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PubMed1986

Effect of cigarette smoke on esophageal epithelium of the rabbit.

Cigarette smoking is a recognized risk factor for esophageal mucosal disease. For this reason we investigated the effects of smoke on esophageal epithelial electrolyte transport and barrier function in the rabbit. Studies were performed using an extract of cigarette smoke (EOCS) prepared from high-tar, high-nicotine cigarettes. Epithelia were exposed to EOCS in vivo or in vitro in the Ussing chamber. Acute in vivo exposure to EOCS lowered in vivo esophageal potential difference by 61%, and in vitro studies established that this was due to inhibition of active Na transport from mucosa to serosa. Exposure to an EOCS had no effect on net Cl transport or epithelial permeability, the latter reflected by the absence of change in electrical resistance or mannitol flux. The ability of an EOCS to lower potential difference (and inhibit Na transport) was dose-related and equally effective whether contact occurred with the luminal or serosal surface of the tissue. Similar studies performed with an EOCS prepared from filtered smoke established that the component(s) in EOCS responsible for the effects on transport resided in the particulate phase of smoke (i.e., nicotine and "tars"). However, nicotine only inhibited Na transport from the serosal side of the tissue, thus indicating that one or more tars either cause or contribute to the effect of an EOCS on transport. The inhibition by smoke of ion transport in esophageal epithelium may well be an early deleterious link in the pathophysiological chain between cigarette smoking and esophageal mucosal disease.

Animals↗
PubMed1986

Phytohemagglutinin from red kidney bean (Phaseolus vulgaris) inhibits sodium and chloride absorption in the rabbit ileum.

Phytohemagglutinin (PHA), derived from red kidney bean (Phaseolus vulgaris), can induce malabsorption and diarrhea when fed to rats. In this study, we determined the effect of PHA on ion transport in the rabbit ileum in vitro. Compared with control tissues, PHA (1 mg/ml) added to the mucosal solution increased short-circuit current (1.1 +/- 0.2 microEq/cm2 X h, p less than 0.001), decreased net Na (-1.0 +/- 0.5 microEq/cm2 X h, p less than 0.02) and Cl (-1.2 +/- 0.6 microEq/cm2 X h, p less than 0.025) absorption, and decreased tissue conductance (-1.8 +/- 0.5 mS/cm2, p less than 0.001). Serosal addition of PHA had no effect on the short-circuit current or tissue conductance. Mucosal PHA did not increase mucosal levels of cyclic adenosine monophosphate or cyclic guanosine monophosphate. Removal of serosal calcium did not affect the increase in short-circuit current induced by mucosal PHA. Utilizing fluorescent microscopy, rhodamine-labeled PHA was found to bind to the luminal border of villus cells, but not to crypt cells, in the ileum. In the descending rabbit colon, PHA did not affect either the short-circuit current or conductance, and rhodaminated PHA did not bind to the epithelial surface. Using the increase in short-circuit current as an indicator of absorption, PHA did not affect Na-coupled glucose or amino acid absorption in the ileum. This study suggests that dietary lectins may play a role in regulating intestinal fluid and electrolyte transport.

Animals↗
PubMed1988

Uptake of polypeptide fragments of proteins by rat intestine in vitro and in vivo.

Minute amounts of intact proteins were previously shown to be taken up from the intestine into the systemic circulation of mature animals; fragments were not detected. In this study, we sought evidence for uptake of fragments in both in vitro and in vivo experiments. Polypeptide fragments produced by pepsin digestion of bovine serum albumin (ranging in molecular weight from approximately 6000 to 25,000) were labeled with 125I. Everted jejunal gut sacs prepared from rat intestine were incubated with labeled fragments. After incubation, fluid exposed to the serosal surface was applied to a Sephadex G-50 gel permeation column. Radioactivity was detected in fractions corresponding to the elution position of the fragments. Transfer of fragments from the mucosal to the serosal surface was temperature-dependent. In in vivo studies, labeled fragments were infused into the jejunum of rats. Blood samples obtained from a mesenteric vein or the portal vein contained labeled fragments. After infusion of unlabeled fragments, nanogram amounts of immunoreactive fragments were detected by radioimmunoassay of mesenteric and portal venous blood. Thus, polypeptide fragments of a potential food protein were capable of being transferred across the mucosa in vitro and in vivo. Failure to detect fragments in the systemic circulation most likely results from their rapid clearance.

Animals↗
PubMed1988

Effect of BW 942C, an enkephalinlike pentapeptide, on sodium and chloride transport in the rabbit ileum.

BW 942C is a novel enkephalinlike pentapeptide that has been shown to have antidiarrheal action in model systems. The effect of BW 942C on rabbit ileal electrolyte transport was studied to gain insight into the mechanism of the antidiarrheal action of opiate-like compounds. Multiple effects were observed, differing with the basal state of the tissue. BW 942C increased Na absorption in tissues that were not absorbing in the basal state, whereas it had little effect on Na absorption in tissues that were previously absorbing at moderate to high rates (greater than 1 microEq/h.cm2. It increased Cl absorption and caused a dose-related decrease in short-circuit current in all tissues. This effect was reversed or inhibited by naloxone (10(-5) M), suggesting that it is mediated by opiate receptors. No significant change in residual flux was noted. BW 942C was effective from both the serosal and mucosal side; however, it required a 2-log higher dose on the mucosal side (10(-4) M, maximal) to achieve a response similar to that observed with serosal application (10(-6) M, maximal). The ability of BW 942C to alter stimulated secretion was studied using theophylline, prostaglandin E2, vasoactive intestinal peptide, and bethanechol. There was significantly less Cl secretion in BW 942C-treated tissues than in control tissues after stimulation with prostaglandin E2 (10(-7) M). However, this effect was not apparent at higher doses of prostaglandin E2 and there was no inhibition of the short-circuit current response to any of the secretory stimuli by BW 942C. Loperamide was also found to be unable to inhibit the Cl secretion or change in short-circuit current stimulated by theophylline. Although opiates have been shown to be moderately effective antidiarrheal agents, their ability to influence mucosal electrolyte transport is weak and may only account for part of their antidiarrheal action.

Animals↗
PubMed1989

Fall in the number of myenteric neurons in aging guinea pigs.

The neurons of the myenteric plexus of the entire small intestine were stained in young adult (3-4 mo old) and aging guinea pigs (26-30 mo old). Total length and circumference of the intestine were measured in the same experiments. The small intestine of the aging guinea pigs was longer, and (in the conditions of distention used) had a total serosal surface approximately 70% greater than in young adult animals. The spatial density of myenteric neurons per unit of serosal surface fell dramatically in aging animals, and the total number of myenteric neurons in the small intestine ranged between 1.1 and 1.6 million, i.e., it was only 40%-60% of the value obtained in young adult guinea pigs (2.75 million). The light microscope appearance of the neurons of the two groups of animals was markedly different and the suggestion is put forward that in aging guinea pigs the substantial reduction in neuron number is accompanied by structural changes and reorganization of the neurons that are left.

Aging↗
PubMed1991

Neuromodulation of guinea pig intestinal electrolyte transport by cholecystokinin octapeptide.

We examined the effect of cholecystokinin octapeptide on electrolyte transport across isolated guinea pig mucosa. Segments of distal ileum stripped of longitudinal muscle and bathed on both sides with a Krebs'-bicarbonate buffer responded to cholecystokinin octapeptide when studied under short-circuited conditions. Cholecystokinin octapeptide (0.5-50 nmol/L) evoked a transient (4-10-minute) increase in transepithelial potential difference and short-circuit current upon application to the serosal side. Maximal increases in short-circuit current, achieved at 50-500 nmol/L, were 67 +/- 11 microA/cm2, whereas half-maximal effects occurred at a concentration of 0.7 +/- 0.2 nmol/L. Pretreatment of the tissues with 0.5 mumol/L atropine reduced the maximal short-circuit response to cholecystokinin octapeptide by 53%. The change in short-circuit current due to cholecystokinin octapeptide was nearly abolished by pretreatment with 0.5 mumol/L tetrodotoxin, suggesting neuronal involvement. Cholecystokinin octapeptide-induced increases in short-circuit current were halved by removal of serosal buffer Ca2+ and were abolished in Cl(-)- and HCO3(-)-free buffer. The cholecystokin-receptor antagonists proglumide and lorglumide shifted the concentration-response curve for cholecystokinin octapeptide competitively to the right, having antagonists potencies of 130 and 0.03 mumol/L, respectively. Cerulein (0.1-500 nmol/L) also increased short-circuit current, whereas nonsulfated cholecystokinin octapeptide was ineffective. In conclusion, cholecystokinin octapeptide seems to act at neuronal cholecystokinin receptors to stimulate mucosal anion secretion, in part, by releasing acetylcholine.

Animals↗
PubMed1991

Electrolyte transport in piglets infected with transmissible gastroenteritis virus. Stimulation by verapamil and clonidine.

The effects of clonidine, an alpha 2-adrenergic agonist, and verapamil, a Ca2+ channel blocker, on Na+ and Cl- absorption were studied in stripped jejunal mucosa from control and transmissible-gastroenteritis-virus-infected piglets. All infected piglets developed severe diarrhea 18-24 hours after oral inoculation. Jejunum from infected animals, as compared with control jejunum, had decreased mucosal-to-serosal, serosal-to-mucosal, and net Na+ and Cl- fluxes. Clonidine and verapamil caused a decrease in short-circuit current and stimulation of Na+ and Cl- absorption in control jejunum. In infected piglets, although the jejunum exhibited severe villus atrophy, both drugs stimulated Na+ and Cl- absorption and the magnitude of Na+ and Cl- absorption was similar in control and transmissible-gastroenteritis-infected jejunum. In contrast, D-glucose stimulated Na+ absorption, and the decrease in short-circuit current caused by verapamil and clonidine, were decreased in transmissible-gastroenteritis-infected jejunum. Such pharmacological stimulation of Na+ and Cl- absorption might be useful in the management and treatment of certain viral diarrheal diseases.

Animals↗
PubMed1992

Inhibition of neuronally mediated secretion in rat colonic mucosa by prostaglandin D2.

The effect of prostaglandin D2 (PGD2) on ion transport across the mucosa of the descending colon was studied in rats. PGD2 dose-dependently decreased baseline short-circuit current of mucosa-submucosal preparations mounted either in the Ussing chamber or mounted as an everted sac. However, with the everted sac technique, the tissue was about 1000 times more sensitive to PGD2. Concomitant with the decrease in short-circuit current, PGD2 increased the mucosal-to-serosal fluxes of sodium and chloride and decreased the serosal-to-mucosal flux of chloride. PGD2 inhibited the secretory action of the PGI2 analogue iloprost, PGD2 alpha, and neurotensin. The action of these secretagogues was dependent on the presence of the submucosal plexus. In contrast, PGD2 had no effect on the increase in short-circuit current caused by PGD2, substance P, or serotonin, the actions of which were not dependent on the presence of the submucosal plexus. The results indicate that the action site of the antisecretory mechanism of PGD2 is localized in the secretomotor neurons.

Animals↗
PubMed1992

Transport of glucose polymer-derived glucose by rabbit jejunum.

Mechanisms for the assimilation of glucose polymers have been inferred from perfusion studies. To further define these mechanisms, the results of measurements of unidirectional glucose fluxes across short-circuited rabbit jejunal segments in vitro are reported. Glucose polymer-stimulated short-circuit current was similar to that of glucose [19 +/- 6.0 microA/cm2 (n = 7) and 26 +/- 5.7 microA/cm2 (n = 13), respectively] and was inhibited by both acarbose and phlorizin. Acarbose, an alpha-glucosidase inhibitor with no effects of glucose transport, was used to uncouple digestion from absorption. Mucosal-to-serosal flux of glucose polymer-derived glucose was lower than that of an equal weight/volume of glucose [124 +/- 62 nmol.h-1.cm-2 (n = 4) vs. 452 +/- 121 nmol.h-1.cm-2 (n = 6); P less than 0.05] and was inhibited by both phlorizin and acarbose. No glucose polymers were detected in the serosal bath solutions by thin-layer chromatography. It is concluded that glucose polymer-derived glucose is transported by a phlorizin-inhibitable process at a rate slower than that of free glucose, a finding that suggests that hydrolysis limits glucose polymer assimilation.

Analysis of Variance↗
PubMed1992

Mucosal ouabain and Na+ inhibit active Rb+(K+) absorption in normal and sodium-depleted rat distal colon.

To determine the effect of mucosal sodium and mucosal ouabain on active Rb+(K+) absorption, unidirectional and net 86Rb+ fluxes were measured under voltage-clamp conditions in the distal colon of normal and sodium-depleted rats. The role of mucosal sodium (independent of serosal sodium) was evaluated in a model of Rb+(K+) absorption in which serosal ouabain markedly enhanced active Rb+(K+) absorption. In normal rats, mucosal sodium was a competitive inhibitor of Rb+(K+) absorption, and Rb+(K+) absorption consisted of a mucosal sodium-sensitive component and a mucosal sodium-insensitive component. Further, mucosal ouabain almost completely inhibited the mucosal sodium-insensitive component but did not affect the mucosal sodium-sensitive component. In sodium-depleted rats, both mucosal sodium-sensitive and mucosal sodium-insensitive fractions of Rb+(K+) absorption were also identified. Aldosterone markedly stimulated the mucosal sodium-sensitive component (1.68 +/- 0.15 vs. 0.60 +/- 0.10 muEq.h-1.cm-2) but not the sodium-insensitive component (0.88 +/- 0.09 vs. 0.64 +/- 0.06 muEq.h-1.cm-2) component of Rb+(K+) absorption; however, in contrast to normal animals, mucosal sodium in sodium-depleted animals was a noncompetitive inhibitor of Rb+(K+) absorption. The mucosal sodium-insensitive component of Rb+(K+) absorption in sodium-depleted animals was substantially inhibited by mucosal ouabain, but the mucosal sodium-sensitive component, unlike that in normal animals, was partially inhibited by mucosal ouabain. These studies indicate that the characteristics of the Rb+(K+) absorptive process in sodium-depleted animals differ significantly from those present in normal animals, suggesting that aldosterone induces an Rb+(K+) absorptive mechanism not present in normal animals.

Animals↗
PubMed1993

Mucosal histamine elimination and its effect on acid secretion in rabbit gastric mucosa.

BACKGROUND: Rapid elimination of histamine near the oxyntic cells is important in the termination of the secretory response when the signal for histamine release is discontinued. The mechanism of this local process is still unclear. METHOD: Gastric mucosal histamine elimination was, therefore, examined in fundic mucosa mounted in flux chambers and in dispersed mucosal cells. RESULTS: [3H]histamine placed into the serosal chamber medium was transported across the mucosal tissue into the lumen, but a greater quantity was methylated to an inactive metabolite, Nt-methylhistamine, and preferentially released to the serosal chamber, the interstitial medium. Both processes were enhanced by increased substrate concentration. They were reduced by lowering the temperature and by sodium replacement. Inhibition of histamine methyltransferase suppressed histamine uptake and methylation and significantly increased histamine-stimulated acid secretion in the tissue preparation and in dispersed mucosal cells. The augmentation was reduced by an H2-receptor blocker. CONCLUSION: Mucosal histamine methylation and the secretion of histamine into the gastric lumen removes histamine from the extracellular space effectively, reducing the histamine concentration near the oxyntic cell surface.

Animals↗
PubMed1993

Bicarbonate secretion in rabbit ileum: electrogenicity, ion dependence, and effects of cyclic nucleotides.

BACKGROUND: Ileal HCO3- secretion is not well understood. The aim of this study was to examine its Na+ and Cl- dependencies, electrogenicity, and responses to amiloride, 4-acetamido-4'-isothiocyano-stilbene-2,2'-disulfonate (SITS), and cyclic nucleotides. METHODS: The serosa to mucosa HCO3- flux (Jsm) across rabbit ileal mucosa mounted between HCO(3-)-free mucosal solution and HCO(3-)-containing serosal solutions was determined by titration. RESULTS: In SO4(2-)-containing Ringer's solution, Jsm varied with [Na+] in two phases, one with a high and one with a low affinity for Na+; amiloride inhibited the high- and SITS inhibited the low-affinity phase. Switching from SO4(2-)- to Cl(-)-containing Ringer's solution caused a SITS-inhibitable 42% increase in Jsm. Changes in Jsm were coupled 3:2 with changes in short-circuit current. Cyclic nucleotide effects on Jsm were as follows. In SO4(2-)-containing Ringer's solution at 141 (but not 80) mmol/L Na+, theophylline caused equal increases in Jsm and short-circuit current that equaled the combined effects of 8-Br-5'-cyclic guanosine monophosphate (cGMP) and 8-Br-5'-cyclic adenosine monophosphate (cAMP). Serosal SITS blocked these effects, but amiloride did not. In Cl(-)-containing Ringer's solution, theophylline and bumetanide together (but not separately) increased Jsm. CONCLUSIONS: (1) Basolateral HCO3- entry occurs via Na+/H exchange and a SITS-inhibitable process (Na(+)-HCO3- cotransport?). (2) Most HCO3- exit across the brush border occurs by a Cl(-)-independent process and some by Cl-/HCO3- exchange. (3) At low cellular [Cl-], HCO3- can be secreted via anion channels activated by cAMP and cGMP. (4) Ileal HCO3- secretion is electrogenic.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1994

Inhibition of short-chain fatty acid absorption and Na+ absorption during acute colitis in the rabbit.

BACKGROUND/AIMS: Short-chain fatty acids (SCFAs) provide energy for colonocytes and stimulate colonic fluid and electrolyte absorption. The impact of acute colitis on SCFA-stimulated Na+ absorption and SCFA absorption was examined. METHODS: Proximal colon from rabbits infected with Yersinia entercolitica, a pair-fed group, and controls was mounted in Ussing chambers, and Na+ transport, short-circuit current, and tissue conductance were examined during a basal period and after stimulation with the SCFAs, butyrate, or propionate. Propionate transport and luminal SCFA concentration were evaluated. RESULTS: Butyrate and propionate stimulated electroneutral Na+ absorption above basal levels in the control and pair-fed groups, as evidenced by significant increases in mucosal-to-serosal and net Na+ fluxes with no change in serosal-to-mucosal flux, short-circuit current, or conductance. Butyrate-stimulated Na+ absorption and propionate absorption were blocked by amiloride, an inhibitor of Na(+)-H+ exchange. In the infected group, both butyrate and propionate failed to stimulate colonic Na+ absorption above basal levels. Propionate absorption was inhibited, and epinephrine failed to stimulate Na+ or propionate absorption. Luminal SCFA concentrations were increased in acute colitis. CONCLUSIONS: Inhibition of SCFA-stimulated Na(+)-H+ exchange and SCFA absorption contribute to the diarrheal fluid loses observed in acute colitis and may reduce colonocyte energy supply.

Acute Disease↗
PubMed1994

Localization of bicarbonate transport along the crypt-villus axis in rabbit ileum.

BACKGROUND/AIMS: HCO3- can be absorbed as well as secreted in the rabbit ileum. With 25 mmol/L HCO3- on the serosal side only, a serosa-to-mucosa flux (Jsm) is found; with 25 mmol/L on the mucosal side only, epinephrine elicits a mucosa-to-serosa flux (Jms). This study aimed to localize these two processes along the crypt-villus axis. METHODS: Excised ileal segments were exposed luminally to 2 mol/L Na2SO4 (hypertonic treatment) or to isotonic Ringer's solution for 15 minutes. Mucosa was then chamber-mounted, and measurements were made of Jsm or Jms and of short-circuit current (Isc) responses to glucose plus alanine and to either theophylline or epinephrine. RESULTS: With HCO3-/CO2 added to the serosal side only, hypertonically treated tissues showed a 22% decline in Jsm; a 25% decline in Isc response to theophylline; and a 71% decline in Isc response to glucose plus alanine compared with control. With HCO3-/CO2 added to the mucosal side only, tissues showed 92% and 87% declines in Jms and Isc responses to epinephrine, respectively, and a 87% decline in Isc response to glucose plus alanine. Histological examination showed destruction of villus caused by hypertonic treatment but sparing of crypt cells. CONCLUSIONS: Both HCO3- and Cl- are secreted mainly by crypt cells and absorbed mainly by villus cells.

Animals↗
PubMed1995

Octreotide promotes gallbladder absorption in prairie dogs: a potential cause of gallstones.

BACKGROUND/AIMS: Gallstone formation during octreotide administration has been causally linked to increased biliary concentrations of calcium, protein, and total lipids, all purported prolithogenic factors. These changes may be caused by octreotide-induced gallbladder stasis or a direct effect of octreotide on gallbladder absorption. We tested the hypothesis that octreotide stimulates gallbladder ion and water transport. METHODS: Prairie dog gallbladders were mounted in Ussing chambers and bathed in oxygenated Ringer's solution. Electrophysiological parameters were recorded, and unidirectional Na+, Cl-, and H2O fluxes were measured before and after serosal exposure to 50 nmol/L octreotide. RESULTS: Octreotide exposure caused a significant decrease in transepithelial short-circuit current and potential difference and an increase in tissue resistance compared with baseline. These alterations in electrophysiological parameters coincided with changes in ion transport. Octreotide stimulated net Na+ and H2O absorption and converted the gallbladder from a state of Cl- secretion to one of Cl- absorption by increasing mucosal to serosal fluxes. Octreotide effects on ion transport were blocked by 4,4'-diisothiocynostilbene-2,2'-disulfonic acid and amiloride and reversed by theophylline. CONCLUSIONS: Octreotide may promote gallstone formation by inducing gallbladder stasis and by directly increasing gallbladder absorption, which may act synergistically to increase the concentration of prolithogenic factors in bile and to facilitate nucleation and stone growth.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Gonadotropin stimulation of K+ secretion and Na+ absorption by brook trout (Salvelinus fontinalis) sperm duct epithelium.

The sperm duct epithelium from mature spermiating brook trout (Salvelinus fontinalis) was mounted in vitro to examine control of Na+ absorptive and K+ secretory transport. Na+ absorption (measured as the short-circuit current) and K+ secretion (measured using 86Rb+ as tracer) were stimulated by 3-isobutyl-1-methylxanthine and cyclic AMP while unstimulated tissues had no net ion transport. Purified chum salmon (Oncorhynchus nerka) Con AII carbohydrate-rich gonadotropin produced a rapid, sustained rise in Rb+ secretion and Na+ uptake in a log linear dose-dependent manner. Addition of gonadotropin to either apical (mucosal) or basolateral (serosal) sides evoked the response, but addition to the apical side produced the more rapid effect, indicating that receptors for the hormone are present on both sides of the transporting cells and suggesting that subepithelial tissue may slow the response to serosally added hormone. This is the first indication that gonadotropin may directly regulate ion transport functions of the blood-testis barrier of vertebrates and in this way regulate seminal plasma ionic composition.

Absorption↗
PubMed1987

Serotonin release is mediated by muscarinic receptors on duodenal mucosal cells.

Serotonin (5-HT), found in abundance in intestinal enterochromaffin cells, has been shown to be released in response to neural, humoral, and intraluminal stimuli but the mechanisms controlling release are poorly understood. The purpose of this study was to determine whether 5-HT release induced by the muscarinic agonist, methacholine, is mediated by enteric nerves or is a direct action at the mucosal cell level. We mounted rabbit mucosal sheets containing intact submucosal neural elements, but stripped of muscularis propria and myenteric plexus, in modified Ussing chambers and measured the release of 5-HT in response to 5 X 10(-5) M methacholine added to both mucosal and serosal surface bathing solutions, in the presence and absence of selective neural blockade with 1 X 10(-6) M tetrodotoxin. 5-HT release in control tissues (no drugs) as measured by radioimmunoassay was 25.7 +/- 6 ng/cm2/30 min (mean +/- SEM). In the presence of mucosal and serosal methacholine, total 5-HT release increased significantly (P less than 0.05) to 66.7 +/- 9 ng/cm2/30 min. When tetrodotoxin alone was applied, 5-HT release significantly increased to 55.2 +/- 9 ng/cm2/30 min compared to matched control. In the presence of tetrodotoxin, methacholine increased 5-HT release to 79.3 +/- 9 ng/cm2/30 min, which was significantly greater than with tetrodotoxin alone. These results provide evidence of an inhibitory neural regulation of basal 5-HT release since release increased in the presence of neural blockade. They also suggest that a muscarinic receptor at or near the enterochromaffin cells mediates mucosal 5-HT release since 5-HT is further increased by methacholine even in the presence of neural blockade.

Animals↗
PubMed1988

Prevention of postoperative pericardial adhesions with hydrophilic polymer solutions.

Pericardial adhesions subject patients requiring cardiac reoperation to potential injuries of the heart, great vessels, and extracardiac grafts during resternotomy. We evaluated polyvinylpyrrolidone (PVP) and a methlycellulose derivative (MCD) as intraoperative irrigating solutions in the prevention of postoperative pericardial adhesions. Fifteen dogs weighing 15 to 20 kg were divided into three equal cohorts and subjected to left thoracotomy with pericardiotomy. Prior to surgical manipulation, the pericardial cavity was irrigated with either PVP, MCD, or Ringer's lactate (RL). Serosal injury stimulating intraoperative trauma was induced by gauze sponge abrasion of the epicardium and inner surface of the pericardium and by allowing desiccation of serosal surfaces for 30 min. The pericardial cavity was evaluated for adhesion formation 6 weeks postoperatively by reoperation. Two independent observers, unaware of the study solution, evaluated the extent and severity of pericardial adhesions on a 0-4 scale. All dogs in the RL control group had surgically significant adhesions and a mean adhesion score of 3.2 +/- 1.1. In contrast, no PVP- or MCD-treated dog had surgically significant adhesions. The mean adhesion scores were 0.2 +/- 0.4 for PVP and 0.5 +/- 0.7 for MCD. Our results indicate that PVP (P less than 0.004) and MCD (P less than 0.024) significantly reduce pericardial adhesion formation when compared to RL. Clinical application of PVP or MCD for the prevention of pericardial adhesions should reduce morbidity and mortality of cardiac reoperation.

Animals↗