当归对正常及肝硬化犬血浆胰高血糖素水平的影响

众所周知，胰高血糖素参与了肝硬化高动力循环和门脉高压的形成。我们以往的研究证实。中药当归对肝硬化门脉高压症有良好的预防及治疗作用。为探讨其作用机理，本文研究了当归对正常及胆道结扎肝硬化犬内脏血浆胰高血糖素水平的影响。结果表明，用药后两组动物血浆胰高血糖素水平均显著下降，且肝硬化组下腔静脉和门静脉内血浆胰高血糖素水平的变化与其门脉和门脉血流量的变化呈显著正相关。提示当归可能通过减少胰高血糖素的分泌和     

胰高血糖素在乙肝后肝硬化门静脉高压症病人血中浓度的变化

胰高血糖素是由29个氨基酸组成的多肽，由胰岛A细胞分泌，具有强大的扩血管作用。我们用放射免疫分析技术测定了乙肝后肝硬化门静脉高压症病人门静脉、肝静脉及外周血中胰高血糖素浓度，旨在探讨胰高血糖素浓度变化的原因及其临床意义。     

奥曲肘对肝硬化病人门脉血流动力学的影响以及与血浆胰高？…

为探讨奥曲肽减少门脉血流量、降低门脉压和血浆胰高糖素水平的关系，我们研究了肝硬化病人应用奥曲肽前、后门脉血流动力学及血浆胰高糖素水平的变化。静滴奥曲肽后，病人门脉系统血流量及血浆胰高糖素水平均显著下降。奥曲肽可明显减少门脉血流量，因此能有效地用于治疗门脉高压。奥曲肽降低门脉压的机制可能在于抑制胰高糖素的释放。     

奥曲肽对肝硬化病人门脉血流动力学的影响以及与血浆胰高糖素水平的关系

为探讨奥曲肽减少门脉血流量、降低门脉压和血浆胰高糖素水平的关系，我们研究了肝硬化病人应用奥曲肽前、后门脉血流动力学及血浆胰高糖素水平的变化。静滴奥曲肽后，病人门脉系统血流量及血浆胰高糖素水平均显著下降。奥曲肽可明显减少门脉血流量，因此能有效地用于治疗门脉高压。奥曲肽降低门脉压的机制可能在于抑制胰高糖素的释放。     

肠系膜上静脉外科干的应用解剖与临床

目前治疗门脉高压症常用分流术有门腔分流术,脾肾静脉、脾门静脉分流术及肠腔分流术等,其中肠腔分流术,由Regnolds和Clatwarthy五十年代首倡以来,一系列国内外医务工作者相继对肠腔分流术疗效进行观察,他们都认为此术治疗门脉高压症其减压效果好,脑病并发率及术后死亡率低,故在临床推荐应用,同时,为了解决此术解剖学变异的难题,法国解剖学家Gillot在1964年对肠系膜上静脉进行了较为详细的报道,并首先将该静脉可供吻合的一段命名为外科干,此后,     

肝前性门脉高压大鼠胰岛功能的变化

目的：探讨肝前性门脉高压大鼠胰岛α、β细胞功能及其与循环血液中胰岛素及胰高血糖素水平变化的关系。方法：采用部分结扎门静脉的方法复制肝前性门脉高压,假手术及正常鼠的胰岛进行分离和纯化,并对其体外生物学活性进行检测。结果：肝前性门脉高压组大鼠循环血液中胰岛素及腹高血糖素水平明显高于正常组大鼠（P＜0．01）。肝前性门脉高压级大鼠分离纯化的胰岛经体外培养48h或在含糖基质中孵育2h后释放胰岛素量明显低于正常,而陵高血糖素明显高于正常（P＜0．01）。结论：胰岛α细胞分泌功能增加可能有助于解释高胰高血糖素血症的发生;门脉高压时,循环血液中胰岛素水平增加,但哪胞功能低于正常。     

门静脉高压症经颈静脉肝内门体分流术(TIPS)血液动力学分析

经颈静脉肝内门体分流术（TIPS）是治疗门静脉高压症的有效手术之一。本文提出了一个集中参数模型对TIPS进行血液动力学分析。首先根据门脉高压的前向血流学说和后向血流学说，计算了门静脉系统血液动力学参数，然后计算了TIPS术后门静脉系统血液动力学参数的变化，并详细分析讨论了这些血液动力学参数随肝硬变梗阻程度的变化，以及TIPS分流道阻力对它们的影响。结果表明所得结果和临床所测参数吻合较好，该模型可进一步应用于门脉高压症和其它分流术血液动力学机理研究，并为临床应用提供参考。     

部分回结肠切除术治疗门脉高压的实验研究

本文根据门脉系的解剖生理学特点,设计了部分回结肠切除术用以治疗门脉高压症。通过对8只猫的实验观察,表明该术式能有效地降低自由门脉压,缓解门脉压高症,并能在一定程度上提高门脉最大灌注压.本文还将该术式与断流术、分流术进行了比较、讨论。     

食管静脉曲张的手术治疗

食管静脉曲张的手术治疗浙江省中医院收治门静脉高压症食管静脉曲张２０４例（其中手术治疗１９３例），病因以血吸虫病肝硬变最多见，其次为肝炎后和门脉性肝硬变。对无上消化道出血史者，采用以脾切除为主的手术。对有出血史者，行周围型门体静脉分流术或断流术，两组效...     

分流手术治疗门脉高压症并发上消化道出血的研究进展

食管、胃底部静脉曲张破裂出血是门静脉高压症最常见、最严重的并发症,出血量大、死亡率高,内科治疗效果不确切,而静脉一旦破裂,就会反复出血,而每次出血必将给肝带来严重损害,因此,应争取即时外科手术治疗。但因门静脉侧支吻合丰富,故治疗方法多种多样,而分流术在其中占有重要一席,它不但可以防止再出血,而且是预防发生肝昏迷的有效措施。目前分流主要有以下五种术式:①脾肾静脉分流术;②门腔静脉分流术;③脾腔静脉分流术;④肠系膜上、下腔静脉分流术;⑤经颈内静脉肝内门体分流术(TIPSS)。它们均切实降低了门脉压力,阻止了出血,取得了良好效果。     

2型糖尿病并发高血压者血清瘦素、胰岛素、胰高血糖素的水平变化及关系研究

目的：探讨2型糖尿病并发高血压者血清瘦素（Leptin）、胰岛素（Insulin）、胰高血糖素（Glucagon）水平变化与关系。方法：采用放射免疫分析对30例2型糖尿病并发高血压者和30例不伴高血压者进行血清瘦素、胰岛素及胰高血糖素含量测定,分析两组瘦素水平及其相关性。结果：两组糖尿病患者上述三指标显著高于健康正常人组（30例）,具有统计学意义（P〈0．01）;合并高血压的糖尿病病人与无高血压病人比较,差异也非常显著（P〈0．05）,且与血压的程度呈正相关关系。结论：糖尿病并发高血压者血清瘦素、胰岛素、胰高血糖素的升高,参与了本病的发生与发展过程,作为判断其病情指标有重要临床价值。     

Rapid changes in glucose metabolism following the administration of ethionine: its role in regulating hepatic protein synthesis

The relationship between the changes in portal glucagon, insulin, glucose, and hepatic protein synthesis were investigated during ethionine intoxication. There was a 50% decrease in blood glucose, a seven-fold increase in portal glucagon and a 90% increase in portal insulin, all of which coincided temporally with the inhibition of hepatic protein synthesis. When reversal of ethionine intoxication was initiated with adenine it simultaneously restored blood glucose, insulin, glucagon, and protein synthesis. Protein synthesis could not be adequately restored by glucose, but in this case hepatic ATP levels did not increase. In addition, glucose given by stomach tube prior to ethionine did not prevent the action of ethionine, though it did maintain plasma glucose levels and prevented the decrease in plasma insulin and increase in plasma glucagon. These results show that in vivo regulation of hepatic protein synthesis during ethionine intoxication is not likely to be mediated by portal insulin, glucose, and glucagon.     

Influence of somatostatin on glucagon- and epinephrine-stimulated hepatic glucose output in the dog.

Glucose kinetics were measured using [3-3H]glucose in conscious dogs during the infusion of: 1) glucagon alone; 2) glucagon plus somatostatin with insulin replacement; 3) epinephrine alone; and 4) epinephrine plus somatostatin with insulin and glucagon replacement. Infusion of glucagon alone resulted in a 10-15 mg/dl rise in plasma glucose and a transient 45% rise in glucose production. When somatostatin and insulin were added, a four- to fivefold greater rise in plasma glucose and glucose production was observed. Glucagon levels were comparable to those achieved with infusion of glucagon alone, whereas peripheral insulin levels increased three- to fourfold above baseline, suggesting adequate replacement of preinfusion portal insulin levels. Infusion of epinephrine alone produced a 40% rise in plasma glucose and a 100% rise in glucose production. When somatostatin, insulin, and glucagon were added to epinephrine, the rise in glucose production was reduced in 65% despite replacement of glucagon levels and presumably mild portal insulin deficiency. These findings suggest that somatostatin: 1) potentiates the stimulatory effect of physiologic hyperglucagonemia on glucose production independent of insulin availability and 2) blunts the stimulatory effect of physiologic increments of epinephrine independent of glucagon availability.     

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.     

Is daytime insulin more physiologic and less atherogenic than bedtime insulin?

The question is whether bedtime insulin, one of the standard therapy regimens of type 2 diabetes, can be more atherogenic than daytime insulin. There is no study to answer this question. However, pharmacokinetics of drugs and physiopathology of type 2 diabetes are considered, we can assume that daytime OAD plus bedtime insulin therapy might be more atherogenic than daytime insulin plus bedtime OAD therapy. The rationale for combination therapy is based on the assumption that, if evening insulin lowers the fasting glucose concentration to normal, then daytime oral agents will be more effective in controlling postprandial hyperglycemia. However, exogenous insulin administration is not a convenient way to inhibit hepatic glucose production which determines fasting plasma glucose because in post absorptive period, hepatic glucose production is determined by high glucagon and low insulin levels. In postprandial period, beta cell-originated insulin inhibits glucagon synthesis by paracrine effect and also inhibits hepatic glucose production by using half of its concentration that administered to portal system. Since half of insulin that found in portal system is exposed to hepatic clearance to inhibit hepatic glucose production, portal insulin concentration is 2-4-folds higher than peripheral insulin concentration. But, exogenous insulin neither inhibits glucagon synthesis via paracrine effect, nor reaches desired portal concentrations because it has a short half-life and in opposition to physiologic states it is not administered to the portal system. On the contrary, its peripheral concentration is higher than portal one. Thus, exogenous insulin that is used to inhibit hepatic glucose production requires higher concentrations than physiologic values. Eventually, peripheral hyperinsulinemic state which is a risk factor of CVD is created iatrogenically. Bearing in mind that PI3K pathway, working synchronously with the diurnal rhythm of other metabolic hormones, is more active during daytime especially in postprandial period when aminoacids and glucose exist in the environment, and that decreased insulin response in PI3K pathway in diabetics, we may propose iatrogenically created hyperinsulinemia can cause more atherogenic effects via MAPK pathway. For that reason, using OAD instead of bedtime insulin may be a more convenient way to inhibit hepatic glucose production. Thus, glucagon synthesis inhibition can be achieved via paracrine effect of OAD-induced insulin secretion, as well as required portal insulin concentration can be reached by the direct secretion of insulin to the portal system. Moreover, lower peripheral hyperinsulinemia state can be provided.     

Nervous control of pancreatic endocrine secretion in pigs

The increases in the concentrations of insulin and pancreatic glucagon in portal venous and arterial plasma in response to electrical stimulation of the vagus nerves were studied in anesthetized splanchnicotomized young pigs. The responses were frequence dependent; threshold frequency was below 1 Hz and maximum response was reached at 8–12 Hz. With maximal stimulation responses of magnitudes comparable to the responses to maximal arginine (glucagon) and glucose stimulation (insulin) were observed. However, both the insulin and the glucagon response were critically dependent on the blood glucose concentration during the stimulation: the glucagon response was inversely correlated to blood glucose, whereas the insulin response was positively correlated to blood glucose at concentrations above 4.5 mmol · 1^-1. Below this glucose concentration there was no detectable insulin response and above 8.0 mmol ·^-1 no glucagon response to vagal stimulation. A stimulated secretion of glucagon as well as insulin was maintained for up to 30 min stimulation, but insulin secretion tended to decrease, whereas glucagon secretion tended to increase. Above blood glucose concentrations of 4 mmol · 1^-1, blood glucose concentrations increased slightly in response to vagal stimulation, whereas no change was noted during stimulations performed at lower blood glucose concentrations.     

Glucagon attenuates the action of insulin on glucose output in the liver of the Goto-Kakizaki rat perfused in situ

The effects of glucagon and insulin on glucose production were explored directly using the isolated perfused liver of the Goto-Kakizaki (GK) rat, an animal model of type-2 diabetes. In the perfused liver of control rats, infusion of glucagon (0.06-1.0 nM) into the portal vein dose-dependently increased glucose output. In the GK rat liver, in which the intracellular distribution of glycogen was heterogeneous, basal glucose output during perfusion was significantly higher than in control, whereas the effect of glucagon on the maximum glucose output was not different. Infusion of insulin inhibited the glucagon-induced hepatic glucose output by 30-40% in control livers, but had no effect on that from the GK rat liver. The increase in hepatic cAMP content after glucagon infusion was antagonized by insulin in control livers, but not in the livers of GK rats. These results indicate that the antagonistic effect of insulin on glucagon-induced hepatic glucose production was attenuated in the isolated liver of the GK rat and suggest that this insulin resistance appeared in the signal transduction process of glucagon upstream from cAMP production.     

Hormonal disorders in borderline arterial hypertension

Measurements of blood plasma ACTH, hydrocortisone, STH, somatostatin, insulin, glucagon levels and plasma renin activity in 70 patients with borderline hypertension (BAH) and in 20 normal male subjects have revealed increased ACTH, hydrocortisone, and somatostatin levels, elevated plasma renin activity, and reduced STH and insulin levels in the patients. A possible role of the pressor hormone system activation in the pathogenesis of borderline arterial hypertension and in BAH transformation into essential hypertension is discussed.