Effect of desympathization on repair of the resected thyroid gland in adult rats

Department of Biology, Izhevsk Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR D. S. Sarkisov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 107, No. 3, pp. 353–356, March, 1989.     

Interaction between endogenous opioids, cholinergic and adrenergic mechanisms during vagally-induced gastrin release in rats

Endogenous opioids are present in neurons of the vagus and the intrinsic nervous system and they are colocalized with gastrin in antral G-cells. This raises the possibility that endogenous opioids modulate gastrin release. Stimulation of both cervical vagi (10V, 5Hz, 5ms) elicited an increase of arterial plasma gastrin levels at intragastric pH7 or pH2. The response at pH2 was 30% of that at luminal pH7. Atropine reduced vagally stimulated gastrin levels substantially. At luminal pH2 the small residual noncholinergic response was mediated neither by adrenergic mechanisms nor by endogenous opioids. At luminal pH 7 adrenergic blockade with phentolamine and propranolol reduced vagally stimulated gastrin by 60%. In the presence of atropine adrenergic blockade elicited only a small inhibitory effect suggesting that vagal activation of adrenergic mechanisms depends on atropine-sensitive cholinergic pathways. Blockade of opiate receptors by naloxone had no effect on vagal gastrin release, however, the noncholinergic gastrin response was reduced significantly by naloxone, suggesting that cholinergic mechanisms normally restrain activation of endogenous opioids during vagal stimulation. Naloxone had no effect on the noncholinergic, nonadrenergic stimulation of gastrin levels. These data suggest that endogenous opioids can contribute to vagal gastrin release provided the cholinergic restraint is blocked and adrenergic mechanisms stimulate endogenous opioids. In conclusion a major role of endogenous opioids in the regulation of vagal gastrin release can not be detected.     

Oncocytic Schneiderian papilloma in a young adult: a rare diagnosis

The oncocytic Schneiderian papilloma (OSP) is a rare neoplasm of the nose and paranasal sinuses. The majority of the approximately twenty patients reported in the literature with this papilloma have been over the age of fifty at the time of diagnosis. The 33-year-old woman reported here is the youngest patient with this lesion to date. The OSP should be considered in the work-up of all unilateral nasal polypoid lesions. This lesion's propensity for recurrence and its documented association with synchronous malignant disease warrant surgical excision by en bloc resection of the lateral nasal wall, with corresponding careful microscopic evaluation of all excised tissue.     

Immunotoxicology studies on octoxynol-9 and nonoxynol-9 in mice

In a double-blind study, mice were injected intraperitoneally with 0.2 ml 0.2% octoxynol-9 (O-9), 0.2 ml 0.2% nonoxynol-9 (N-9), or 0.2 ml saline (control) daily for 24 days. Another control group received no treatment. All mice were immunized twice with sheep red blood cells (SRBC) and bled by caudal incision. Mice receiving N-9 lost weight (P less than 0.02), had smaller livers (P less than 0.05), and showed enlarged spleens (P less than 0.05). The N-9-treated mice did not differ from either control group in the primary or secondary anti-SRBC responses, leukocyte (WBC) counts, or in the sizes of the kidneys, hearts, lungs, or thymuses. Mice receiving O-9 showed no significant differences from either control group in any of these tests. Serum immunoglobulin M (IgM) and immunoglobulin G (IgG) levels were similar in mice treated with O-9, N-9, or saline. All 3 groups had higher levels of both classes of immunoglobulins on day 16 than did untreated controls. This study shows that O-9, given to mice in doses 3 times that used by humans, is nontoxic, whereas the same dose of N-9 has minor deleterious effects.     

Release of cholecystokinin from rat cerebral cortex in vivo: role of GABA and glutamate receptor systems

Using cortical cups in chloralose-urethanized rats, the in vivo release of cholecystokinin-like immunoreactivity (CCK-LI) from cerebral cortex was examined. Resting levels of cholecystokinin-like immunoreactivity ranged from 20 to 30 pg/20 min sample. The addition of potassium (40 mM) in excess, resulted in a highly significant elevation in the levels of CCK-LI in the cortical superfusate. Deletion of calcium and the substitution of cobalt (10 mM), resulted in a significant reduction in both resting release and the release otherwise evoked by the addition of potassium. Focal electrical stimulation of the cortex (20 Hz), resulted in a significant (1.9 +/- 0.2-fold, n = 8) increase in the levels of CCK-LI. The addition of glutamate (10(-6)-10(-4) M) of kainic acid (10(-8)-10(-6) M), also resulted in significant elevations in the levels of CCK-LI. The co-administration of a putative glutamate receptor antagonist, kynurenic acid (10(-4) M) resulted in a significant reduction in the levels of release otherwise evoked by the addition of glutamate, but not by electrical stimulation. The addition of GABA (10(-5)-10(-3) M) resulted in a dose-dependent decrease in the resting release of CCK-LI, and the release evoked by glutamate. Picrotoxin (10(-6)-10(-4) M), resulted in a highly significant increase in the levels of CCK-LI in the cortical effluent. These results are consistent with a tonic GABAergic inhibition of CCK-releasing neurons. The treatment of the animal with diazepam (30 mg/kg, i.p.) also resulted in a significant reduction in resting release and the release otherwise evoked by focal cortical stimulation.     

Inborn errors of the urea cycle

Inborn errors of the urea cycle are an important cause of hyperammonaemia throughout childhood, and are associated with high morbidity and mortality rates. If they are diagnosed early and treated appropriately, the outcome for affected children is significantly improved.     

Inhibition of vessel allograft rejection by endothelial removal. Morphologic and ultrastructural changes.

The vascular endothelium plays an important and complex role in vascular allograft rejection. Antigens expressed by the endothelium can act to promote and be the target of rejection reactions, which often lead to thrombosis and ischemic necrosis of the allograft. In this study, segments of femoral artery and femoral vein with or without endothelium were grafted between allogenic or autologous control rats. Immunocompetent Lewis (RT1(1] recipient rats were randomly selected for groups (N = 14 for each) receiving the following: ACI- (RT1a) allografts with intact endothelium, allografts with endothelium removed before operation, autografts with endothelium, and autografts with endothelium removed. Rejection was assessed by graft patency as well as morphologic and ultrastructural changes. At 5 days, the allografts with intact endothelium were totally occluded, whereas allografts without endothelium remained patent, as did autologous control grafts with or without endothelium. Two additional groups (N = 14 each) receiving the de-endothelialized allografts or autografts were examined at 120 days after operation, revealing that grafts in both groups were still patent and had been re-endothelialized. These findings indicate that physical removal of vascular endothelium may depress vessel allograft rejection without immunosuppressive therapy.