Gastric Blood Flow Research Articles

Evaluation of endoscopic laser Doppler flowmetry for measurement of human gastric blood flow. Methodologic aspects.

Endoscopic measurement of gastric blood perfusion by laser Doppler flowmetry (LDF) has been evaluated in 28 patients and 15 healthy volunteers. During the recordings it was necessary to keep the probe in light contact with the mucosa to obtain stable curves and to avoid artificial Doppler signals caused by relative movements between the gastric wall and the probe. Gastric distention by air insufflation did not influence the recorded flow level significantly when air insufflation was moderate. The intravenous injection of 0.6 mg atropine did not cause any significant alteration in recorded blood flow, and this drug may be used as premedication before endoscopic blood flow measurements. Recordings with both 4- and 12-kHz bandwidth of the LDF instrument showed a relative constant relationship for different flow levels, the flow values measured with 12 kHz being about twice the corresponding values measured with 4 kHz. With 12-kHz bandwidth more of the disturbance signal is recorded, which makes analysis of endoscopic recorded flow curves difficult and inaccurate. It is therefore recommended to use 4-kHz bandwidth during endoscopic measurements in conscious humans. Blood flow measurements from both sides of the gastric wall were consistently of the same order of magnitude (r = 0.91), and the endoscopically recorded output signal increased in three of five patients when a reflecting mirror was placed at the serosal side. The results indicate that endoscopic LDF usually represents blood perfusion in all layers of the gastric wall.

The effects of alpha adrenergic blockade on central haemodynamics and regional blood flows during positive pressure ventilation. An experimental study in the pig.

The effects of alpha receptor blockade on cardiac output distribution in pigs were studied. Recordings were made during spontaneous breathing (SB), during ventilator treatment with 8 Pa positive end-expiratory pressure (8 PEEP), after alpha blockade during SB (SB-alpha) and at 8 PEEP (8 PEEP-alpha). The microsphere method was used for blood flow determinations. The animals received either 5 ml.kg-1.h-1 (Group A) or 10 ml.kg-1.h-1 (Group B) of fluids. In Group A on SB-alpha, CO was maintained due to tachycardia but mean arterial pressure (MAP) decreased, renal blood flow and urine production decreased. At 8 PEEP-alpha, CO decreased despite increased heart rate (HR), MAP decreased alarmingly, renal blood flow decreased, urine production ceased and cerebral blood flow decreased, reflecting failing autoregulation. In Group B, CO increased during SB-alpha, SVR decreased, myocardial blood flow increased and organ blood flows were otherwise unchanged. At 8 PEEP-alpha, MAP, SVR, renal, pancreatic and splenic blood flows decreased in Group B. Gastric, intestinal and muscular blood flows were unchanged at 8 PEEP-alpha in Group B which is interpreted as an effect of the alpha blockade. In both groups peripheral arterio-venous shunting increased after alpha blockade.

Distribution of blood flow to the gastrointestinal tract of swine during T-2 toxin-induced shock

Swine (6 per group) were used to study gastrointestinal blood flow during T-2 toxin-induced shock. Low- and high-dose groups were given T-2 toxin at 0.6 or 2.4 mg/kg via the pulmonary artery; controls were given the ethanol vehicle. Radiolabeled microspheres were administered into the left atrium to assess organ blood flow predosing and at 90-min intervals for 6 hr. Gastric blood flow decreased in both T-2 groups, and at 6 hr the high-dose group's value was 17% of the predose value. In the low-dose group, the lowest gastric blood flow (30% of predose) was observed 3 hr postdosing. Small-intestinal blood flow of the control group declined to 64% of the predose value. In the high-dose group, small-intestinal blood flow at 3 hr was 174% of predose, followed by a reduction to 62% at 6 hr, coinciding with a severe decline in cardiac output. Small-intestinal blood flow of the low-dose group was 159% of predose at 1.5 hr, then declined to the control value. The high-dose group's large-intestinal blood flow increased to 177% of predose at 3 hr, then declined to 66% at 6 hr. The low-dose group's large-intestinal blood flow increased to 200% of the predose value. The severe decline in gastric blood flow is probably related to the development in swine (given high doses of T-2 toxin) of a grossly bright red gastric fundus, with histologic evidence of vascular congestion and mucosal deterioration. The initial increase in blood flow to the intestine may contribute to its tolerance to sublethal doses of T-2 toxin and may facilitate the rapid intestinal absorption of the toxin.

Gastric epithelial restitution at low luminal pH during influence of pentagastrin or cimetidine in the cat

This study examines restitution of the gastric surface epithelium at luminal pH 1 after damage to the gastric mucosa by instillation of 2 M NaCl for 10 min. After mucosal damage, potential difference decreased to zero and H+ back-diffusion increased. Gastric blood flow increased after exposure to 2 M NaCl, irrespective of the secretory state of mucosa. Neither pentagastrin nor cimetidine showed any protective effect against mucosal damage produced by 2 M NaCl. Ninety minutes after mucosal exposure to 2 M NaCl there was an almost complete restitution of the gastric surface epithelium in pentagastrin-stimulated and cimetidine-treated animals, whereas about 15% of the gastric surface still showed damage in animals in which acid secretion was not interfered with. These findings show that restitituion of the surface epithelium, in vivo, is a rapid and resistant process even at a very low luminal pH. The secretory state of mucosa may have some influence on this process.

Acute gastric ulceration in rats with obstructive jaundice with special reference to gastric mucosal blood flow.

The mechanism of acute gastric ulceration in rats with obstructive jaundice was investigated in terms of the changes in the gastric mucosal blood flow, and the effect of vagotomy on ulceration was examined. 188 Sprague-Dawley rats weighing about 250 g were prepared and divided into 4 groups as follows; control group (sham operation), jaundiced group (ligation of the bile duct), vagotomized group (vagotomy with pyloroplasty), jaundiced and vagotomized group (simultaneous ligation of the bile duct and vagotomy with pyloroplasty). Two weeks after the operation, water immersion and restraint stress procedures were performed in these 4 groups. The gravity of acute gastric ulcerations was calculated by ulcer index. The gastric mucosal blood flow was measured by hydrogen clearance technique. The following results were obtained: In control group, ulcer index was increased and gastric mucosal blood flow was decreased after the stress procedures. The jaundiced group showed significantly higher ulcer index and early significant decrease of gastric mucosal blood flow after the stress procedures compared to the control group. The vagotomized group showed significantly decreased ulcer index after the stress procedures compared to the control group, however, the gastric mucosal blood flow showed almost the same values as the control group. The jaundiced and vagotomized group showed significant decrease of ulcer index and improvement of decrease of gastric mucosal blood flow compared to the jaundiced group. These results indicated that the gastric mucosal blood flow plays an important role in the occurrence of acute gastric ulceration in rats with obstructive jaundice, and vagotomy might be useful to prevent them by maintaining gastric blood flow in obstructive jaundice.

The Role of H2Receptors in Gastric Mucosal Blood Flow

To determine the relation between H2 receptors and gastric mucosal blood flow, we measured the latter in rats by the electrolytically generated hydrogen gas clearance technique. The blood flow increased significantly after intravenous injection of 0.1 mg/kg of impromidine, a very potent and specific agonist of H2 receptors. On the other hand, gastric mucosal blood flow decreased significantly after intravenous administration of 5 or 20 mg/kg of cimetidine or 2 mg/kg of famotidine. However, 2 or 20 rng/kg of omeprazole, whose anti-secretory effect is as strong as that of H2 blockers such as cimetidine and famotidine, caused no significant change in the gastric rnucosal blood flow. This indicates that H2 receptors regulate gastric mucosal blood flow in rats.

Effect of somatostatin on human gastric blood flow evaluated by endoscopic laser Doppler flowmetry.

The effect of somatostatin on human gastric blood flow has been evaluated by endoscopic laser Doppler flowmetry. A bolus injection of 250 micrograms somatostatin intravenously caused a transitory decrease in the gastric blood flow of 40%. After continuous infusion of somatostatin for 1 h no change in the gastric microcirculation could be demonstrated in spite of significantly elevated somatostatin-like immunoreactivity in plasma. The results do not give evidence that somatostatin has a possible beneficial effect in patients with gastric bleeding caused by a significant gastric blood flow reduction.

Autonomic nervous control of fundic secretion of somatostatin and antral secretion of gastrin and somatostatin in pigs.

By selective catheterization of gastric veins, we studied the secretion of gastrin and somatostatin from the antrum and of somatostatin from the gastric fundus-corpus region in anaesthetized pigs with or without acute adrenalectomy. The secretion was studied during electrical stimulation of the vagus nerves and the splanchnic nerves and simultaneous irrigation of gastric lumen with fluids of high, low, and neutral pH. The corpus-fundus somatostatin response to vagal stimulation was biphasic with a short-lasting initial increase followed by a lasting inhibition, which was little influenced by intraluminal pH or adrenalectomy. In pigs with intact adrenals, antral somatostatin secretion was increased by vagal stimulation, whereas in adrenalectomized pigs, the effect was inhibitory. The vagally induced inhibition was abolished when the intragastric pH was kept at pH 2. The antral gastrin secretion was strongly stimulated by vagal stimulation. The magnitude of the secretory response was inversely related to the pre-stimulatory somatostatin levels, but not to the nerve stimulation responses. Splanchnic stimulation increased arterial blood pressure and gastric blood flow, but had inconsistent effects on somatostatin and gastrin secretion.

An approach to the mechanism of acute ulceration in obstructive jaundice.

Changes of noradrenaline (NA) and prostaglandin (PG) E2 in gastric mucosa and gastric wall blood flow (GWBF) were investigated after stress load in rats with obstructive jaundice. We found that water immersion and restraint stress more easily increased the ulcer index and decreased GWBF, corresponding to a decrease of the NA and PGE2 contents in the gastric mucosa, as the duration of jaundice increased. Administration of PGE2 reduced the increase of the ulcer index and the decrease of the GWBF and NA contents in the gastric mucosa. It is suspected that the rapid decrease of NA and PGE2 is connected with the rapid decrease of GWBF after stress load in obstructive jaundice, and we reached the hypothesis that both PGE2 and NA mutually regulate local GWBF.

Secretory state and acute gastric mucosal injury in sepsis.

Cats were subjected to a standardized 3-h septicemia by intravenous infusion of live Escherichia coli in an LD50 dose. The effect of pentagastrin stimulation on the development of gastric mucosal injury was studied. There was no hemodynamic difference between the series during septicemia. Thus, pentagastrin did not induce increased gastric blood flow during the period of E. coli infusion. Intraluminal gastric pH was lower in the series given pentagastrin during the last 2 h of septicemia. Nevertheless, the extent of gastric mucosal injury was similar in the two groups, whereas the depth of injury was, if anything, less pronounced in the pentagastrin-stimulated group.

Blood flow responses to small bowel resection.

The objective of this study was to determine whether the gastrointestinal blood flow response to small bowel resection is related to the compensatory hyperplasia resulting from resection. In one group of rats, a laparotomy was performed and 80% of the small bowel resected, reanastomosing proximal jejunum with distal ileum. In the second group (controls), a transection followed by reanastomosis was performed either in the jejunum or ileum. One, two, three, or five days later, the animals were anesthetized, and blood flows to the stomach, jejunum, ileum, cecum, colon, and pancreas were measured using the radioactive microsphere technique. Samples of these tissues were obtained for determination of thymidine incorporation and DNA content. Growth, as evidenced by increases in tissue weight, DNA content, and rate of DNA synthesis, occurred in all tissues. Blood flow was elevated in the pancreas and in bowel segments (ileum and cecum) distal to the site of resection. Gastric, jejunal and colonic blood flows were not affected by bowel resection, in spite of similar trophic changes. Paired-value analyses did not reveal any correlation between blood flow and rate of DNA synthesis. The results of these studies suggest that humoral, rather than metabolic, factors are responsible for the gastrointestinal and pancreatic hyperemia that occurs after small bowel resection.

Gastric Bleeding and/or (?) Enteral Feeding

Upper gastrointestinal bleeding from stress ulceration is a serious complication of critical illness which is associated with increased morbidity and mortality. 1 Zinner MJ Zuidema GD Smith PL Mignosa M The prevention of upper gastrointestinal tract bleeding in patients in an intensive care unit. Surg Gynecol Obstet. 1981; 153: 214-220 PubMed Google Scholar , 2 Harris (Pingleton) SK Bone RC Ruth WE Gastrointestinal hemorrhage in patients in a respiratory intensive care unit. Chest. 1977; 72: 301-304 Abstract Full Text Full Text PDF PubMed Scopus (69) Google Scholar , 3 Schuster DP Rowley H Feinstein S McGue MK Zukerman GR Prospective evaluation of the risk of upper gastrointestinal bleeding after admission to a medical intensive care unit. Am J Med. 1984; 76: 623-630 Abstract Full Text PDF PubMed Scopus (191) Google Scholar Efforts to prevent gastric bleeding have centered on prevention of stress ulceration. Stress ulcers are caused by a complex interaction of systemic, tissue and luminal factors which destroy the ability of the intact gastric mucosa to maintain homeostasis. 4 Silen W Pathogenetic factors in erosive gastritis. Am J Med. 1985; 79: 45-48 Abstract Full Text PDF PubMed Scopus (22) Google Scholar Preservation of gastric mucosal integrity is a dynamic process dependent upon normal gastric blood flow, systemic acid-base balance and normal metabolic and secretory state of the mucosa. Experimental evidence suggests gastric acid plays a key role in the formation of gastric erosions, not from excessive acid secretion, but rather from a temporary failure of gastric mucosal defense mechanisms to deal with the acid present. 5 Marrone GC Silen W Pathogenesis, diagnosis and treatment of acute gastric mucosal lesions. Clin Gastroenterology. 1984; 13: 635-649 PubMed Google Scholar Therefore, prophylactic measures have centered on neutralizing gastric acidity with antacids and decreasing gastric acid secretion with histamine2-receptor blockers, such as cimetidine or ranitidine. An array of clinical studies suggest antacids are superior in elevating gastric pH and decreasing gastric bleeding. 1 Zinner MJ Zuidema GD Smith PL Mignosa M The prevention of upper gastrointestinal tract bleeding in patients in an intensive care unit. Surg Gynecol Obstet. 1981; 153: 214-220 PubMed Google Scholar , 2 Harris (Pingleton) SK Bone RC Ruth WE Gastrointestinal hemorrhage in patients in a respiratory intensive care unit. Chest. 1977; 72: 301-304 Abstract Full Text Full Text PDF PubMed Scopus (69) Google Scholar , 6 Priebe HJ Skillman JJ Bushnell LS Long PC Silen W Antacid versus cimetidine in preventing acute gastrointestinal bleeding. N Engl J Med. 1980; 302: 426-430 Crossref PubMed Scopus (263) Google Scholar , 7 Martin LF Staloch DK Simonwitz DA Failure of cimetidine prophylaxis in the critically ill. Arch Surg. 1979; 114: 492-496 Crossref PubMed Scopus (42) Google Scholar However, recent data indicate that cimetidine may prevent progression of established stress ulceration. 8 Peura DA Johnson LF Cimetidine for prevention and treatment of gastroduodenal mucosal lesions in patients in an intensive care unit. Ann Intern Med. 1985; 103: 173-177 Crossref PubMed Scopus (154) Google Scholar

Nicotine and smoking do not decrease basal gastric mucosal blood flow in anesthetized rats.

The literature regarding the effect of nicotine and cigarette smoke on gastric blood flow is conflicting. The hydrogen gas clearance technique was used to measure the effects of nicotine and cigarette smoke on basal gastric mucosal blood flow in anesthetized rats. Blood flow was measured before, during, and after treatment with either intravenous nicotine (4 or 40 micrograms/kg/min) or inhaled cigarette smoke (nicotine or nicotine free). Neither intravenous nicotine nor cigarette smoke significantly altered gastric mucosal blood flow. On the other hand, hypotension produced by hemorrhage significantly decreased mucosal blood flow (P less than 0.05). Thus the technique used could detect a decrease in blood flow. These findings indicate that in the anesthetized rats, hypotension but not intravenous nicotine or cigarette smoke, in the doses given, reduce gastric mucosal blood flow.

Indomethacin‐induced changes in canine gastric mucosal haemodynamics and haemoglobin oxygenation, and the effects of topical anti‐ulcer agents

Abstract Changes in gastric mucosal haemoglobin concentration (mucosal blood volume), mucosal haemoglobin oxygenation, mucosal blood flow and gastric arterial blood flow caused by indomethacin, an ulcerogenic agent, and anti‐ulcer agents were investigated in the stomach flap of anesthetized dogs. Indices of mucosal haemoglobin concentration and haemoglobin oxygenation, mucosal blood flow and arterial blood flow to the stomach flap were measured simultaneously. The intravenous injection of indomethacin (10 mg/kg) caused an immediate decrease in mucosal haemoglobin concentration with a gradual decrease in mucosal and arterial blood flow, and a slight decrease in mucosal haemoglobin oxygenation. The topical application of prostaglandin E2 (10 μg/ml) and spizofurone (a new anti‐ulcer agent, 1 mg/ml) to the mucosa significantly increased these parameters, and remedied the decreases of these parameters caused by indomethacin. Cimetidine (20 mg/ml), pirenzepine (10 mg/ml) and proglumide (40 mg/ml) given topically did not significantly increase these parameters in the resting state or the indomethacin‐induced ischaemic state. This study indicates that: indomethacin decreases gastric haemodynamics, and that improvement occurred with application of mucosal protective agents (i.e. prostaglandin E2 and spizofurone) and changes in mucosal blood concentration were closely correlated with those in mucosal blood flow and arterial blood flow, but correlated less well with those in the case of haemoglobin oxygenation.

Esophageal Blood Flow in the Cat: Normal Distribution and Effects of Acid Perfusion

The radioactive microsphere technique was used to estimate blood flow to different regions of the esophagus and to adjacent regions of the stomach before and after perfusion of the esophagus with hydrochloric acid (pH 1.5) for 5 min. Under resting conditions total blood flow, as well as blood flow to the mucosal-submucosal layer and the muscular layer, to both sphincters was significantly higher than to the esophageal body. Blood flow to the adjacent regions of the stomach was significantly higher than esophageal blood flow. Acid perfusion resulted in a large increase in total blood flow in both sphincters and the lower esophageal body. Gastric blood flow was not altered by acid perfusion. The esophageal hyperemia resulted primarily from an increase in blood flow to the muscular layer; mucosal-submucosal blood flow was increased only in the lower esophageal sphincter. The present study indicates that short periods (5 min) of gastroesophageal reflux may increase esophageal blood flow.

Hemodynamics of the gastric mucosa and gastric ulceration in rats and in patients with gastric ulcer.

The microcirculation is the fundamental nutrient supply and waste removal system of all tissues. Recent improvements in spectrophotometric technique have made possible the noninvasive assessment of oxygen supply and utilization in the gastric mucosa. The authors have utilized such methods to assess gastric mucosal hemodynamics. The technique permitted further clarification of the roles of the gastric microcirculation, mucosal oxygenation, and acid secretion in the pathogenesis of stress ulcers in the stomach of rats. Furthermore, it provided important information on the function of gastric mucosal hemodynamics in the healing of gastric ulcers in man. The technique is described along with the authors' correlation studies between spectrophotometric data and other techniques for measuring gastric blood flow (hydrogen gas clearance and aminopyrine clearance methods and direct electromagnetic flowmeter techniques) and the prevention of ulcerogenesis.

Changes of Tissue Blood Flow in Mice Loaded with SART (Repeated Cold) Stress or Restraint and Water Immersion Stress and the Effect of Administered Neurotropin

In order to explore the peripheral microcirculation and to obtain an outline of autonomic innervation in SART (specific alternation of rhythm in temperature)-stressed (repeated cold-stressed) animals, which are regarded as model animals for clinical vagotonic-type dysautonomia, peripheral tissue blood flow was determined in mice, using the hydrogen clearance method. SART-stressed mice showed a decrease in gastric blood flow, no change in hepatic blood flow and an increase in dermal blood flow. In the mice exposed to the restraint and water immersion stress (RWIS), a type of acute stress, in contrast with SART stress which is a subacute type, remarkable decreases were observed in gastric, hepatic and dermal blood flows. Changes of both gastric and dermal blood flow in SART-stressed mice were dose-dependently prevented and maintained within normal limits by the treatment with Neurotropin, a sedative analgesic which is an extract isolated from vaccinia virus-inoculated and inflamed skin of rabbits. In RWIS-loaded mice. Neurotropin exhibited a great preventive effect on changes of blood flow in the stomach, a slight effect in the liver, and no effect in the cutis. When mice were loaded with SART stress after left-cervical vagotomy, SART stress failed to elicit any decrease in gastric blood flow. In SART-stressed mice treated with 6-hydroxydopamine, gastric and dermal blood flows tended to show a further decrease and increase, respectively, over and above the changes caused by SART stress. From these results, it is suggested that SART-stressed mice may have decreased gastric parasympathetic tone, a decrease in sympathetic tone and also other anomalies such as increased tension of the sympathetic cholinergic vasodilator nerves in the cutis.

Body Temperature Dependency of Gastric Regional Blood Flow, Acid Secretion and Ulcer Formation in Restraint and Water-Immersion Stressed Rats

The effect of water temperature during restraint and water-immersion stress (RWIS) on gastric regional blood flow, acid secretion and ulcer formation were compared to those of restraint stress (RS) alone in rats. RS had no effect on the gastric regional blood flow. In contrast, the gastric regional blood flow was significantly decreased by RWIS. A water temperature dependent reduction of gastric regional blood flow induced by RWIS was observed between 20°C and 30°C. The decrease in gastric regional blood flow for RWIS rats was related to a lowering of the body temperature, which almost coincided with the temperature of water for the immersion. The gastric acid output was not influenced by RS. However, RWIS significantly increased the gastric acid output. The temperature of water in order of increasing acid output induced by RWIS was 25°C>30°C>20°C. Little ulcer formation was found in RS rats, while exposure to RWIS caused marked ulceration. The temperature of water in order of severity of ulceration by RWIS was 25°C>20°C>30°C. The severity of ulceration was not related to the decrease in gastric regional blood flow or increase of acid output, but was correlated to the ratio of the gastric blood flow/the acid output. These findings suggest that the decrease of gastric regional blood flow is in good agreement with the fall of body temperature, and the combined effects of the gastric blood flow and the acid secretion are involved in the ulceration caused by RWIS.

Gastric blood flow in ethanol injury and prostaglandin cytoprotection.

Studies performed in the author's laboratory concerning the role of gastric mucosal blood flow in ethanol-induced gastric mucosal injury and prostaglandin cytoprotection are reviewed. Fluorescent in vivo microscopic and hydrogen gas clearance studies revealed total absence of blood flow in the gross ethanol-induced lesions. Prostaglandin pretreatment not only prevented gross lesion formation but flow was present throughout the mucosa. A cytoprotective dose of the prostaglandin analogue did not increase blood flow. Transmitted light in vivo microscopy revealed rapid cessation of blood flow through mucosal microvessels within 1 min of ethanol application. The microvessels remained filled with red blood cells, suggesting an intravascular coagulation phenomenon. Histologic studies revealed no necrotic lesion formation 1 min after ethanol, but increasing necrosis from 10 to 60 min. These findings suggest that the rapid ethanol-induced cessation of blood flow renders the gastric mucosa more susceptible to ethanol injury and prostaglandin acts by preventing this blood flow change.

Body temperature dependent decrease of gastric blood flow in restraint and water-immersion stressed rats.

The effects of restraint and water-immersion stress (RWIS) on the cardiovascular system (including blood pressure, heart rate, blood flow in the gastric region, and blood flow in the common carotid artery and descending aorta) and body temperature were studied in rats. The blood pressure of RWIS rats did not differ from that of restraint stress (RS) rats. The heart rate, blood flow in the gastric region, common carotid artery and descending aorta as well as body temperature were significantly decreased by RWIS, but not by RS. The decrease in heart rate in RWIS rats was not influenced by pretreatment with atropine, hexamethonium or vagotomy. The reduction of gastric regional blood flow was not influenced by pretreatment with atropine and phenoxybenzamine. The changes in these three parameters were closely correlated in all the RWIS rats tested. These results suggest that the decrease in gastric regional blood flow is due to a lowering of the body temperature via decreasing cardiac output.