Biomedical subjects

I T Beck

Publications and source records attributed to I T Beck.

At least 19 recordsLinked to original sources

PubMed1992

The role of histamine1 and histamine2 receptors in the ethanol-induced jejunal plasma protein loss.

Histamine and other mediators have been shown to be involved in the ethanol-induced jejunal plasma protein loss. In this study we have investigated whether the histamine (H)-related component of this protein loss is mediated by H1-receptors, H2-receptors or both. Four groups of dogs (n = 12 in each) were studied. They were: untreated, H1 + H2-receptor blockade, H1-receptor blockade and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptor blockade. Chlorpheniramine and ranitidine were used to block H1 and H2-receptors respectively. In all animals, jejunal protein loss was measured over 10 min periods for 90 min. Ethanol increased protein loss in all time periods (p less than 0.001). This protein loss was depressed by H1 + H2-receptors blockade throughout 90 min (p less than 0.01). H1-receptor blockade caused a similar depression of ethanol effect but only during 20 to 40 min (p less than 0.05). In contrast, H2-receptor blockade aggravated the protein losing effect of ethanol throughout 90 min (p less than 0.01). Analyses of data tend to suggest that the ethanol-induced protein loss is mediated principally by H1-receptors, and that a complete inhibition of the histamine-related ethanol-induced protein loss can be achieved only by a simultaneous blockade of both H1 and H2-receptors, and not by H1- or H2-receptor blockade alone.

Animals↗

PubMed1992

The role of angiotensin in the intestinal vascular response to hypotension in a canine model.

It was previously shown that the vasoconstrictory response to hypotension was similar in the mucosa of the small bowel and the colon but was significantly higher in the muscularis of the latter than that of the former. To understand the mechanism of this differential response of the muscularis of the small bowel and the colon, the present study investigated the effect of an angiotensin II inhibitor (saralasin) on the hypotension-induced vasoconstriction of the mucosa and the muscularis of these two locations of the gastrointestinal tract. Dogs were used. Hypotension was induced by hemorrhage to reduce blood pressure by 40 mm Hg. Blood flow was measured by 15-microns radiolabeled microspheres. Saralasin was infused intravenously for 20 minutes at a rate of 0.05 mg.kg-1 bolus followed by 1 microgram.kg-1.min-1. Saralasin had no effect on the basal blood flow of the mucosa or the muscularis of the small bowel or on the hypotension-induced vasoconstriction of these two layers of the small bowel. In contrast, saralasin decreased blood flow to the mucosa (-28%; P less than 0.001) and increased blood flow to the muscularis (+140%; P less than 0.001) of the colon under basal conditions and also reduced the hypotension-induced vasoconstriction of the colonic muscularis (P less than 0.01). These and supplementary data indicate that there is a difference between the small bowel and the colon in local activity of vascular angiotensin system and that this system is most active in the colonic muscularis where it plays a significant role in the vasoconstrictory response to hypotension.

Angiotensin II↗

PubMed1991

The microvascular anatomy of the canine stomach. A comparison between the body and the antrum.

To investigate whether there is a difference in the microvascular architecture between the body and the antrum of the canine stomach, these two locations were compared with respect to microsphere entrapment and the microvascular architecture and diameter in relation to histology by corrosion casting and by intraarterial injection of india ink. There was 63% shunting of 9-micron microspheres in the antrum, but none in the body. Corrosion cast and Indian ink studies showed that in the body there was a single microvascular network of capillaries that appeared to originate from the arterioles in the submucosa and were in close apposition to the epithelial cells of the gastric glands. The diameter of these capillaries was 8.6 +/- 0.2 microns. In contrast, there were two distinct capillary networks in the antrum: a basal and a superficial. The capillaries of the basal network of the antrum originated from the arterioles at the level of the muscularis mucosa and drained into the capillaries of the superficial mucosa. The capillaries of the superficial network had a significantly larger diameter (10.8 +/- 0.4 microns) than those of the basal network (7.3 +/- 0.2 microns). In many instances the capillaries of the superficial network originated directly from the ascending arterioles passing through the basal network. These direct arteriocapillary connections may have permitted the shunting of 9-microns spheres in the antrum.

Animals↗

PubMed1991

Microvascular permeability increases early in the course of acid-induced esophageal injury.

To test the hypothesis that microvascular injury is involved in the pathophysiology of acid-induced esophagitis, the effect of acid perfusion on intraluminal plasma protein loss was studied in relation to histological changes. Four groups of opossums (n = 6 in each) were perfused with either normal saline control) or 10, 20, or 100 mmol/L isoosmolar hydrochloric acid at 2 mL/min for 90 minutes using a midesophageal catheter. The distal esophagus was cannulated via a gastrostomy, and the effluent was collected and measured for intraluminal loss of IV injected 125I-bovine serum albumin. Plasma protein loss in the control group was constant with a total loss of 3.40 +/- 0.69 mg/g dry wt. Perfusion of 10, 20, and 100 mmol/L hydrochloric acid increased total protein loss to 8.06 +/- 2.62, 13.94 +/- 2.72, and 27.34 +/- 4.34 mg/g dry wt, respectively. The protein loss was not associated with intraluminal blood loss, as measured by previously injected 51Cr-labeled autologous red blood cells. Histological changes, scored by a blinded observer, were significant only between control animals and those perfused with 100 mmol/L hydrochloric acid. Separate studies using the vascular tracer monastral blue B demonstrated an increase in labeling of lamina propria blood vessels that varied directly with the concentration of acid perfusate, thereby providing direct morphological evidence of microvascular injury. These studies suggest that increased microvascular permeability occurs early in the course of acid-induced esophageal injury.

Animals↗

PubMed1991

Transition from nutcracker esophagus to achalasia. A case report.

We report a middle-aged woman with nutcracker esophagus who progressed to classic achalasia in two years. Several previous reports have documented progression of nutcracker esophagus to diffuse esophageal spasm and diffuse esophageal spasm to achalasia, but the only previous report of nutcracker esophagus progressing to achalasia was in a child. Our case suggests that, in some instances, nutcracker esophagus and achalasia may share the same pathogenesis.

Esophageal Achalasia↗

PubMed1991

The effect of pitressin on esophageal blood flow of the dog.

In a previous study on canine esophagus, we reported that intravenous infusion of isoproterenol caused mucosal (i.e., mucosal + submucosal) vasodilation only in the lower esophageal sphincter (but not in the body) and muscularis vasodilation only in the body (not in the lower esophageal sphincter). In the present study, we have investigated in dogs whether these esophageal tissues also exhibit a similar difference in their vasoconstrictory response to intravenous infusion of pitressin. All measurements were made before (basal) and after infusion of 0.02 U pitressin.min-1.kg-1 for 15 min. Pitressin significantly decreased portal venous pressure and blood flow, and increased vascular resistance of all tissues of the esophagus. This vasoconstriction of the tissues, however, was higher in the squamous mucosa of the body than in the columnar mucosa of the lower esophageal sphincter. In contrast, it was higher in the smooth muscle of the lower esophageal sphincter than in the striated muscle of the body. These data together with those of our previous report on isoproterenol demonstrate that pitressin causes a pronounced vasoconstriction in those esophageal tissues where isoproterenol had no effect. Conversely, pitressin causes least vasoconstriction in those tissues where isoproterenol produced a significant vasodilation. These differences could be the result of partial agonist actions or differences in receptor density or in receptor-effector coupling mechanism.

Animals↗

PubMed1990

Omeprazole in H2 receptor antagonist-resistant reflux esophagitis.

We conducted a retrospective review of 25 patients with severe reflux esophagitis treated with omeprazole because of failure of H2 receptor antagonists to heal their esophagitis. Prior to beginning omeprazole (40 mg/day), all patients were on H2 antagonists for at least 9 months and still had endoscopic evidence of longitudinal (grade II) or circumferential (grade III) distal esophageal ulceration. Omeprazole therapy brought about complete endoscopic healing in 24 of 25 patients (96%). Twenty-three of 24 healed patients were then restarted on H2 antagonists as maintenance therapy. Repeat endoscopy was performed if symptoms recurred. Fourteen of 24 patients (58%) had recurrence of endoscopic esophagitis documented between 26 and 300 days from the time of starting maintenance therapy. Two of these 14 patients opted for antireflux surgery, whereas the remaining 12 were once again given omeprazole, which again resulted in symptom resolution in all patients. These data suggest that most patients with H2 receptor antagonist-resistant ulcerative esophagitis cannot be successfully maintained on H2 antagonists even after the ulcers have been healed with omeprazole. Further studies are required to determine the role of omeprazole compared to other treatments in the long-term maintenance therapy of these patients.

Adolescent↗

PubMed1990

Gastrointestinal blood flow in the opossum with special reference to the esophagus.

The opossum esophagus, like that of the human, is composed of striated muscle fibres proximally and smooth muscle fibres distally. Because of this similarity the opossum has been used extensively as an animal model for esophageal studies, but to date no data on esophageal blood flow have been reported in this species. The purpose of this study was to establish the basal blood flow characteristics of different regions of the opossum gastrointestinal tract with particular reference to the esophagus. Intracardiac injection of 15-microns microspheres was used to provide an estimate of blood flow (mL.min-1.g-1 dry tissue) to the whole wall, the combined layer of mucosa plus submucosa, and the muscularis propria. Basal blood flow in the whole tissue and mucosa-submucosa was significantly higher in the lower esophageal sphincter than in the proximal or distal esophagus. The muscularis propria blood flow displayed an aborally increasing gradient with flow to proximal esophagus (striated muscle) less than distal esophagus (smooth muscle) less than lower esophageal sphincter. Regional differences in blood flow to other regions of the gastrointestinal tract were similar to that described in other species. In addition, no changes in basal blood flow occurred despite repeated microsphere injections, suggesting that this species provides a good animal model for the study of gastrointestinal blood flow.

Animals↗

PubMed1990

Comparison of vascular response of different locations of the gastrointestinal tract to isoproterenol and nifedipine.

In the present study we have compared the effect of intravenous infusion of a calcium channel blocker, nifedipine (1.0 micrograms.kg-1.min-1 for 20 min), with that of isoproterenol (0.1 micrograms.kg-1.min-1 for 20 min) on the hemodynamic parameters and the vascular response of different locations and tissue layers of the gastrointestinal tract. Heart rate increased with isoproterenol but not with nifedipine. Both agents caused a similar increase in cardiac output and a similar fall in mean arterial pressure. After 20 min infusion, nifedipine increased the blood flow of the axillary artery, but isoproterenol had no such effect. Isoproterenol caused vasodilation of the mucosa in the antrum but not in the fundus and the body of the stomach or in the duodenum, jejunum, mid small intestine, ileum, and colon. The mucosal effect of nifedipine was similar, except that it also caused vasodilation in the small bowel and in the ascending colon. Nifedipine caused vasodilation of the muscularis throughout the gastrointestinal tract, but isoproterenol had no such effect. These differences are discussed in relation to the mechanism of action of these two vasodilators. It is suggested that the vascular response of different locations and tissue layers of the gastrointestinal tract to vasodilators is locally regulated by a variety of mechanisms may include beta- and alpha-receptor density and (or) sensitivity, angiotensin II activity, and metabolic need of the tissues.

Animals↗

PubMed1990

A randomized prospective trial comparing oral sodium phosphate with standard polyethylene glycol-based lavage solution (Golytely) in the preparation of patients for colonoscopy.

One hundred and two patients were randomized to receive either oral sodium phosphate or standard polyethylene glycol-based lavage solution (Golytely) prior to colonoscopy in order to establish whether the much smaller volume of the former agent enhanced patient tolerance while maintaining or improving effectiveness and safety. Overall, patients found sodium phosphate preparation much easier to complete. In 37 patients who had had a previous colonoscopy prepared with Golytely, 100% of those now receiving sodium phosphate found it easier to complete and over 90% felt it caused less discomfort, compared with their previous experience with Golytely. Colonoscopists, unaware of the type of lavage solution used, scored the degree of colonic cleansing significantly higher for sodium phosphate-prepared colons compared with colons prepared with Golytely. Serial measurements of blood tests and postural pulse and blood pressure changes did not reveal any clinically significant changes in intravascular volume. Hyperphosphatemia was noted with sodium phosphate, but was transient, and no concomitant decrease in calcium was seen. Histological assessment for possible preparation-induced changes revealed no difference between the two agents. Sodium phosphate is significantly less expensive than Golytely. We conclude that, in the group of patients studied, sodium phosphate is a safe colonic cleansing agent that is better tolerated and more effective than Golytely.

Colonoscopy↗

PubMed1989

Regional differences in the vascular response of the canine esophagus to vasodilators.

The basal blood flow of the proximal and distal body of the esophagus, and that of the lower esophageal sphincter, and the vascular response of these sites to intravenous infusion of nifedipine (1.0 microgram/kg.min) and isoproterenol (0.1 microgram/kg.min) were studied. The basal blood flow of the mucosa plus submucosa, muscularis propria, and the whole wall was significantly higher in the lower esophageal sphincter than in the proximal or the distal body. Intravenous nifedipine caused a similar decrease in vascular tone of the mucosa and the muscularis propria in all sites of the esophagus. Isoproterenol infusion significantly decreased the vascular tone of the mucosa with columnar epithelium (i.e., mucosa overlying the lower esophageal sphincter), but not of the mucosa with squamous epithelium (i.e., mucosa overlying the body). In the muscularis propria the vasodilatory effect of isoproterenol and nifedipine was significant at all sites, but this effect was greater in the striated muscle of the body than in the smooth muscle of the lower esophageal sphincter (p less than 0.05). Thus, not only do different vasodilators have different effects on the vasculature of the esophagus, but also a single agent may have differing effects on the various sites and layers of this organ.

Animals↗

PubMed1989

Mechanism of ethanol-induced jejunal microvascular and morphologic changes in the dog.

To study the mechanism of morphologic and microvascular effects of intraluminal ethanol, we perfused jejunal segments of the dog with 6% (wt/vol) ethanol for 0 (control), 10, 20, 30, 60, and 90 min, and measured the time-dependent changes in (a) the prevalence of villi with epithelial damage (i.e., villi with intact blebs plus those with broken blebs) and those without epithelial damage (undamaged villi), (b) the height of the villus core and the patency of lacteals, (c) jejunal albumin loss, and (d) permeability of microvessels of the villus tip by colloidal carbon vascular labeling. We found that (a) the prevalence of villi with epithelial damage or with intact bleb increased progressively during the first 20 min of ethanol perfusion and then declined gradually; (b) the height of the villus core and the patency of lacteals in the undamaged villi and in those with intact bleb decreased during the first 20 min and then gradually increased; and (c) jejunal albumin loss and the prevalence of villi with carbon labeling increased for the first 30 min, after which the former declined gradually whereas the latter remained at a plateau. These findings suggest that contraction of the villus core and compression of the lymphatics are the primary cause of ethanol-induced epithelial damage, which is accentuated by increased microvascular permeability and consequent protein leakage. The mechanism of recovery of most parameters, in spite of continuous ethanol perfusion, remains to be investigated.

Animals↗

PubMed1989

Time-related changes in microsphere entrapment in canine jejunum.

To assess the validity of repeated blood flow measurements using the microsphere technique, the apparent blood flows in the anatomic layers of the jejunum were determined from the entrapment of 9-, 11.5-, and 17-micron microspheres at 1.5, 15, 30, and 60 min after their injection. The entrapment of 17-micron spheres in the mucosa plus submucosa and in the muscularis propria remained similar at all times, but these spheres migrated (P less than 0.01) from the submucosa to the mucosa. By 1.5 min, 5 +/- 2% of 11.5-micron spheres had shunted, but no subsequent shunting was observed. No migration of 11.5-micron spheres from the mucosa, submucosa or the muscularis was observed. The shunting of 9-micron spheres from the whole wall increased from 19 +/- 4% at 1.5 min to 40 +/- 4% at 60 min (P less than 0.001). These data suggest that 17-micron spheres can only fractionate the blood flow of the whole wall into that of the mucosa plus submucosa and that of the muscularis propria, while 11.5-micron spheres may measure fractional flow to the submucosa separately. The continued washout of 9-micron microspheres precludes their use for repeated blood flow measurements.

Animals↗

PubMed1988

Vasculature of various locations of canine gastrointestinal tract responds differently to intravenous isoproterenol.

In this study we investigated the relative vascular response of different locations of the gastrointestinal tract to continuous intravenous infusion of isoproterenol (0.1 microgram kg-1 min-1 for 10 min). The vascular response of some nonsplanchnic organs was also examined. Blood flow of the arteries was measured by electromagnetic flowmetry and that of the tissues by 15-micron microspheres. Isoproterenol increased (P less than 0.05) blood flow of the axillary artery (+52%), and the superior mesenteric artery (+45%), but not that of the inferior mesenteric artery. In the nongastrointestinal tissues, isoproterenol increased (P less than 0.05) the blood flow of the left (+46%), and right ventricle (+85%), and the skeletal muscle (+100%). In the gastrointestinal tract, isoproterenol increased (P less than 0.05) blood flow in the esophagogastric junction (+505%) and antrum (+1511%) only, but not in the gastric body or in any location of the small or large intestine. The drug also caused a large fall in resistance in the esophagogastric junction (-74%) and antrum (-94%), and a small, but significant fall in the duodenum, jejunum, and in the mid-small intestine. It had no significant effect on vascular resistance in the gastric body, ileum, or colon. In those locations of the gastrointestinal tract where isoproterenol caused an increase in blood flow, this effect was confined to the combined mucosal plus submucosal layer, and the drug had no effect on the muscularis. These data suggest that different locations of the gastrointestinal tract respond differently to the same circulating concentration of isoproterenol. The mechanism of this difference in response merits further investigation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

16,16-Dimethyl prostaglandin E2 alleviates jejunal microvascular effects of ethanol but not the ethanol-induced inhibition of water, sodium, and glucose absorption.

To examine the relation between ethanol-induced microvascular and absorptive changes, we have investigated the effect of 16,16-dimethyl prostaglandin E2 on the jejunal intraluminal plasma albumin loss (which was taken as a measure of microvascular changes) and the inhibition of water, sodium, and glucose transport caused by intraluminal ethanol. A group of 8 dogs received intravenously 16,16-dimethyl prostaglandin E2 at a dose of 0.1 microgram/kg as a bolus followed by 0.05 microgram/kg.hour for 2 h (prostaglandin-treated group). A second group of 8 dogs received no 16,16-dimethyl prostaglandin E2 (untreated group). In each dog of both groups, one jejunal segment was perfused with an ethanol-free solution (control segment) and an adjacent segment was perfused with the same solution containing 6% (wt/vol) ethanol (ethanol-perfused segment). The albumin loss (mg/g dry gut wt.90 min, mean +/- SE) by the control and the ethanol-perfused segments was 0.76 +/- 0.23 and 8.29 +/- 1.27, respectively, in the untreated group, and 0.66 +/- 0.23 and 4.81 +/- 0.67, respectively, in the prostaglandin-treated group. The ethanol-induced increase in albumin loss was significant in both groups, but was significantly lower (p less than 0.05) in the prostaglandin-treated group than in the untreated group. Intraluminal ethanol depressed net water, sodium, and glucose transport by 74%, 52%, and 22%, respectively, in the untreated group, and by 92%, 65%, and 38%, respectively, in the prostaglandin-treated group. The magnitude of this depression did not differ significantly between the two groups. As 16,16-dimethyl prostaglandin E2 attenuated the ethanol-induced plasma albumin loss, but not the inhibition of water, sodium, or glucose transport, we conclude that the microvascular and the absorptive changes produced by ethanol are not mediated by the same mechanism.

16,16-Dimethylprostaglandin E2↗

PubMed1988

Histamine is involved in ethanol-induced jejunal microvascular injury in rabbits.

To examine for the possible involvement of histamine in the jejunal microvascular effects of ethanol, we investigated the effects of (a) intraluminal ethanol on histamine release by the jejunum and (b) simultaneous inhibition of both histamine1 and histamine2 receptors (using promethazine and cimetidine, respectively) on ethanol-induced intestinal plasma protein loss in rabbits. Ethanol increased histamine release by the jejunum both in vivo (p less than 0.01) and in vitro (p less than 0.05). To investigate the effect of antihistamines on ethanol-induced plasma protein loss, we determined the dose of blockers that would completely inhibit the histamine1 and histamine2 receptors. In the absence of antihistamines, ethanol caused a 10-fold increase in jejunal protein loss over the controls (p less than 0.001). Simultaneous inhibition of histamine1 and histamine2 receptors attenuated (p less than 0.025), but did not abolish, the ethanol-induced protein loss. These data are discussed in relation to the literature, and it is concluded that histamine may play a role in the jejunal microvascular effects of ethanol. As the ethanol-induced protein loss was not completely inhibited, other mediators or mechanisms were probably involved.

Animals↗

PubMed1988

Evidence for the involvement of 5-lipoxygenase products in ethanol-induced intestinal plasma protein loss.

In this study we investigated whether the products of 5-lipoxygenase (5-LO) were involved in the jejunal microvascular injury induced by intraluminal ethanol (ETH). A group of rabbits was given orally a selective inhibitor of 5-LO (L-651,392, Merck Frosst Canada) in two 10-mg doses, 24 and 2 h before the experiments (treated group). Another group received no such treatment (untreated group). In each animal of both groups, a jejunal segment was perfused with a control solution (control segment) and an adjacent segment with an ETH-containing (6% wt/vol) solution (ETH-perfused segment). In a series of experiments, we measured 5-LO activity of the jejunal segments of both groups using the generation of leukotriene B4 (LTB4) as an index. In a second series of experiments, we determined the ETH-induced intraluminal protein loss, which was taken as a measure of mucosal microvascular damage. In the untreated group, LTB4 generation (pg/mg tissue) by the ETH-treated segment (2.49 +/- 0.70) was higher (P less than 0.005) than that by the control segment (0.68 +/- 0.14). In the treated group, the LTB4 generation decreased (P less than 0.05) both in the control (0.15 +/- 0.03) and the ETH-perfused segments (0.44 +/- 0.09), but the difference between the two segments still remained significant. ETH caused a 13-fold increase (P less than 0.01) in jejunal protein loss in the untreated group but only a 5-fold increase (P less than 0.05) in the treated group. The ETH-induced increase in protein loss was significantly lower in the treated than in the untreated group (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Indium-111-labeled autologous leukocyte imaging and fecal excretion. Comparison with conventional methods of assessment of inflammatory bowel disease.

This study was designed to evaluate the role of 111In-labeled leukocyte imaging and fecal excretion in the assessment of inflammatory bowel disease. We compared these tests to various indices of disease activity in Crohn's disease, to Truelove's grading in ulcerative colitis, and to endoscopy, x-ray, and pathology in both diseases. Eleven controls, 16 patients with Crohn's disease, 13 with ulcerative colitis, and 3 with other types of acute bowel inflammation were studied (positive controls). Indium scanning was performed at 1, 4, and 24 hr. Fourteen of 16 patients with active Crohn's disease had positive scans but in only five was localization accurate. One patient had inactive ulcerative colitis, and the scan was negative. Of 12 patients with active ulcerative colitis, 10 had positive scans but disease localization was accurate in only four. Disease extent was correctly defined in 1 of the 3 Positive Controls. There was no significant difference in the accuracy of scanning at 1, 4, or 24 hr. 111In fecal excretion was significantly higher in patients with inflammatory bowel disease than in controls, and there was correlation between 111In fecal excretion and most of the indices of disease activity in Crohn's disease. In ulcerative colitis, 111In fecal excretion did not correlate with Truelove's grading but reflected colonoscopic assessment of severity. In conclusion, 111In-labeled leukocyte scanning lacks sensitivity with respect to disease extent, but fecal excretion of 111In correlates well with disease severity as determined by other methods.

Colectomy↗