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Biomedical subjects

I T Beck

Publications and source records attributed to I T Beck.

At least 55 records · Page 3Linked to original sources
PubMed1986

Ethanol-induced vascular permeability changes in the jejunal mucosa of the dog.

We have demonstrated previously that ethanol causes alterations in jejunal morphology and fluid secretion, and that these changes are accompanied by an increase in mucosal arteriolar blood flow, shunting of blood through noncapillary microvessels, hyperemia, hemoconcentration, and an enhanced loss of plasma protein into the gut lumen. All the microcirculatory changes are compatible with an ethanol-induced mucosal microvascular stasis. The present study was undertaken to examine whether these changes are accompanied by an enhanced mucosal microvascular permeability. Using a colloidal carbon vascular labeling technique, we demonstrated that 6% wt/vol intraluminal ethanol caused marked accumulation of carbon particles in the walls of the capillaries and microvenules of the villus tips. The effect of 3% ethanol was much less pronounced, and the extent of carbon entrapment did not significantly differ from microvessels in villi perfused with Krebs-Ringer solution without ethanol. Electron microscopy indicated that the carbon was localized between the endothelial cell and the basal lamina of the microvessels. Because the carbon accumulation was always localized at the vicinity of endothelial cell junctions, the escape of carbon particles from the lumen probably occurred through these cell junctions. This could have been the result of a transient retraction of endothelial cells. Electron microscopic examination also demonstrated that the lumina of some capillaries and venules of the villus tip of jejunal segments perfused with 6% ethanol were clogged with carbon particles. This latter finding indicates that there was stasis in these vessels at the time of carbon injection. Similar intraluminal carbon accumulation was never seen in control jejunum or jejunum perfused with 3% ethanol. Thus the results of this study indicate that 6% (wt/vol) ethanol causes microvascular injury and stasis. The findings with 6% ethanol are reminiscent of those described by others in the early phases of acute inflammation, and thus it is possible that the microvascular changes caused by ethanol may be related to the liberation of some of the chemical mediators of the immediate response to acute injury.

Animals↗
PubMed1986

The effect of acid and bethanechol stimulation in patients with symptomatic hypertensive peristaltic (nutcracker) esophagus. Evidence that this disorder may be a precursor of diffuse esophageal spasm.

The hypertensive peristaltic (nutcracker) esophagus represents a motility disorder characterized clinically by squeezing retrosternal chest pain and manometrically by high amplitude esophageal peristaltic contractions. This study was designed to examine whether the nutcracker esophagus is: (a) a distinct entity, (b) a member of the spectrum of primary esophageal dysmotilities (e.g., diffuse esophageal spasm and achalasia), or (c) is secondary to reflux-induced acid sensitivity. Thirteen patients with a nutcracker esophagus by baseline manometry were subsequently studied after acid perfusion and bethanechol stimulation (0.08 mg/kg). Records were analyzed for symptomatic response and motility changes. Eight of 13 (62%) experienced chest pain during acid perfusion, but none had significant motility changes documented during this period. After bethanechol injection, chest pain occurred in six of 12 (50%) patients; two had burning pain and in the other four (33%) their squeezing chest pain was reproduced. Changes in the motility tracing with evidence of disordered motility suggestive of diffuse esophageal spasm were seen after bethanechol in seven of the 12 tracings analyzed (58%), including all six patients who developed chest pain. We conclude that patients with nutcracker esophagus on baseline manometry may develop motility patterns consistent with diffuse esophageal spasm after provocation with bethanechol. We take this to suggest that the nutcracker esophagus is part of the continuum of primary motility disorders and may actually be a precursor of diffuse esophageal spasm.

Adult↗
PubMed1986

Arteriolar, capillary, and shunt flow gradients along the intestine in relation to the weight distribution of the mucosa, submucosa, and muscularis--a microsphere study.

The objective of this study was to establish the basal arteriolar (ART), capillary (CAP), and shunt (SH) flow of the three anatomical layers of the gut wall (mucosa, submucosa, and muscularis) along the intestinal tract of the dog employing a microsphere technique. We also examined whether a gradient of blood flow (BF) exists along the intestine, and if so, how this is related to the blood flow and weight distribution of the three anatomical layers along the intestine. We found the following. (i) In all locations of the intestine a higher proportion of the ART inflow passed through the capillaries of the layers with higher metabolic need, i.e., mucosa (68-79%) and the muscularis (50-79%), than through the capillaries of the submucosa (34-46%). Thus, the distribution between CAP and SH flow in the three anatomic layers of the gut wall, as measured by the microsphere technique, appears to correspond to the functional requirements of these tissue layers. (ii) From the duodenum to the ascending colon (but not along the colon), there was a significant decreasing gradient of ART flow (R2 = 50.6%) and a small and barely significant gradient of CAP (R2 = 11.6%) and SH flow (R2 = 9.7%) of the whole gut wall. (iii) All these gradients were present in the mucosa, but their slopes were higher than those in the whole gut wall; the R2 for the mucosal ART, CAP, and the SH flow was 60.5, 52.7, and 21.6%, respectively. (iv) The ART, CAP, or the SH flow of the submucosa and the muscularis showed no such decreasing gradient. Thus, the gradient of blood flow of the whole gut wall appears to be a reflection of a more prominent gradient of ART and CAP flow of the mucosa. (v) Similar to the mucosal blood flow, the weight distribution of the mucosa showed a craniocaudal gradient (R2 = 69.3%). The latter was found to be directly related to the mucosal blood flow of all locations from the duodenum to the ascending colon, except for the duodenum, which had a higher ART and SH flow than those of several, but not all, distal locations. This higher blood flow of the duodenum could be due to a functional difference of this location.

Animals↗
PubMed1985

Ultrasound in the diagnosis of sphincter of Oddi spasm.

Biliary colic from spasm of the sphincter of Oddi has been a difficult diagnosis to prove. We describe a patient in whom the diagnosis was arrived at using a pharmacological provocative test employing codeine to reproduce pain and a change in liver and pancreatic serum enzymes, and ultrasound to demonstrate a transient increase in common bile duct diameter. Testing carried out before surgical sphincteroplasty reproduced symptoms, and brought about marked pancreatic and liver enzyme elevation and an increase in common bile duct diameter measured by ultrasound (0.4 to 1.0 cm). Such events did not occur after sphincteroplasty. This case study suggests that codeine may be a useful provocative agent and that ultrasound measurements of changes in common bile duct diameter may provide a useful method in the diagnostic approach to Sphincter of Oddi Spasm.

Acetaminophen↗
PubMed1984

Effects of ethanol on cytoplasmic peptidases of the jejunal epithelial cell of the hamster.

Although ethanol has been reported to inhibit intestinal amino acid absorption and peptide hydrolysis by the brush border membrane (BBM) peptidases, its effect on other events of protein absorption (such as peptide hydrolysis by cytosol peptidases, absorption of peptides across the BBM, and translocation of amino acids across the basolaterial membrane) has not yet been reported. To obtain a better understanding of the overall effect of ethanol on intestinal protein absorption, in the present study we have investigated the influence of ethanol on the cytosol peptidases. In order to examine the activity of these enzymes, without the influence of brush border digestion and translocation of peptides, the present study was carried out in vitro using a preparation of cytosol peptidases. Results show that exposure of the enzymes to 1-5% (w/v) ethanol caused a dose-dependent inhibition of hydrolysis of L-leucylglycine (Leu-Gly), glycyl-L-tyrosine (Gly-Tyr), and L-phenylalanylglycine (Phe-Gly) by the cytosol peptidases. These inhibitions were completely reversible. Kinetic studies indicated that ethanol depressed the hydrolysis of Leu-Gly and Gly-Tyr by a mixed type of inhibition, in which the Vmax decreased and the Km increased. In the hydrolysis of Phe-Gly, two enzymes were involved, and ethanol depressed the Vmax of both, without affecting their Km. These findings suggest that ethanol alters only the catalytic center of both enzymes involved in the hydrolysis of Phe-Gly and alters both the catalytic center and the substrate binding site of the enzymes involved in the hydrolysis of Leu-Gly and Gly-Tyr. The results of this study together with those of our previous investigation on BBM peptidases indicate that ethanol interferes with the intestinal hydrolysis of peptides and, therefore, probably with the absorption of protein.

Animals↗
PubMed1984

Ethanol-induced mucosal microvascular stasis and enhanced plasma protein loss in the dog jejunum.

On the basis of previous studies in our laboratory, we have proposed that ethanol-induced alterations in the mucosal microcirculation, particularly vascular stasis, may be responsible for the genesis of the mucosal morphologic lesions and enhanced fluid secretion observed during acute perfusion of the jejunum with ethanol. In an attempt to substantiate this in the present study, we examined (a) the effects of acute intraluminal alcohol perfusion (3.0% and 6.0% wt/vol) on canine mucosal arteriolar blood flow, mucosal red blood cell volume, and mucosal "plasma volume" (as reflected by total mucosal albumin volume), and (b) whether ethanol induces an enhanced secretory filtration of plasma from the jejunal mucosal microvasculature into the gut lumen. These studies indicate that intraluminal perfusion of the jejunum with 6% ethanol leads to a significant (p less than 0.05) increase in both mucosal arteriolar blood flow and red blood cell volume. Despite these changes, mucosal "plasma volume" (total albumin volume) remained unaltered, indicating that hemoconcentration had occurred in the mucosa of the ethanol-perfused segments. These events could result in congestion or stasis within the blood vessels of the mucosa. Perfusion with 6% ethanol also caused a significant increase (p less than 0.05) in the loss of plasma proteins from the mucosal microvasculature into the gut lumen. These results are consistent with our previous proposal that ethanol leads to mucosal microvascular stasis and plasma transudation and that these conditions may in turn lead to the mucosal morphologic lesions and altered fluid transport induced by ethanol.

Animals↗
PubMed1983

Effect of ethanol on morphology and total, capillary, and shunted blood flow of different anatomical layers of dog jejunum.

On the basis of previous studies in our laboratory we postulated that the ethanol-induced alteration in jejunal morphology was the result of its effect on the microcirculation. The present study was undertaken to examine the validity of this hypothesis. Accordingly, the effects of intraluminal ethanol perfusion (3.0 and 6.0% w/v) on mucosal morphology; water, glucose, and sodium transport; and regional blood flow were examined in in vivo jejunal segments of pentobarbital-anesthetized dogs. Compared to control segments, those perfused with ethanol exhibited a significant increase in the prevalence of morphological alterations of the mucosa, consisting of subepithelial fluid accumulation (bleb formation) and exfoliation. Those villi with epithelial damage exhibited villus cores significantly shorter than those with a normal, undamaged epithelium. Segments perfused with ethanol exhibited a depressed net water absorption, to the point that net secretion occurred in the segments perfused with 6% ethanol. Net absorption of glucose was similarly depressed by intraluminal perfusion with ethanol, whereas net absorption of sodium was unaffected. Regional jejunal blood flows were estimated using a dual, radiolabeled microsphere technique. Both total jejunal wall and total mucosal blood flow (in ml/min/100 g dry tissue) in the ethanol-perfused segments were significantly increased over control. Similarly, jejunal wall and mucosal capillary blood flows were increased by ethanol perfusion. Neither submucosal nor muscularis blood flows were affected by intraluminal perfusion with ethanol. Compared to control, shunting or nonentrapment of 9-micron microspheres was increased in the mucosa of the ethanol-perfused segments. In contrast to this, shunting of 9-micron microspheres in the submucosa and muscularis was unaffected by intraluminal perfusion with ethanol. It therefore appears that the ethanol-induced mucosal morphological alterations are accompanied by a localized mucosal hyperemia, and an increased shunting of blood through the mucosa. Based on the results of this and other studies, a microvascular mechanism was tentatively proposed to explain the pathogenesis of the ethanol-induced morphological changes.

Animals↗
PubMed1983

Simultaneous estimation of arteriolar, capillary, and shunt blood flow of the gut mucosa.

Microspheres of 15 and 9 microns diameter were injected simultaneously into the left ventricle of the dog, and the entrapment of these microspheres in different layers of the gut wall was measured under resting conditions, vasoconstriction, and subsequent vasodilation. Results show that some of the 9-microns spheres passed into the portal blood through all layers of the gut wall, whereas 15-microns spheres were completely entrapped in the tissue. The pattern of entrapment of 15-microns spheres during vasoconstriction and during subsequent vasodilation suggests that these microspheres measure adequately the arteriolar inflow of the muscularis, submucosa, and mucosa (i.e., villus plus crypt) but, due to series arrangement between the arterioles of the villus and the crypt, cannot measure the arteriolar flow of the villus and crypt separately. The entrapment of 9-microns microspheres in the muscularis, submucosa, crypt, and villus that occurred during vasoconstriction did not change during subsequent vasodilation. This suggests that these microspheres became lodged in the precapillary sphincter or capillary and therefore measured the capillary flow of these layers. Accordingly, the difference between the arteriolar (measured by 15 microns) and the capillary (measured by 9 microns) flow of the muscularis, submucosa, and mucosa may provide an estimate of the noncapillary (shunt) flow of these layers.

Animals↗
PubMed1983

Effect of ethanol on jejunal regional blood flow in the rabbit.

The effects of intraluminal ethanol perfusion (3.0% and 6.0% vt/vol) on mucosal morphology, water transport, and regional blood flow were examined in in vivo jejunal segments of pentobarbital-anesthetized rabbits. Compared with control segments, ethanol-perfused segments exhibited morphological alterations of the mucosa consisting of subepithelial fluid accumulation (bleb formation), exfoliation of enterocytes, and vascular congestion. The prevalence of epithelial damage was significantly increased in the segments perfused with 6% ethanol. Net water transport was significant (p less than 0.025) depressed in segments perfused with 3.0% and 6.0% wt/vol ethanol. In animals in which the control segment was absorbing water, ethanol led to a depression in net water absorption or to the reversal of absorption to net secretion. In animals in which the control segment exhibited secretion, ethanol led to an enhanced net secretion. Blood flow through the total jejunal wall and through the luminal layer (consisting of mucosa plus submucosa) was significantly (p less than 0.05) increased by the presence of 3.0% and 6.0% wt/vol ethanol in the intestinal lumen. Blood flow in the external layer of the jejunum (consisting of muscularis plus serosa) did not change significantly. It therefore appears that the ethanol-induced alterations in jejunal mucosal morphology and water transport are accompanied by a localized mucosal or submucosal hyperemia, or both. However, a direct cause and effect relationship between these remains to be established.

Animals↗
PubMed1982

Evidence that L-sucrose is resistant to hydrolysis catalyzed by jejunal brush border enzymes.

The sucrase-isomaltase complex of the intestinal brush border membrane (BBM) catalyzes the hydrolysis of sucrose. The stereospecificity of this enzyme, however, is not known. To investigate this, BBM of hamster jejunum was incubated with D-sucrose or L-sucrose, and the reaction mixture was analyzed using a gas-liquid chromatograph. It was found that D-sucrose was hydrolyzed to its monomers, but L-sucrose remained unhydrolyzed. It is concluded that the sucrase-isomaltase of intestinal BBM of hamster jejunum does not hydrolyze L-sucrose and therefore this enzyme is stereospecific.

Animals↗
PubMed1982

Effect of ethanol on peptidases of hamster jejunal brush-border membrane.

This study was undertaken to investigate the effect of ethanol on the brush-border activity of the small intestine. Brush-border membrane isolated from hamster jejunum was incubated with L-phenylalanylglycine (Phe-Gly), L-leucylglycine (Leu-Gly), or glycyl-L-tyrosine (Gly-Tyr) in the absence and presence of 1-5% (wt/vol) ethanol, and the L-amino acids liberated were determined. Ethanol was found to depress the hydrolysis of all peptides in a dose-dependent manner. The inhibitory effect of ethanol on the peptidases does not appear to be time dependent. The ethanol-induced inhibition of peptidase activity is completely reversible. Kinetic studies indicate that ethanol caused a decrease in the Vmax of the enzymes responsible for the hydrolysis of the Phe-Gly and Gly-Tyr but did not have any effect on their Km. In the hydrolysis of Leu-Gly, two enzymes were involved, and ethanol depressed the Vmax of both without affecting the Km of either. These findings suggest that ethanol produces conformational changes of the peptidases involved in the hydrolysis of these three dipeptides.

Animals↗
PubMed1981

Ethanol-induced inhibition of glucose transport across the isolated brush-border membrane of hamster jejunum.

Acute exposure of jejunal mucosa to ethanol has been reported to produce a depression of transmural glucose transport across this organ in vitro and in vivo. In an attempt to understand the mechanism of action of ethanol on intestinal transport, in the present study we have investigated the effect of ethanol on glucose uptake by purified brush-border membrane vesicles of hamster jejunum. Ethanol, in concentrations found in man after moderate drinking (1-5% w/v), was found to depress glucose uptake by the brush-border membrane in a dose-dependent and time-dependent manner. Mannose was used to measure nonspecific uptake, and we found that the ethanol-induced depression of glucose uptake was not related to an alteration of the nonspecific uptake of this sugar. The inhibition of glucose uptake of the ethanol-treated membranes completely disappeared after repeated washing of the membranes with ethanol-free buffer. Accordingly, the ethanol-induced depression of glucose uptake was not the result of irreversible damage to membrane proteins but was related to a direct effect of ethanol on the brush-border membrane. On the basis of these findings, it is concluded that a direct interference with glucose translocation across the brush border plays an important role in the ethanol-induced depression of transmural jejunal glucose absorption.

Animals↗
PubMed1980

Villous damage induced by suction biopsy and by acute ethanol intake in normal human small intestine.

Previous studies by us indicated that ethanol in concentrations of 2.0-4.8% produced subepithelial blebs in the jejunum of the hamster. In the rat, due to rupture of the blebs, there was denudation of the villus tip epithelium. There are nos similar data on humans. Ethanol, in quantities equivalent to 4.8-6.4 ounces of 80 proof whiskey (diluted to 20% w/v), was infused into stomachs of 20 normal human volunteers. Subjects were divided into groups (Gr) according to the amount or type of alcohol given, and site of biopsies (SB). Gr 1:60 g ethanol, SB = jejunum. Gr 2:45 g ethanol, SB = jejunum. Gr 3:45 g ethanol, SB = duodenum. Gr 4:45 g ethanol as 4.8 oz 80 proof whiskey, SB = duodenum. To compare the morphology in the absence and presence of ethanol, biopsies were obtained from each volunteer before ethanol administration (control period), immediately after peak ethanol concentration in the duodenum or jejunum (ethanol period), and when intraluminal ethanol concentration fell towards zero (recovery period). The mean peak intraluminal ethanol concentrations in the four groups varied between 5.69% and 9.37% (w/v). Ethanol-induced damage was evaluated using strict preset criteria. Coded slides were evaluated by two observers. Suction biopsy damaged 18% of the villi even in biopsies obtained during the control period. Ethanol produced a statistically significant increase in the number of damaged villi (mean of all groups 45%, range: 32% in Gr 2 to 62% in Gr 3). During the recovery period the number of damaged villi fell to that seen in control period biopsies. Ethanol, in quantities equivalent to those ingested during moderate drinking, may produce transient damage to the upper small intestine of man. Conversely, ethanol may simply increase the susceptibility of the mucosa to the unavoidable trauma of suction biopsy. However, the histological and ultrastructural changes were similar to those induced by ethanol in small laboratory animals.

Adolescent↗
PubMed1979

A syndrome of acute self-limiting ulcerative esophagitis in young adults probably due to herpes simplex virus.

Five healthy young adults developed an acute self-limiting ulcerative esophagitis. Two had definite evidence of herpes virus being present and a third one had appropriate changes in herpes simplex viral titer. All cases followed a characteristic and similar course consisting of sudden onset of odynophagia, multiple discrete small ulcers in the esophagus and herpetiform lesions elsewhere in the skin or mouth. Although most previous reports of herpes esophagitis indicate that it is an "opportunistic" infection in debilitated hosts, the present report indicates that this infection, in patients who are otherwise well, may occur more frequently than one would have previously suspected. Therefore, herpes simplex virus should be considered as a possible etiological agent in the differential diagnosis in patients presenting with a sudden onset of odynophagia.

Acute Disease↗