Pathophysiology of venous insufficiency during pregnancy.

Pregnancy is a risk factor for venous insufficiency. Up to 30 percent of women will develop venous insufficiency during their first pregnancy, and with each next pregnancy its prevalence is higher. Several pathophysiologic mechanisms are involved in the pathophysiology of venous insufficiency during pregnancy. The role of these mechanisms in the pathophysiology of venous insufficiency during pregnancy is still a point of discussion. Mechanical compression of enlarged uterus on pelvic veins was the first considered responsible for the occurrence of venous insufficiency during pregnancy. Soon, it was found that hormonal changes in pregnancy cause reduction in venous tone, and this reduction was postulated to be a major factor in pathophysiology of venous insufficiency. In a large number of subsequent studies both hypotheses were tested, being confirmed or rejected, but no consensus has been reached. This paper reviews current knowledge regarding pathophysiology of venous insufficiency during pregnancy, and discusses the possible role that some as yet uninvestigated mechanisms might have in it.

[Small gastrin (G-17) serum levels after stimulation with food during conservative treatment of patients with chronic renal insufficiency]. / Koncentracija malog gastrina (G-17) u serumu poslije podrazajnog obroka u konzervativno lijecenih bolesnika s kronicnom bubresnom insuficijencijom.

The physiological release mechanism for gastrin is complex, including both mechanical and chemical stimuli. Distention of the antrum is the main mechanical stimulus, and proteins and their degradation products constitute the most potent chemical stimuli. The aim of the present study was to examine the little gastrin (G-17) response to a test meal and to study the relationship between the G-17 concentration and gastric acid secretion in patients with various degrees of chronic renal failure (CRF). In 14 CRF patients under conservative treatment and 12 healthy control subjects, fasting and stimulated G-17 concentrations, as well as basal (BAO), maximal (MAO) and peak acid secretion (PAO) were measured. Mean fasting serum G-17 in CRF patients was 7.8 +/- 0.8 pmol/L, significantly higher (p less than 0.001) than in control subjects (5.9 +/- 1 pmol/L). However, the range of basal G-17 concentrations in both groups of subjects was not different from the normal values (4.2 +/- 11.3 pmol/L). The serum G-17 response to the food stimulation was significantly higher (p less than 0.001) in the control subjects than in the CRF patients. In normal subjects, the increment in the serum G-17 concentration rose to a peak at 30 min, but in the CRF patients the peak increment occurred at 60 min, and the response was more prolonged. There was a little difference in meal-stimulated serum G-17 concentrations in patients with various degrees of renal functional impairment. Basal acid output (BAO) was significantly higher (p less than 0.001) in the control subjects (2.62 +/- 0.51 mmol/h) than in the CRF patients (1.68 +/- 0.4 mmol/h). No significant difference in both the maximal acid output (MAO) and peak acid output (PAO) was found between the groups of CRF patients and control subjects. There was no relationship between G-17 concentrations and the gastric acid output in the CRF patients. From the results of the present study it is concluded that the human kidney is unimportant in the catabolism of G-17 but that the renal failure seems to decrease the rate of the peripheral extraction of gastrin by other tissues. The raised basal and meal-stimulated G-17 concentrations sometimes seen in CRF patients are associated with decreased rather than increased gastric acid secretions.