSH-stimulated inhibin production was increased at 3 and 12 days after cryptorchidism, but similar at 6 days after cryptorchidism, compared to the response of tubules obtained from scrotal testes. Furthermore, using seminiferous tubules from normal adult rats, FSH-stimulated inhibin production was increased by raising the incubation temperature from 32 C to 37 C. These in vivo and in vitro data suggest a dual stimulatory and inhibitory effect of higher temperature on inhibin production with an initial rise in basal and FSH-stimulated inhibin secretion by the cryptorchid testis which seems to be due to a direct effect of temperature on Sertoli cells. The subsequent decline in inhibin secretion could be due to the disruption of the seminiferous epithelium.