Postprandial redistribution of regional blood flow at rest and during exercise in conscious dogs with experimental heart failure

The effects of eating and of exercise on regional hemodynamics were studied in conscious dogs with chronic right heart failure induced by tricuspid avulsion and progressive pulmonary constriction. Eating a meal induced transient increases in heart rate, arterial pressure and resistance levels in the mesenteric, renal and iliac beds. This response was followed by a prolonged period of increased mesenteric blood flow (+10 percent) and decreased mesenteric vascular resistance (?44 percent), at a time when heart rate and arterial pressure had returned to control levels. Postprandial mesenteric vasodilation was associated with a reduction in iliac blood flow (?20 percent) and an increase in iliac resistance ( + 19 percent) but with little change in renal blood flow and resistance. Strenuous exercise during the period of postprandial mesenteric vasodilation resulted in a 53 percent fall in mesenteric flow from the preprandial control level and a substantial increase in mesenteric vascular resistance. Thus, in dogs with heart failure the ability of the mesenteric bed to respond postprandially with substantial vasodilation persists. However, when the stress of exercise is superimposed, the mesenteric vasodilation is abolished as blood flow to the gut is drastically reduced.     

提高缺血性肠病的临床认识

缺血性肠病是一组因小肠、结肠血液供应不足导致的不同程度的肠壁局部组织坏死和一系列症状的疾病,可分为急性肠系膜缺血（AMI）、慢性肠系膜缺血（CMI）及缺血性结肠炎（IC）,以IC最多见。临床表现主要为腹痛、血性腹泻、血便及腹胀等消化道症状。该病与动脉粥样硬化、肠系膜动静脉栓塞及血栓形成、心搏量减少及血管炎等有关,患者可同时存在高血压、糖尿病及急性心肌梗死等老龄化疾病。DSA及CT检查对于诊断AMI及CMI价值较高,而IC则主要依赖于结肠镜的诊断。预后也各不相同,AMI病情凶险,死亡率高,须早期诊断及手术治疗;而IC临床症状多为自限性,预后良好。缺血性肠病临床误诊率较高,应引起临床医师重视。     

Evidence for a role of capsaicin-sensitive mucosal afferent nerves in the regulation of mesenteric blood flow in the dog

Capsaicin injected into the lumen of the small intestine produced marked changes in mesenteric blood flow in anesthetized dogs. In the majority of cases capsaicin evoked a significant increase in mesenteric blood flow, the time-course of which indicated it was of a reflex nature. The response to capsaicin was completely abolished by a previous intraluminal application of the local anesthetic lidocaine, and was inhibited by an intraarterial injection of somatostatin. The present findings suggest that the effects of capsaicin may be related to a release of vasoactive peptides from afferent nerves associated with the vascular system of the gastrointestinal tract. It is concluded that capsaicin-sensitive mucosal afferent nerves, possibly provided with an axon reflex arrangement, may play a role in the regulation of local intestinal blood flow.     

The integrated response of the cardiovascular system to food.

To obtain information about the integrated response of the cardiovascular system to food, cardiac output and regional blood flow (superior mesenteric artery, renal artery and calf blood flow) were measured in 14 normal young healthy subjects after an overnight fast and following a standard 800-kcal meal. Results were compared with 8 subjects who remained fasted throughout the study. Cardiac output increased from a mean (SEM) fasting value of 4.8 (0.3) l/min to a peak after 30 min of 6.1 (0.5) l/min (p < 0.001). Superior mesenteric blood flow increased from a fasting value of 463 (45) to a peak of 854 (110) ml/min also after 30 min (p < 0.001). These changes were accompanied by a significant fall in both systemic vascular resistance and superior mesenteric vascular resistance (p < 0.001). Only at the 15-min postprandial measurements was there a significant relationship between the increase in cardiac output and superior mesenteric artery blood flow (r = 0.62, p = 0.02). Calf blood flow increased and vascular resistance fell postprandially (p < 0.05), but there was little change in right renal artery blood flow. There was an insignificant fall in renal vascular resistance. Heart rate increased from a resting value of 65 (3) to a peak of 77 (4) beats/min after 15 and 30 min (p < 0.001), diastolic blood pressure fell postprandially with little change in systolic blood pressure. These results suggest that in healthy young subjects the increase in gut blood flow is met by an increase in cardiac output, with little evidence of redirection from other vascular beds. The early postprandial increase in superior mesenteric blood flow may account for the increase in cardiac output, although the magnitude of the change is much greater for cardiac output than superior mesenteric artery blood flow.     

Vasomotion influences airflow in peripheral airways

The purpose of this study was to test the hypothesis that blood flow, by its effect on blood volume, influences airflow resistance in peripheral airways. In conscious ewes, forced sinusoidal flow oscillations (5 Hz) were applied through a balloon-tipped, dual-channel fiberoptic bronchoscope placed in a segmental bronchus, and peripheral airflow resistance (Rp) was determined from flow and bronchial pressure. Drugs with predominant vascular or airway smooth muscle effects were administered locally through the bronchoscope. Nitroglycerin (NTG) produced a dose-dependent increase in mean Rp (+288% at 1,000 micrograms), which was blocked by methylene blue (p less than 0.05) and not reversed by atropine. Carbachol (CARB) also increased mean Rp in a dose-dependent manner (+605% at 400 micrograms); this effect was not blocked by methylene blue, but it was reversed by atropine (p less than 0.05). The increase in mean Rp after a single dose of NTG (250 micrograms) was sustained for at least 20 min and transiently reversed by vasopressin (0.2 units, p less than 0.05) but not by isoproterenol (100 micrograms). Conversely, the sustained increase in Rp after a single dose of CARB (50 micrograms) was transiently reversed by isoproterenol (p less than 0.05) but not by vasopressin. We conclude that NTG increased Rp by vasodilation and CARB by bronchoconstriction. This supports the hypothesis that vasodilation limits airflow in the lung periphery, presumably because of vascular congestion.     

The impact of endothelin on renal hemodynamics in conscious rats

Endothelin (ET), a peptide recently isolated from the supernatant of cultured endothelial cells, is the most potent vasoconstrictive and hypertensive agent known up till now. We have examined the effect of ET-1 intravenous injection on regional hemodynamics in conscious unrestrained rats. Normal rats are instrumented with an arterial catheter for measurement of mean arterial pressure (MAP) and with pulsed Doppler flow probes on renal and mesenteric arteries and the abdominal aorta for simultaneous recording of blood flow velocities (V). These parameters allow calculation of vascular resistance (R) (R = MAP/V). Thus, ET-1 induces an initial and sharp hypotension, concomitant with tachycardia and a marked vasoconstriction of renal and mesenteric arteries, but a vasodilatation of aorta. This response is followed by a dose-dependent and long-lasting increase of MAP and of renal, mesenteric and aortic vascular resistances accompanied by a decrease of heart rate. The greatest impact of ET-1 constrictive effects is seen on the renal vascular bed whereas the abdominal aorta appears to be far less sensitive. In fact, the dose of 2 nmol/kg of ET-1 induces a dramatic and long-lasting fall of renal blood flow (-86%) resulting from an important vasoconstriction (+1818%). Finally, an elevation of proteinuria is revealed in ET-1 (2 nmol/kg) treated rats, but not in those treated with the same dose of Angiotensin II. This proteinuria is characterized by the appearance of proteins with a molecular weight from 20,000 to 140,000 and sometimes 280,000, and an increase of excreted albumin, seeming to reflect an alteration of glomerular permeability.(ABSTRACT TRUNCATED AT 250 WORDS)     

Eosinophilic esophagitis: A subset of eosinophilic gastroenteritis

Eosinophilic gastroenteritis (EG) was first described over 50 years ago. Despite its long history, it remains an ill-defined and poorly understood entity. EG can present in a number of ways, none of which are exclusive to the disorder. EG has features of allergy and immune dysregulation but does not clearly fit into the category of allergic or immune disorder. While EG has been reported to affect all locations and layers of the gastrointestinal tract, the vast majority of reported cases have demonstrated mucosal involvement of the gastric antrum and small intestine in addition to disease activity of other locations of the gastrointestinal tract. Recently, several reports have identified a disease consisting of an isolated esophageal eosinophilia. Eosinophilic esophagitis (EE), also known as primary eosinophilic esophagitis or idiopathic eosinophilic esophagitis, occurs in adults and in children and represents a subset of EG with an isolated severe esophageal eosinophilia. Patients with EE present with symptoms similar to those of gastroesophageal reflux but are unresponsive to antireflux medication. Reports have demonstrated that patients with EE respond to either dietary restriction or corticosteroids.     

Mesenteric blood flow during cardiopulmonary bypass in pigs

BACKGROUND: Gastrointestinal complications represent a serious problem after cardiopulmonary bypass. Hypoperfusion of the gastrointestinal tract during bypass has been implicated as the cause. We therefore investigated blood flow in the superior mesenteric artery during cardiopulmonary bypass. METHODS: Mature female pigs (n = 12) were investigated. While six sham-operated animals served as control (group I), six pigs underwent normothermic cardiopulmonary bypass for 180 minutes (group II). Bypass flow was 2.4 l/m2/minute. Standard regimens for anesthesia and cardiopulmonary bypass were used. Blood flow in the superior mesenteric artery was assessed by Doppler flowmetry. RESULTS: Blood flow in the superior mesenteric artery did not change significantly in group I. In group II, mesenteric blood flow increased significantly from baseline at 120, 150, and 180 minutes. Oxygen consumption in the mesenteric circulation increased significantly in group II at 90 and 180 minutes compared to baseline, as well as oxygen extraction. Lactate content in the mesenteric vein in group II increased compared to control at 30, 90 and 180 minutes. CONCLUSION: Overall gastrointestinal blood flow is not impaired during cardiopulmonary bypass in this animal model. Instead, gastrointestinal blood flow increased during normothermic cardiopulmonary bypass as well as oxygen consumption.     

Acute intestinal ischemia and infarction

Acute intestinal ischemia is a gastrointestinal emergency resulting from a sudden decrement in intestinal blood flow. It may occur as a consequence of mesenteric vascular occlusion and/or hypoperfusion and may involve the small intestine or colon. Bowel infarction, sepsis, and death may result, making prompt diagnosis and management imperative. Acute mesenteric ischemia generally stems from interruption of blood flow within the superior mesenteric artery or vein, and leads to small intestinal hypoperfusion and infarction. It carries with it a mortality rate of approximately 70%, but improved survival may be achieved as a result of early diagnostic consideration, undelayed angiography, and surgical intervention, when appropriate. Acute colonic ischemia occurs typically as a result of a transient mismatch between intestinal blood flow and the metabolic demands of the colon. Although infarction may occur, colonic ischemia is often a reversible condition with mortality rates considerably lower than those witnessed in acute mesenteric ischemia. This article reviews the pathophysiology, clinical features, diagnostic, and therapeutic options applicable to patients with acute intestinal ischemia.     

Unsuspected mesenteric hypoperfusion despite apparent hemodynamic recovery in the early phase of septic shock in piglets

We have developed an animal model of group B beta Streptococcal sepsis especially conducive to observation of hemodynamic sequelae of the early phases of septic shock. In piglets (N = 7), direct continuous measurements were made of aortic pressure (AOP), left atrial pressure (LAP), central venous pressure (CVP), mesenteric artery blood flow (QMES), and pulmonary artery blood flow, equivalent to cardiac output (CO). Systemic vascular resistance (SVR) and regional mesenteric vascular resistance (MVR) were calculated. Sepsis was induced by bolus intravenous administration of live, washed, type 1b group B beta Streptococcus (GBS) at approximately 1 X 10(10) organisms/kg. Early in septic shock, AOP, LAP, CO, and QMES fell to 66%, 20%, 62%, and 34% of pre-GBS levels, respectively, while SVR and MVR rose to 139% and 224% of control. The decrease in QMES and increase in MVR were significantly more extensive than the fall in CO or the rise in SVR, respectively. Subsequently, systemic hemodynamic function improved over time while regional mesenteric circulation did not. AOP and CO recovered to 86% and 88% of pre-GBS levels, respectively, and SVR returned to 105% of baseline. However, QMES remained only 48% of control, and MVR continued at 173% of pre-GBS levels. Mesenteric blood flow could not accurately be inferred from measurements of either AOP or CO during sepsis in these piglets. Relative mesenteric hypoperfusion persisted despite systemic hemodynamic recovery during this GBS sepsis protocol.     

Use of selective mesenteric vasodilator peptides in experimental nonocclusive mesenteric ischemia in the dog

Three structurally related peptides, ovine corticotropin-releasing factor, sauvagine, and urotensin I are selective mesenteric vasodilators in dogs. To assess the possible benefit of these peptides in nonocclusive mesenteric ischemia, they were compared with a nonselective vasodilator, sodium nitroprusside, in the anesthetized dog. Mesenteric blood flow was reduced by approximately 30%, without lowering of systemic arterial pressure, by either digoxin or pericardial tamponade. In the digoxin model, i.v. infusions of corticotropin-releasing factor, sauvagine, and urotensin I restored intestinal vascular resistance and mesenteric blood flow to control values, without causing a fall in systemic arterial blood pressure. In the tamponade model, only urotensin I was assessed, and it produced the same restoration of hemodynamic variables. On the other hand, in both models, i.v. infusions of nitroprusside, which were effective in correcting intestinal vascular resistance, produced a fall in arterial blood pressure (presumably because of systemic dilatation), which prevented restoration of mesenteric blood flow. Intestinal oxygen uptake was not altered by tamponade, but was reduced by 23% in the digoxin model, where it was restored to control values by both the peptides and nitroprusside. The increased oxygen extraction seen in both models was corrected by the peptides but not by nitroprusside, suggesting that nitroprusside may have a direct and offsetting metabolic effect on the gut.     

Hemodynamic effects of intravenous sodium nitroprusside in the conscious dog

The hemodynamic effects of 7 min i.v. sodium nitroprusside (NP) were studied in conscious dogs previously instrumented for measurement of arterial pressure, cardiac output, regional blood flow distribution, left ventricular (LV) pressure, and internal dimensions. Nitroprusside, 25 microgram/kg/min, reduced mean arterial pressure by 23 +/- 3%. Cardiac output increased initially by 39 +/- 7% and returned toward control by the end of the infusion. Regional blood flows increased initially; the relative rise was greatest in the coronary (+ 225 +/- 39%), intermediate in the mesenteric (+ 98 +/- 23%) and iliac (+ 38 +/- 6%), and least in the renal (+ 10 +/- 3%) bed. By the end of the infusion period the vasodilation was unchanged in the iliac bed, less intense in the coronary and mesenteric, while in the iliac bed, blood flow was reduced and resistance was actually increased by 33 +/- 11% above control. A generalized vasonconstriction ensued after cessation of infusion. In contrast, when the drug was administered intra-arterially to the iliac bed, arterial pressure did not fall and only iliac vasodilation was observed. Peak cardiac effects were characterized by increases in heart rate and LV dP/dt, along with marked reduction in LV end-systolic diameter (- 13 +/- 2%), and in end-diastolic diameter (-17 +/- 2%) and pressure. LV end-diastolic diameter fell even heart rate was maintained at a constant rate by pacing. Thus, in the conscious dog, NP reduced LV dimensions substantially, while inducing changes in peripheral beds. The differences in these effects depend on interactions between the direct effects of NP and the opposing effects of reflex adjustments which appear sufficiently powerful to result in net constriction of the iliac bed late during the infusion.     

Vascular anatomy of the gastrointestinal tract

The blood supply of the gastrointestinal system has intramural and extramural components. The intramural vascular distribution is generally well developed with plexuses in the different layers of the bowel wall and with specializations in the liver, small intestine and gastroesophageal junction, adapted to the function of these organs. The extramural arterial supply for the oesophagus is derived from the thoracic aorta or its major branches. Blood supply to the abdominal organs is provided by three major unpaired vessels arising from the abdominal aorta, namely the coeliac trunk and the superior and inferior mesenteric arteries. The branches of these vessels form anastomotic systems that provide a rich blood supply to the adjoining organs. In many areas the systems overlap while in other regions linkages are limited. Interrelations and weak points are of significant clinical importance. As well as this, there is a great individual variability in the anatomy of the gastrointestinal vasculature.     

Effects of omeprazole on gastric mucosal blood flow in the conscious rat

Regional blood flow in the gastrointestinal tract (forestomach, corpus, antrum, duodenum, jejunum, and colon) was determined in the conscious rat by means of the microsphere technique. The effects on blood flow were determined after omeprazole (orally and intravenously) and cimetidine (intravenously) during both basal and pentagastrin-stimulated gastric acid secretion. Under basal conditions neither omeprazole nor cimetidine decreased the blood flow in the gastrointestinal tract in spite of pronounced inhibition of acid secretion. On the contrary, there was a tendency towards an increased blood flow in the mucosal layer of the corpus after the oral (80 mumol/kg) and the high intravenous (10 mumol/kg) dose of omeprazole. When omeprazole was given intravenously to rats during pentagastrin-stimulated acid secretion, blood flow in the gastric mucosa was unaffected in spite of complete or almost complete inhibition of acid secretion. In contrast, cimetidine decreased the mucosal blood flow, indicating that the pentagastrin-induced increase in blood flow to some extent is mediated by H2 receptors.     

The role of cyclic AMP in mesenteric vasodilation

We tested the hypothesis that one mechanism regulating vasodilation in the mesenteric arterial circulation involves an increase in the cyclic AMP (cAMP) content of vascular smooth muscle. In anesthetized dogs, mesenteric blood flow measured with an electromagnetic flowmeter increased during intra-arterial infusion of isoproterenol, prostaglandin E₁, papaverine, and cAMP. Propranolol blocked the vasodilator response to isoproterenol but not the dilatory effects of the other drugs. Segments of mesenteric arteries were incubated with the preceding drugs (except cAMP), and tissue concentrations of cAMP were measured. Mesenteric artery cAMP content was increased by isoproterenol, prostaglandin E₁, and papaverine. The effect of isoproterenol on tissue cAMP was blocked by propranolol. For comparison we studied the effect of oxygen tension on arterial cAMP content. Varying the pO₂ of the bathing solution from 680 to 0 mm Hg did not significantly alter mesenteric artery cAMP content except for a small reduction at zero pO₂. The present results are consistent with the concept that isoproterenol, prostaglandin E₁, and papaverine induce dilation of mesenteric arteries via increases in intracellular cAMP.     

The effect of octreotide on gastroduodenal blood flow measured by laser Doppler flowmetry in rabbits and man

OBJECTIVE: The somatostatin analogue, octreotide is valuable in the management of variceal bleeding, and it has been suggested that it may stop peptic ulcer hemorrhage by reducing gastroduodenal blood flow or increasing intragastric pH. The aim of this study was to determine the effect of intravenous octreotide infusion on gastroduodenal mucosal blood flow and gastric pH. METHODS: Seven New Zealand white rabbits and five healthy human volunteers were used. Mucosal blood flow was measured using a laser Doppler flowmeter (LDF). The Doppler probe was positioned in the upper gastrointestinal tract of the seven rabbits and five human volunteers. Blood flow was measured before and after octreotide infusion. RESULTS: In the animal experiments, mucosal blood flow was decreased in a dose dependent manner in the gastric body (209.1-56.3 U) (p < 0.008), antrum (143.3-33.3 U) (p < 0.02) and duodenum (254-67.6 U) (p < 0.016) by doses of octreotide ranging from 10-50 microg/kg of body weight. In the human studies, mucosal blood flow was decreased in the gastric body (p < 0.016) and antrum (p < 0.009) after octreotide infusion (dose 1-1.5 microg/kg). Intragastric pH was significantly increased (p < 0.05). The change was not associated with systemic hemodynamic changes. CONCLUSIONS: Gastroduodenal mucosal blood flow was reduced and intragastric pH increased by octreotide. This agent could be helpful in the management of gastroduodenal mucosal bleeding.     

Nicardipine Infusion Improved Hepatic Function But Failed to Reduce Hepatic Venous Pressure Gradient in Patients with Cirrhosis

We investigated the effects of nicardipine on systemic and splanchnic hemodynamics and on liver function in 16 patients with cirrhosis and portal hypertension. Patients received a continuous infusion of 0.3 mg/min of nicardipine (n = 10) and a control infusion (n = 6). No significant changes were observed after a control infusion. In contrast, systemic vasodilatation, evidenced by a significant fall in mean arterial pressure (-14%, p less than 0.01) and systemic vascular resistance (-30%, p less than 0.01), increased heart rate (+8%, p less than 0.01) and cardiac output (+21%, p less than 0.01), and increased hepatic blood flow (+43%, p less than 0.01) were observed at 60 min after a continuous infusion of nicardipine. Although nicardipine improved hepatic function (intrinsic clearance from 0.29 +/- 0.13 to 0.33 +/- 0.15 L/min, p less than 0.05), portal pressure evaluated by hepatic venous pressure gradient was not reduced significantly (from 16.3 +/- 4.9 to 15.1 +/- 5.7 mm Hg; NS). We conclude that a continuous infusion of nicardipine improves liver function but has no beneficial effect on portal pressure in patients with cirrhosis.     

Intestinal phase of superior mesenteric artery blood flow in man.

Duplex ultrasound was used to investigate superior mesenteric artery haemodynamics in humans in order to study the contribution of the small intestine to the postprandial splanchnic hyperaemia, and to determine the relative potencies of the major food components in the postprandial mesenteric flow response. Duplex parameters of vessel diameter, mean velocity, and volume flow were determined serially in the basal state and after stimulation. Flow parameters were significantly (p less than 0.05) increased after liquid and solid oral meals. Modified sham feeding did not alter mesenteric blood flow. Intestinal perfusion of an isocaloric liquid test meal induced flow increases comparable with oral intake. Superior mesenteric artery blood flow also significantly (p less than 0.05) increased after isocaloric and iso-osmolar loads of intraduodenal carbohydrate, fat, and protein meals. Responses were similar after the test meal, fat, and protein, but were significantly (p less than 0.05) less for carbohydrates. Different osmolar loads of saline did not affect flow responses. We conclude that the intestinal phase is the major regulator of the postprandial mesenteric blood flow response in healthy humans and that the chemical nature of food determines the mesenteric response pattern.     

Evidences for vagus nerve in maintenance of immune balance and transmission of immune information from gut to brain in STM-infected rats

AIM：To determine whether salmonella Typhimurium(STM) in gastrointestinal tract can induce the functional activation of brain,whether the vagus nerve involves in signaling immune infomation from gastrointestinal tract to brain and how it influences the immune function under natural infection condition.METHODS:Animal model of gastrointestinal tract infection in the rat was established by an intuation of Salmonella Typhimurium(STM) into stomach to minic the condition of natural bacteria infection,Subdiagphragmatic vagotomy was performed in some of the animals 28 days before infection The changes of Fos expression visualized with immunohistochemistry technique in hypothalamic paraventricular nucleus(pVN) and superaoptic nuclesu (SON)were conted.Meanwhilie,the percentage and the Mean Intensities of Flurescent (MIFs)of CD4+ and CD8+ T cells in peripheral blood were measured by using flow cytometry(FCM),and the pathological changes in ileum and mesenteric lymph node were observed in HE stained sections.RESULTS:In bacteria-stimulated groups,inflammatory pathological changes were seen in ileum and mesenteric lymph node,The percentages of CD4+ T cells in peripheral blood were decreased from 43%&#177;4.5%to 34%&#177;4.9%(P&lt;0.5)and MIFs of CD8+ T cells were also decreased from 2.9&#177;0.39to 2.1&#177;0.36(P&lt;0.05)with STM stimulation.All of them proved that our STM-infection model was reliable Fos immunoreactive(Fos-ir) cells in PVN and SON incerased significantly with STM stimulation,from 189&#177;41 to467&#177;62(P&lt;0.05)and from 64&#177;21 to 282&#177;47(P&lt;0.05)individually,which suggested that STM in gastointestinal tract induced the functional activation of brain Subdiagphragmatic vagotomy attenuated FOs expression in PVN and SON induced by STM,from 467&#177;62to 226&#177;45(P&lt;0.05)and from 282&#177;47to 71&#177;19(P&lt;0.05)individually,and restored the decreased percentages of CD4+ T cells induced by STM from 34%&#177;4.9% to original level 44%&#177;6.0%(P&lt;0.05).In addition,subdiagphragmatic vagotomy itself also decreased the percentages of CD8+ T cells (from 28%&#177;3.0%to 21%&#177;5.9%),P&lt;0.05 and MIFs of CD4+(from 6.6&#177;0.6to4.9&#177;1.0P&lt;0.05)and CD8+ T cells (from 2.9&#177;0.39to 1.4&#177;0.34,P&lt;0.05).Both of them manifested the important role of vagus nerve in transmitting immune information from gut to brain and maintaining the immune balance of the organism.CONCLUSION:Vagus nerve dose involve in transmitting adbominal immune informaton into the brain in STM infection condition and play an important role in maintenance of the immune balance of the oranism.     

糖尿病胃肠功能紊乱模型胃肠道超微结构变化的研究

目的：明确糖尿病胃肠功能紊乱时胃肠道的超微结构变化。以明确其发病机制。方法：建立四氧嘧啶-糖尿病大鼠模型，对其胃肠道各个部位的超微结构变化进行观察。结果：糖尿病大鼠模型在胃窦与结肠的超微结构变化比较显著，病变主要发生在平滑肌细胞和微血管，未观察到神经末梢有明显的超微结构上的改变。结论：糖尿病胃肠功能紊乱的发生与其胃肠道超微结构的变化有关。