Effect of anaesthetizing the region of the paraventricular hypothalamic nuclei on energy metabolism during exercise in the rat

The ventromedial and posterior hypothalamic nuclei are known to influence glucoregulation during exercise. The extensive projections of the paraventricular hypothalamic nucleus (PVN) to the sympathetic nervous system suggest that the PVN also may be involved in glucoregulation during exercise. The region of the PVN was anaesthetized with bupivacaine before running (26 m min^-1) or continued rest, via previously implanted bilateral brain cannulas aimed at the dorsal aspect of the PVN. Control rats were treated identically to PVN-anaesthetized rats, but were not infused. Blood, for determination of plasma concentrations of metabolites and hormones, was drawn from a tail artery, and ³H-glucose was infused in a tail vein for glucose turnover determinations. At rest, no significant changes in plasma concentrations of metabolites or hormones were induced by anaesthesia of the region of the PVN. During exercise, glucose production and utilization and plasma concentrations of glucose, lactate, glycerol, noradrenaline, adrenaline, corticosterone, and glucagon increased (P < 0.02) and plasma insulin decreased (P < 0.02) in all rats. However, initially in exercise, adrenaline (4.3 ±0.8 vs. 7.9 ± 1.0 nmol 1^-1 in controls, P < 0.05, t= 6 min) and later corticosterone levels (1.37 ± 0.06 vs. 1.69 ± 0.10 nmol 1^-1 in controls, P < 0.05, t = 20 min) were attenuated by PVN anaesthesia. Initially during exercise, glucose utilization was higher and plasma glucose lower in PVN-anaesthetized rats compared to controls (16.6 ± 0.8 vs. 12.7 ± 0.6 μmol min^-1 100 g^-1 and 7.1 ± 0.2 vs. 8.1 ± 0.2 mmol 1^-1, respectively. P < 0.05, t= 6 min) and exercise-induced liver glycogen breakdown was only significant in the controls. In conclusion, the region of the PVN does not influence glucoregulation at rest, but affects glucoregulation during exercise, by stimulating adrenaline and corticosterone secretion during exercise.     

Pathology of the lung in leukaemia and lymphoma: a study of 87 autopsies

Histopathological findings in the lungs in a series of autopsies on 87 patients suffering from various types of leukaemia or lymphoma who had received no treatment, or various combinations of radiotherapy, chemotherapy and bone marrow transplantation were reviewed. Thirteen untreated patients showed neoplastic infiltration (4), thromboembolism (4), infection (5) or amyloidosis (1). Seventy-two treated cases showed malignant infiltration (14), vascular damage (21), infections (32) and/or diffuse alveolar damage (47). One patient treated with local irradiation for myeloma had acute bronchopneumonia alone and another treated with [32P] for polycythaemia rubra vera had extensive thrombo-embolism of the large pulmonary vessels. Clinical and autopsy evidence of infection correlated very poorly. Non-infective pulmonary disease was a frequent finding. Bacterial, fungal or pneumocystis pneumonia particularly affected the chemotherapy and radiotherapy groups, while cytomegalovirus infection was seen only in the bone marrow transplant group. This study shows that diffuse alveolar damage is a common and important problem in patients treated with radiotherapy and chemotherapy.     

Dominant T-Cell Receptor β-Chain Gene Rearrangements Indicate Clonal Expansion in the Rheumatoid Joint

Miltenburg, A.M.M., van Laar, J.M., Daha, M.R., de Vries, R.R.P., van den Elsen, P.J. & Breedveld, F.C. Dominant T-Cell Receptor β-Chain Gene Rearrangements Indicate Clonal Expansion in the Rheumatoid Joint. Scand. J. Immunol. 31, 121-125, 1990
T-cell receptor (TcR) β and δ gene rearrangements were studied in anti-CD3 expanded T-cell populations cultured from the synovial membrane (SM) (n=5) or synovial fluid (SF) (n=2) of rheumatoid arthritis (RA) patients. Dominant TcR β-chain gene rearrangements to Cβ1 were demonstrated in all the patients tested and 1-3 expanded clones per patient were found. Clonal rearrangements to Cβ2 were detected in one SM sample (two clones) and one SF sample (one clone). The TcR δ gene was deleted in all the samples tested. We conclude that clonal dominance may be present, either using the Cβ1 or Cβ2 gene segment.     

Contribution of liver nerves,glucagon, and adrenaline to the glycaemic response to exercise in rats

The contribution of hepatic sympathetic innervation, glucagon and adrenaline to the glycaemic response to exercise was investigated in rats. Hepatically denervated (LDX) or sham operated (SHAM) rats with permanent catheters were therefore submitted to swimming with or without infusion of somatostatin in combination with adrenodemedul–lation. Blood samples were taken for measurements of blood glucose, plasma free fatty acids (FFA), adrenaline (A), noradrenaline (NA), insulin and glucagon. Liver denervation by itself did not influence glucose levels during exercise. Infusion of somatostatin in SHAM animals, which inhibited the exercise–induced glucagon response, led to enhanced sympathoadrenal outflow (measured as plasma A and NA) and a reduced blood glucose during exercise, suggesting that glucagon serves as a powerful mediator of the glycaemic response during swimming. Infusion of somatostatin in LDX animals failed to enhance plasma NA levels and led to a more pronounced reduction in blood glucose levels. This indicates that liver nerves do contribute to the glycaemic response to exercise when glucagon secretion is suppressed. Reduced blood glucose levels after adrenodemedullation revealed that adrenal A is another important mediator of the glucose response to exercise. Infusion of somatostatin in adreno–demedullated SHAM or LDX animals was not accompanied with increased NA outflow, suggesting that adrenal A is necessary to allow the compensatory increased outflow of NA from sympathetic nerves. In conclusion, the study shows that pancreatic glucagon and adrenal A are the predominant factors influencing the glycaemic response to exercise, whereas a role of the sympathetic liver nerves becomes evident when glucagon secretion is suppressed.