The effect of neurotensin and secretin on gastric acid secretion and mucosal blood flow in man

Neurotensin stimulates pancreatic secretion directly and by potentiating the effect of secretin. Neurotensin also inhibits gastric secretion. Secretin inhibits gastric secretion as well, but whether it also interacts with neurotensin is not known. Secretin is known to inhibit gastric mucosal blood flow (GMBF). The effect of neurotensin on GMBF is not known. Acid secretion (triple lumen perfused orogastric tube) and GMBF ([14C]aminopyrine clearance) were therefore measured in 6 subjects during neurotensin, secretin and neurotensin plus secretin infusions. Neurotensin plus secretin reduced acid secretion by a median 130 (range 34-394) mumol/min which was significantly greater than either neurotensin at 36 (7-67) mumol/min or secretin 54 (20-347) mumol/min alone (P less than 0.05). This effect appeared independent of GMBF. Neurotensin plus secretin reduced GMBF by 14 (12-27) ml/min but not significantly more than neurotensin at 11 (3-20) ml/min or secretin 18 (2-27) ml/min alone. Further, there was no correlation between changes in acid output and GMBF during infusion of the peptides. We conclude that the inhibitory effects of neurotensin and secretin on gastric secretion are at least additive and together they may function as an 'enterogastrone'.     

Cardiovascular responses to intrathecal administration of arginine vasopressin in rats

Arginine vasopressin (AVP) has been localized in numerous extrahypothalamic brain regions and in the spinal cord. The results of intracerebroventricular AVP injections and microinjection of AVP into the brain stem suggest that this peptide, acting centrally at higher levels, may influence cardiovascular function. No function for the AVP occurring at spinal levels has been reported. In this study we report that AVP, in picomole quantities, increased arterial blood pressure and integrated heart rate in a dose-dependent manner following intrathecal application to the thoracic region in the rat. This response was not blocked by intravenous administration of the AVP antagonist d(CH₂)₅-d-Tyr-VAVP. These results suggest that AVP, acting within the spinal cord, may alter neural outflow regulating blood pressure and heart rate.     

Reproductive and metabolic hormones during estrus after fasting in Holstein heifers

The estrous cycles of 23 Holstein heifers were synchronized with three prostaglandin F₂α (PG) injections at 0600 h 11 d apart, designated as Days ?11, 0 and 11. Twelve of the animals were randomly assigned to receive no solid food (Group F) from Day 6 to 14, while the other animals remained on full feed to serve as controls (Group C). Jugular blood samples were collected at 6-h intervals beginning with PG injection at 0600 h on Day 0 until 1800 h on Day 4 and at 0600, 1200 and 1700 h on Day 8 through 10. Samples were collected again at 6-h intervals from PG Day 11 (0600 h) until 1800 h on Day 15. Period 1 was defined as those samples collected from Day 0 through 4.5, Period 2 from Day 7 through 10, Period 3 from Day 11 through 14.25, and Period 4 from Day 14.5 through 15. Plasma growth hormone concentrations were increased (P<0.01) in F as compared with C animals during Periods 2, 3 and 4. Plasma concentrations of prolactin (P<0.01) were decreased in F as compared with C animals during Periods 2 and 3. Plasma urea concentrations were increased (P<0.01) in F as compared with C animals during the first 3 d of the fast (Period 2) but were decreased (P<0.01) during the remainder of the experiment (Periods 3 and 4). Thus, fasting was effective in altering several metabolic parameters. Although plasma progesterone and luteinizing hormone (LH) concentrations remained similar (P>0.05) between F and C animals, plasma estradiol-17β concentrations decreased in F as compared with C animals during Periods 2, 3 and 4. No differences (P>0.05) between F and C animals were found in duration to LH peak after PG injection, estrous behavior, or pregnancy rates. Results from this study indicate that fasting reduced plasma estradiol-17β concentrations during estrus but did not alter occurrence of estrus or pregnancy rate.     

Blood typing invalidates alleged evidence of fertility of XO mare

A mare with XO gonadal dysgenesis was reported to have produced two foals. Blood samples from the mare, her two foals, their sire and the mare's sire were typed for blood-group and serum protein variants in conjunction with registry requirements. Both foals qualified as offspring of the reported parents. However, the blood-typed mare could be excluded as an offspring of her alleged sire. An alternative hypothesis to explain the blood-type and karyotype findings was that a fertile mare had been substituted for the XO mare, as surrogate mother and blood-type donor. A computer search of 120,000 blood-type records identified only one other horse with the same blood type as the dam of the foals. That horse was a mare of the same breed and owned by the person who had attempted to register foals from the XO mare. These blood-type findings invalidated the allegation of XO fertility and emphasize the need for parentage verification to support reports of unusual reproductive performance.     

安定减低家兔膈神经放电幅度的机制分析

本实验室曾经报道静脉注射安定对于清醒、麻痹、人工呼吸的家兔具有减低膈神经放电幅度、加快呼吸频率,缩短吸气时程(T_I)和呼气时程(T_E),降低动脉血压等作用。本工作在35只家兔中进一步分析了某些药物对安定的这些作用的影响。GABA 降低膈神经放电幅度和动脉血压,这与安定的作用相同,但 GABA 延长T_I、T_E和减慢呼吸频率,与安定的作用相反。事先用氨基酸脱羧酶抑制剂异烟肼处理,或用 GABA 受体拮抗剂印防己毒素处理,可阻遏安定减低膈神经放电幅度的作用。在事先用印防己毒素处理的家兔中,可见安定缩短 T_IT_E的作用不受影响。异烟肼或印防己毒素还能部分对抗安定的降压效应。阿片受体拮抗剂纳洛酮和5-HT 受体拮抗剂赛庚啶都不能阻遏安定降低膈神经放电幅度和动脉血压的作用。上述结果提示安定降低膈神经放电幅度的作用可能通过 GABA 这一中间环节,而内啡肽和5-HT可能不起重要作用。安定的降压作用需要有内源性 GABA 参与才得以持续较长时间,在减少GABA 或阻断 GABA 受体后,安定只有短暂的降压作用。     

Effects of monovalent cations on red cell shape and size

Human erythrocytes were incubated in isotonic solutions of different monovalent cations. The apparent size of the red cells measured on scanning electron microscopic pictures decreases in the order Li⁺>Na⁺=K⁺>Rb⁺. These differences in size are abolished after pretreatment with trypsin, which removes a large part of the charges associated with membrane glycoproteins. Shape alterations are also observed. Normal biconcave shapes are visible after Na⁺ or K⁺ incubation, whereas Li⁺ leads to flabby, flattened cells with a certain tendency to crenation, and Rb⁺ causes more pronounced biconcavity with a certain tendency to cupping. The overall effects of pretreatment with trypsin are similar to those of Li⁺. Our results provide evidence that the electrostatic repulsion of glycoproteins and other charged membrane components may play an essential role in maintaining red cell shape.     

蟾蜍红细胞与网织红细胞染色质蛋白的比较研究Ⅲ·HMG蛋白质

从亚洲蟾蜍(Bufo bufo asiaticus)与鸡红细胞核内分离纯化了HMG蛋白(Highmobility group proteins),经聚丙烯酰胺凝胶电泳鉴定,证明两者的电泳图谱不完全相同,在蟾蜍的红细胞内也能观察到与鸡HMG_(17)相对应位置上的蛋白质区带,但在鸡HMG_(14)相对应的位置上,却能观察到两条显著的蛋白质区带(A及B带)。此外,我们已把蟾蜍成熟红细胞与苯肼诱发后的网织红细胞内的HMG蛋白进行比较,证明两者有显著的差异。网织红细胞内HMG_A和HMG_B蛋白在含量上起了变化,却与成熟的红细胞相反。另外还出现了二条新的蛋白区带(C与D带)。初步的结果暗示了,HMG蛋白类似于非组蛋白、染色质蛋白,在量上的变化将会引起功能上的变化。     

Characterization of proteolytic enzymes of the midgut and excreta of the biting fly Stomoxys calcitrans

Proteolytic enzymes were characterized in the midgut and the excreta of the stable fly Stomoxys calcitrans (L) with proteins, synthetic substrates, and inhibitors. Inhibition studies suggested trypsinlike activity in sugar-fed fly midguts, whereas excreta and blood-fed fly guts exhibited other proteases. Trypsinlike activity in midguts removed 20 and 30 h after a blood meal increased from 20% to 50% of the total proteolytic enzymes present. Trypsinlike activity was inhibited with human sera, trypsin-specific inhibitors, and a protein isolated from the stable fly thorax. When human albumin and globulin fractions were incubated with trypsinlike enzymes isolated from the midgut and excreta, the albumin fraction was less inhibitory than the globulin fractions and was readily hydrolyzed by the proteolytic enzymes. These results may indicate that the proteolytic enzymes produce an abortive complex with the globulin fractions of the sera. Such a complex may explain the temporary inhibition of proteolysis by the blood meal. Soybean trypsin inhibitor fed to stable flies caused 50% inhibition in proteolytic activity in the midguts of sugar-fed stable flies and 25% inhibition in the midguts of blood-fed stable flies. Complete inhibition of proteolytic enzyme activity was achieved only in vitro. pH profiles of proteolytic enzyme activity isolated from the excreta of blood-fed stable flies indicated that several proteolytic enzymes were excreted.     

The effect of chronic alcohol feeding on lipid peroxidation in microsomes: lack of relationship to hydroxyl radical generation

Chronic alcohol feeding causes microsomal induction including increased generation of hydroxyl radicals. Ethanol induced liver injury may be mediated by lipid peroxidation for which hydroxyl radicals have been proposed as major mediators. Ethanol promotes lipid peroxidation when given acutely but also may serve as a hydroxyl radical scavenger. Therefore, we studied the acute and chronic effects of alcohol on microsomal lipid peroxidation and hydroxyl radical generation. Chronic alcohol feeding in rats increased microsomal generation of hydroxyl radicals but lipid peroxidation of endogenous lipid was inversely related to hydroxyl radical generation. Ethanol (50mM) had a slight inhibitory effect on hydroxyl radical production in peroxidizing microsomes, no effect on endogenous lipid peroxidation and enhanced the lysis of RBCs added as targets of peroxidation. Enhanced microsomal generation of hydroxyl radicals following chronic alcohol feeding is not an important mediator of lipid peroxidation.     

Effect of Folate Deficiency on Local Cerebral Glucose Utilization in the Rat

There is considerable debate on the role of folate in CNS function. Recent work indicates that folate deficiency may affect CNS serotonin metabolism, and clinical studies describe many consequences of such a deficiency. On the other hand some workers maintain that folate deficiency alone causes CNS abnormalities. We maintained rats, through dietary deprivation, at folate levels below 4 ng/ml for more than 6 weeks and showed that at that time both their liver and brain folate levels were significantly reduced. We then studied their local cerebral glucose utilization (LCGU) using the [14C]deoxyglucose technique. This method assesses cerebral function by measuring regional metabolic activity. We also determined LCGU in rats given the same diet but replenished with folate (folate control) and in others given free access to commercially available food (normal controls). Our results show that this degree of folate deficiency has no effect on cerebral function. This contrasts with the focal suppression of LCGU we previously reported in a model of vitamin B12 deficiency.