1. The human spleen sequesters 200-250 mL densely packed red blood cells. Up to 50% of this viscous blood is actively expelled into the systemic circulation during strenuous exercise or simulated apnoea (breath-hold) diving. The contribution of splenic contraction to changes in the circulating volume of red blood cells (RBCV), as well as the venous concentration of white blood cells (WBC) and platelets (PLT), was investigated following repeated breath-hold apnoeas. 2. Eighteen trained apnoea divers and 18 intact and six splenectomized subjects without diving experience repeated five maximal apnoeas with face immersion in cold water, with 2 min intervals between successive attempts. Venous blood samples were taken before and between consecutive apnoeas, as well as at 0, 10 and 20 min after the last breath hold. Arterial pressure, heart rate and transcutaneous partial pressure of oxygen and carbon dioxide were monitored continuously. 3. Plasma protein concentration decreased by 5.8, 2.2 and 9% in apnoea divers, untrained and splenectomized subjects, respectively, indicating an expansion of plasma volume. The RBCV and venous concentration of WBC, corrected for changes in plasma volume, increased in both trained apnoea divers (4.9+/-1.0 and 14.9+/-3.1%, respectively) and intact subjects (1.7+/-0.8 and 7.2+/-1.8%, respectively), whereas in splenectomized subjects there was no change in RBCV and a delayed increase in WBC concentration. Furthermore, an initial lymphocytosis detected during repeated breath holds in divers and intact subjects was completely absent in splenectomized subjects. None of the groups showed significant changes in PLT concentrations. The well-recognized diving response to apnoea (bradycardia and increased blood pressure) was seen during all breath-hold attempts in all subjects. 4. Repeated breath-holds (apnoeas) contribute to increased RBCV and venous blood concentrations of WBC through splenic contraction.

No abstract

In various stressful conditions, the thymus is subjected to incidental involution, mostly due to the thymocytolytic effect of secreted glucocorticosteroids. The aim of this study was to examine acute thymic involution in sick neonates and to compare the morphological grade with some clinical and laboratorial parameters. The influence of the illness on thymus tissue was investigated in 100 neonates who were treated and died in a neonatology intensive care unit. The preterm infants (n = 73) were born before the 37th week of gestation. Analysis of 57 placentas showed inflammation in 32% and circulatory disturbances in 23% of the cases. The causes of death were confirmed by autopsy: 35 were preterm infants with respiratory distress syndrome without infection, 22 were malformed, and 10 had birth trauma or asphyxia. In contrast, 29 of the preterm infants had an infection, mostly pneumonia or sepsis, and 4 of the term infants had such infections. Acute thymus involution was histologically graded (0–4) according to the method of van Baarlen (see text). Resting state (grade 0) was found in 25 of 38 neonates who lived <12 h. In 13 of 38 neonates who lived <12 h, thymus involution suggested prenatal stress. The grade of thymus involution related to the duration of illness (p < 0.001). Placental inflammation was associated with features of thymus involution (p < 0.048). Infection as a cause of death was connected to advanced thymus involution (p < 0.001). In preterm newborns, infection was more often connected with acute thymus involution than was respiratory distress syndrome (p < 0.003). Among the parameters measured in all avaiable peripheral blood samples taken 24 h before death, only the lymphocyte count related to the grade of acute thymus involution (p < 0.05), with an increase in percentage of lymphocytes in peripheral blood smears from grade 0 to 2 and a decrease from grade 2 to 4. Although the white blood cell count is highly variable, a low percentage of lymphocytes might be a sign of advanced accidental thymus involution following acute stress.

No significant differences between female and male patients harboring ureteral stones with respect to intraoperative complications were detected. Although stone characteristics were comparable between groups, a small number of women had significantly more severe UTI's postoperatively. Our current therapy regimen for URS seems to be efficient and safe both for females and males.

Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the postapneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by a 2-min resting interval, with face immersion in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 min after the last apnea. The arterial oxygen saturation level and blood pressure, heart rate, and transcutaneous partial pressures of CO(2) and O(2) were monitored continuously. At 20 min after breath holds, IVC diameter increased (27.6 and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8 and 21.4%, respectively) and the control group (74.6 and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes in the presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO(2) increased in all participants during breath holding, returned to baseline between apneas, but remained slightly elevated during the postdive observation period (approximately 4.5%). Thus increased right ventricular afterload and decreased cardiac output were associated with CO(2) retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.