Effect of apomorphine on peripheral venous gastrin and insulin levels in conscious dogs

Apomorphine 0.001, 0.005, 0.05 and 0.1 mg/kg were given i. v. to conscious dogs and gastrin and insulin levels were measured in peripheral venous blood. The lowest dose of apomorphine (0.001 mg/kg) did not change gastrin levels but some times caused a decrease of insulin levels, whereas the higher doses (0.005–0.1 mg/kg) induced a dose dependent increase of both hormone levels. The peak shaped release responses appeared within a few minutes and the basal values were reached again within 20 to 30 min. Apomorphine within the dose range which induced a response of insulin and gastrin also caused nausea and vomiting. Añer pretreatment with haloperidol (0.1 mg/kg) no signs of sickness were observed and the response of gastrin to 0.01 and 0.05 mg/kg of apomorphine was almost completely blocked, whereas the insulin response to both these doses was inhibited to ?50%. We conclude that the release of gastrin and insulin can be activated by stimulation of dopaminergic receptors, the anatomical location of which is not clear. Possible sites for the dopaminergic receptors are the hypothalamic region or the vagal centres in the medulla oblongata.     

Influence of suckling and feeding on insulin, gastrin, somatostatin and VIP levels in peripheral venous blood of lactating sows

Blood samples were collected in peripheral venous blood of seven lactating sows, when their piglets were suckling. In four of the experiments samples were also taken when the sows were fed a meal. Gastrin, insulin, somatostatin and VIP levels were measured by radioimmunoassay. Insulin levels increased by approximately 100% for about 10 min in response to suckling, in some experiments even before the suckling occurred, i.e. when the sows saw, heard and smelled their piglets. In four of the sows suckling caused a biphasic twofold increase in gastrin levels - one immediate peak which lasted for a few min and a second peak of longer duration (about 30-60 min), whereas gastrin levels remained unchanged in three animals. Somatostatin levels usually reflected gastrin levels in a reciprocal way. Thus, a biphasic decrease of somatostatin levels occurred in the high gastrin responders. In contrast, somatostatin levels increased in the experiments, in which gastrin levels did not change. Immediate and short-lasting (a few minutes long) increases of VIP levels were also induced by suckling. Large litters and long suckling periods appeared to be related to greater changes of the levels of all the peptides measured. Feeding influenced insulin, gastrin and somatostatin levels in the same way as did suckling from both a qualitative and a quantitative point of view. In contrast, VIP levels were not increased by feeding. The possible functional effects of the suckling-induced release of gastrointestinal hormones and possible mechanisms of their release are discussed.     

L-vasopressin inhibits oxytocin-induced increases of plasma levels of insulin conscious dogs

Oxytocin is known to increase plasma levels of insulin, glucagon and glucose in dogs. Plasma levels of vasopressin rise during stressful conditions. Since vasopressin counteracts several oxytocin-induced effects, it was decided to study how vasopressin influences the oxytocin-induced elevation of plasma levels of insulin, glucagon and glucose. Therefore oxytocin at 0.11 (which gives rise to physiological plasma concentrations) was infused i.v. for 10 min into fasted, conscious dogs either alone or in combination with 0.033 or 0.17 nmol kg-1 h-1 of L-vasopressin. Accordingly, 1.1 nmol kg-1 h-1 of oxytocin was infused alone or in combination with 0.67 or 1.7 nmol kg-1 h-1 of L-vasopressin. Repeated blood samples were drawn during and after the infusions and insulin and glucagon levels were determined by radioimmunoassay. Plasma levels of insulin increased three- and six-fold in response to 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, respectively, and the elevations were inhibited by L-vasopressin. Slight (1.5-fold) increases in plasma levels of glucagon were observed following 0.11 and 1.1 nmol kg-1 h-1 of oxytocin, although the effect was significant only after the latter dose. Concomitant infusion with L-vasopressin did not markedly influence the effect caused by oxytocin. Small, insignificant increases in blood glucose levels were induced by both doses of oxytocin. These effects were not affected by concomitant infusions of L-vasopressin. The insulin levels rose before glucose levels suggesting that oxytocin stimulates the release of insulin without a previous rise in glucose levels. In conclusion, it has been shown that vasopressin, in amounts which give rise to physiological plasma concentrations, inhibits oxytocin-induced effects on insulin levels, and that oxytocin stimulates the release of insulin via a mechanism which is independent of elevations in blood glucose levels.     

Interaction between gastrin-17 and oxytocin on plasma levels of insulin, glucagon and glucose in conscious dogs

The aim of the present study was to investigate how infusion of gastrin-17 and oxytocin affects plasma levels of insulin, glucagon and glucose in order to elucidate how the two hormones contribute to metabolic changes seen in situations where they are released, e.g. feeding and suckling during lactation. Thus, gastrin-17 (0.5 and 2.0 nmol kg-1 h-1) and oxytocin (0.11 and 1.1 nmol kg-1 h-1) were infused separately or simultaneously into conscious dogs. Both gastrin-17 and oxytocin induced significant, dose-dependent increases in insulin levels. An additive effect on insulin levels was obtained when gastrin-17 and oxytocin were infused simultaneously. Glucagon levels were not affected by gastrin-17 whereas infusion of 1.1 nmol kg-1 h-1 of oxytocin was followed by a significant increase. In contrast to a slight transient increase in the glucose level induced by oxytocin, infusion of gastrin-17 caused a sustained period of hypoglycaemia. Thus, infusion of gastrin-17 and oxytocin, respectively, gave rise to different ratios between circulating concentrations of insulin and glucagon reflected in different effects on the glucose level. The gastrin-induced hypoglycaemia could reflect that gastrin, via a release of insulin, promotes storing of glucose, e.g. in connection with feeding. That infusion of oxytocin caused a parallel increase in insulin and glucagon levels together with a slight increase in the glucose level could imply that oxytocin favours mobilization of glucose, e.g. during lactation.     

Influence on plasma levels of somatostatin, gastrin, glucagon, insulin and VIP-like immunoreactivity in peripheral venous blood of anaesthetized cats induced by low intensity afferent stimulation of the sciatic nerve

The objective of the present study was to investigate whether gastrointestinal hormones can be released in response to low intensity afferent activation of the sciatic nerve. Experiments were performed on anaesthetized cats in which the sciatic nerve was stimulated electrically at 3 Hz, to V and 0.2 ms. Blood samples were collected in a peripheral vein and the plasma levels of somatostatin, gastrin, glucagon, insulin and VIP-like immunoreactivity (below referred to as somatostatin, gastrin, glucagon, insulin and VIP) were recorded by radioimmunoassay. Afferent stimulation of the sciatic nerve caused immediate (approximately 15 min long) changes of the levels of all the above mentioned peptides. Somatostatin, gastrin and glucagon levels rose significantly, whereas in the case of insulin and VIP a significant relationship between the effect of sciatic nerve stimulation and basal levels was established. Thus, insulin and VIP levels decreased when basal levels were high and increased when basal levels were low. The secretion of gastrointestinal and pancreatic hormones is in part regulated by the autonomic nervous system. It is suggested that afferent stimulation of the sciatic nerve causes a reflex activation of the vagal and/or the splanchnic nerves, which in turn affects the release rate of the above-mentioned hormones. In conclusion, these data show that the release of gastrointestinal hormones can be influenced by low intensity stimulation of the sciatic nerve. The physiological trigger of these responses may be touching of the skin.     

Hepatic insulin and glucagon extraction after their augmented secretion in dogs

Effects of intravenous arginine and cholecystokinin-pancreozymin (CCK-PZ) infusion on hepatic extraction of insulin (EI) and glucagon (EGG) and also on hepatic glucose output (HGO) were studied in anesthetized dogs. Because insulin and glucagon exert antagonistic effects on HGO, insulin:glucagon (I/GG) molar ratios were determined in the portal vein and also in peripheral vessels. During the arginine-CCK-PZ infusion the amount of insulin and glucagon coming to the liver increased 12- and 15-fold, respectively. In contrast EI decreased significantly from a control value of 62 +/- 6% to a nadir of 22 +/- 13%. EGG (control value 19 +/- 9%), however, was unaffected by arginine-CCK-PZ. The absence of any alteration in EGG cannot be attributed to the molecular heterogeneity of the immunoreactive glucagon. HGO increased fourfold in response to the pancreatic stimulation, whereas portal I/GG decreased significantly from 8.2 +/- 0.9 to 5.0 +/- 0.7. The concurrent femoral arterial I/GG (control 3.7 +/- 1.0) and mesenteric venous I/GG (control 2.1 +/- 0.5) increased significantly. These observations indicate that portal, but not peripheral, I/GG measurements reflect hepatic events in anesthetized dogs, probably because of the different extraction patterns for insulin and glucagon.     

Release of gastrin and insulin in response to suckling in lactating dogs

The concentration of gastrin and insulin was determined in peripheral blood of 4 lactating dogs during suckling. Suckling induced an immediate rise of gastrin and insulin levels, twofold and threefold, respectively. A peak was reached at approximately 5 min after suckling was started, and basal levels were reached again within 15-20 min. The increase in gastrin and insulin levels coincided with the let-down reflex, i.e. it occurred when the puppies started to obtain milk from their mothers. Sham feeding and feeding induce a vagally mediated increase of gastrin and insulin release in dogs. We suggest that the changes in the gastrin and insulin levels observed by us in the lactating dogs, reflect a similar vagal activation induced by suckling. Possible effects of the suckling induced release of gastrin and insulin on milk ejection and secretion are discussed.     

Regulation of peripheral glucagon concentrations in cyclic, pregnant, and lactating rats.

In the rat, peripheral glucagon concentrations were studied throughout pregnancy and lactation. Basal glucose concentrations were decreased during late pregnancy and during lactation, but basal glucagon concentrations were not affected. Infusion of glucose (7.4 mg/min) caused an elevation of the glucose concentrations, which became lower in the course of lactation, and a suppression of the glucagon concentrations which was the same throughout pregnancy and lactation. Ingestion of 336 mg of glucose or 1 g of rat chow throughout pregnancy and lactation induced a transient increase of the glucose concentrations and a biphasic glucagon response: following a short-lasting elevation, the glucagon concentrations became suppressed. The glucagon responses to these tests did not change during pregnancy and lactation. It is concluded that the regulation of the peripheral glucagon concentration is not affected by pregnancy or lactation, and that the response of the glucagon concentration to a metabolic challenge varies with the kind of test (oral or intravenous) used.     

600名新生儿末梢血与静脉血的血象对比

全自动血液分析仪的广泛应用,使静脉血的检测明显优于末梢血的检测。由于新生儿的生理条件有别于成人,采取末梢血检测新生儿各项血细胞参数仍受到重视,我科对600名新生儿末梢血与静脉血的血象结果进行了比较,现报告如下。1资料与方法我院产科健康新生儿600名,男398名,女202名,平均年龄(4.31±2.06)d。采用美国雅培公司CELL-DYN1600及配套稀释液、溶血素、清洁液。采用足底加温采血和股静脉血采血法,取新生儿足跟血50u l和静脉血0.5 m l,分别置于含有0.5?TA-K2的干燥试管中,迅速摇匀,室温1 h内完成检测。采用配对t检验和直线相关分析…     

Suckling reduces allergic skin responses and plasma levels of neuropeptide and neurotrophin in lactating women with atopic eczema/dermatitis syndrome

BACKGROUND: Lactation is associated with an inhibited hypothalamic-pituitary-adrenal axis response to physical and psychological stress in women and female rats. However, suckling also improved mood and calmness in nonatopic lactating women. Relaxation by humor reduced allergen-induced skin wheal responses, while various forms of stress enhanced those responses in allergic patients. Moreover, enhancement and reduction in allergen-induced skin wheal responses are associated with up- and down-regulation of plasma levels of substance P (SP) and vasoactive intestinal peptide (VIP), respectively. In addition, plasma levels of SP, VIP and nerve growth factor (NGF), but not neurotrophin-3 (NT-3), are elevated in allergic patients. Therefore, the effects of suckling on allergic responses and plasma levels of neuropeptides and neurotrophins were studied in lactating women with atopic eczema/dermatitis syndrome (AEDS). METHODS: Before and after suckling, allergic skin responses to allergens were studied by skin prick test; simultaneously plasma levels of substance P, vasoactive intestinal peptide, nerve growth factor and neurotrophin-3 were measured in lactating women with atopic eczema/dermatitis syndrome. RESULTS: Suckling reduces allergen-induced, but not histamine-induced, skin wheal responses, while holding infants without suckling failed to do so. Suckling also reduced plasma levels of SP, VIP and NGF, but not NT-3 in these patients, while holding infants without suckling failed to do so. CONCLUSIONS: These results indicate that suckling reduces allergic responses with a concomitant reduction in plasma levels of SP, VIP and NGF. Collectively, suckling may have some implication in the study of maternal allergy in atopic patients.     

Arterialization of peripheral venous blood in sickle cell disease

Arterialization of the venous blood is thought to be indicative of cutaneous shunting, and occurs in patients with sickle cell disease (SCD) during vaso-occlusive crisis (VOC). We performed the present study to quantify the amount of shunting that occurs in sickle cell patients presenting at the Howard University Sickle Cell Center, Washington, D.C., as outpatients and for hospitalizations associated with sickle cell crisis. Peripheral venous blood was drawn anaerobically into heparinized syringes from 9 normal control subjects (NC), 24 outpatients (steady-state group), and 14 inpatients during crisis (VOC group). Spectrophotometric measurements were made for the following species of hemoglobin (Hb): oxy-Hb (O2Hb), reduced Hb (RHb), carboxy-Hb (COHb), and met-Hb (MHb). In addition, fetal hemoglobin (HbF) was measured by high-pressure liquid chromatography (HPLC). The O2Hb saturations of the steady state group were not significantly different than those of the NC group (55 +/- 4% vs. 40 +/- 6%). However, the O2Hb saturations of the VOC group were 73 +/- 3%, and this value was found to be significantly greater than those of both the steady-state and the NC groups (p < 0.05). Reduced hemoglobin saturations were inversely related to the O2Hb values, as expected. Compared to the NC group, the steady-state, and VOC groups had greater dyshemoglobin (COHb and MHb) levels (p < 0.05). These findings suggest that the percentages of venous O2Hb and dyshemoglobins may be increased in sickle cell disease even in the absence of VOC. Therefore, the venous O2Hb saturation may be a useful biochemical marker for the arteriovenous shunting and hemodynamic adaptations associated with sickle cell disease.     

Influence of peripheral and intracerebroventricular glucose and insulin infusions on peripheral and cerebrospinal fluid glucose and insulin levels

There is much evidence that glucose and insulin are related to the regulation of food intake and the maintenance of peripheral glucose homeostasis through actions of the central nervous system. However, evidence concerning the penetration of peripheral glucose and insulin into the cerebrospinal fluid (CSF) and the relationship between both peripheral and CSF glucose and insulin levels is still missing. In the reported experiments it is shown that insulin is present in the CSF (17 +/- 3.6 microU/ml CSF versus 44 +/- 6.0 microU/ml plasma) but that CSF insulin does not follow rises of peripheral insulin to 136 microU/ml plasma during 4.5 hours. On the other hand CSF glucose (55 +/- 3.1 mg/dl CSF) follows rises of peripheral glucose levels with a delay of about 30 min. Increase of CSF glucose by infusing glucose into the third brain ventricle elicits a prolonged decrease in peripheral glucose levels. Infusion into the third ventricle of insulin only does not change peripheral glucose. However, infusion of a combination of insulin and glucose in the third ventricle leads to a gradual increase in peripheral glucose and elicits a disappearance of the decrease in peripheral glucose after glucose only infusion into the CSF. During third ventricle infusion experiments no change in peripheral insulin could be observed. It will be argued that changes in CSF glucose and insulin contribute to maintenance of peripheral glucose homeostasis.     

Effect of inflammatory and noninflammatory stress on plasma ketone bodies and free fatty acids and on glucagon and insulin in peripheral and portal blood

Inflammatory stress as characterized by infection withStreptococcus pneumoniae, administration of endotoxin, or the induction of a turpentine abscess is characterized by the inhibition of the ketosis associated with fasting and a decline in the level of free fatty acids in the plasma. Moreover, rats subjected to these inflammatory stresses demonstrate a significant rise in peripheral and portal insulin and glucagon. Rats subjected to noninflammatory stresses, screen-restraint, or noninvasive femoral fracture did not demonstrate the inhibition of ketosis but did show a decrease in plasma free fatty acids. The noninflammatory stresses did not show an abnormal elevation of plasma or portal insulin or glucagon.The views of the authors do not purport to reflect the positions of the Department of the Army or the Department of Defense.In conducting the research described in this report, the investigators adhered to the Guide for the Care and Use of Laboratory Animals, as promulgated by the Committee on the Revision of the Guide for Laboratory Animal Facilities and Care of the Institute of Laboratory Animal Resources, National Research Council. The facilities are fully accredited by the American Association for Accreditation of Laboratory Animal Care.     

Isolation of lymphocytes from peripheral blood of dogs

Previous methods for the isolation of canine peripheral lymphocytes have not consistently produced cells of adequate purity. By means of centrifugation over a layer of Ficoll-sodium diatizoate of appropriate density, followed by passage through a simple column using nylon fibers, relatively pure lymphocyte fractions were isolated from canine peripheral blood. This simple and rapid technique requires no special equipment. Sixty percent of the total lymphocyte population was recovered. The fractions were composed of 96% normal small lymphocytes with a viability of 98%. The lymphocytes thus obtained were suitable for a lymphocytotoxicity assay.