Oceans. Dis-crediting ocean fertilization.
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Atmosphere↗
Biomedical subjects
J J Cullen
Publications and source records attributed to J J Cullen.
Lipopolysaccharide temporarily impairs sphincter of Oddi motility.
The aim of our study was to determine the effect of lipopolysaccharide (LPS) on sphincter of Oddi (SO) motility. Opossums received saline, Escherichia coli LPS (1.0 mg/kg), or E. coli LPS (1.0 mg/kg) and aminoguanidine (50 mg/kg), and the SO was removed 6-24 h later. At 12 h LPS decreased electrical field stimulation (EFS)-induced relaxation and increased baseline tone. These changes were reversed when the animals were pretreated with aminoguanidine. The dose-dependent decrease in EFS-induced relaxation by N(omega)-nitro-l-arginine was impaired after LPS, but not in animals that received LPS and aminoguanidine. The impaired EFS-induced relaxation after LPS was reversed when l-arginine was added to the tissue bath. Serum levels of NO(-)(2)/NO(-)(3) were increased with LPS as compared to saline or both LPS and aminoguanidine. Inducible nitric oxide synthase mRNA was readily seen in SO segments after LPS. LPS impairs EFS-induced relaxation and increases baseline tone of the SO. The effects of LPS on SO motility appear to be mediated by nitric oxide.
Animals↗
Are gastric, jejunal, or both forms of enteral feeding gastroprotective during stress?
BACKGROUND: Clinical data suggest enteral nutrition prevents stress ulceration and intragastric nutrients prevent restraint-induced gastric injury. The purpose of these studies was to determine if jejunal nutrients can protect without gastric contact and to determine if gastric pH, motility, or mucosal perfusion is affected. METHODS: In Experiment 1, 27 rats were restrained for 2 h at room temperature followed by 2 h in cold (4 degrees C), with intragastric (IG) or intrajejunal (IJ) 2 ml/h infusions of saline or 25% glucose. Gastric lesions, pH, volumes, and glucose concentrations were measured postmortem. In Experiment 2, 23 rats had gastric strain gauges implanted >5 days prior to a 0.5 ml/h IG or IJ infusion during stress. In Experiment 3, 40 rats were anesthetized for laser Doppler measurements of gastric mucosal perfusion and arterial catheter monitoring of systemic hemodynamics. Rats received 0.5-ml boluses of concentrated glucose or saline IG or IJ, and were monitored for 60 min. RESULTS: (1) The 2 ml/h IJ and IG glucose infusions prevented gastric injury, but the elevated gastric glucose concentrations suggested equal gastric contact. (2) The 0.5 ml/h glucose IG and IJ infusions decreased gastric injury without reflux of the IJ glucose into the stomach and suppressed stress-induced hypercontractility, but not acidity. (3) Systemic perfusion pressures were unaffected by enteral glucose. IG glucose had little effect on gastric mucosal perfusion, while IJ glucose decreased gastric perfusion within 5 min. CONCLUSIONS: These studies show that large volumes of enteral glucose prevent restraint injury but IJ glucose refluxes into the stomach. The gastroprotective effects of small, nonrefluxing volumes of IJ glucose are associated with suppression of stress-induced gastric hypercontractility, but not with suppressed acidity or enhanced perfusion.
Animals↗
Characterization of the off response to electrical field stimulation in gallbladder smooth muscle.
BACKGROUND: Low-frequency electrical stimulation of intramural nerves of gut smooth muscle produces an "off response," that is, a contraction that occurs after electrical field stimulation (EFS) of the intramural nerves is stopped. The off response coincides with a depolarization of the muscle following an EFS-induced hyperpolarization of that muscle. The aims of our study were to determine if the off response is present in gallbladder smooth muscle and to determine the mechanisms involved in this nerve-mediated response. MATERIALS AND METHODS: Gallbladder strips from opossums were placed in Krebs solution and passed through bipolar ring electrodes for EFS of intramural nerves, and isometric force measurements were recorded. Dose-response curves were determined with N(G)-nitro-L-arginine (L-NNA) a competitive inhibitor of nitric oxide (NO) synthase; 1H-¿1,2,4ŏxadiazolol¿4, 3aquinoxalin-1-one (ODQ), an inhibitor of soluble guanylate cyclase; and oxyhemoglobin, a scavenger of nitric oxide. RESULTS: A contraction termed the off response occurred shortly after EFS ended. The off response was abolished with tetrodotoxin and atropine. The amplitude of the off response increased with increasing voltage. The amplitude of the off response decreased by 41% with L-NNA 1.5 mM. Preincubation of the tissue with L-arginine (1 mM) prevented the inhibition of amplitude seen with L-NNA. The amplitude of the off response decreased by 43% with oxyhemoglobin (40 microM) and by 56% with ODQ (250 microM). CONCLUSION: We conclude that the off response is present in gallbladder smooth muscle after low-frequency EFS. NO may be a mediator of this off response and of nonadrenergic noncholinergic responses in gallbladder smooth muscle.
Animals↗
Effect of endotoxin on opossum oesophageal motor function.
Endotoxin induces nitric oxide (NO*) synthase and alters gastrointestinal functions. We explored the effect of lipopolysaccharide (LPS) on oesophageal motor function at 6, 12, 24, and 48 h. The effects of inhibiting inducible NO* synthase (iNOS) were studied 12 h after administration of LPS with/without aminoguanidine (AG). Oesophageal manometry was performed and tissue bath studies were performed with muscle strips from the oesophagus and lower oesophageal sphincter (LOS). Plasma nitrite/nitrate concentrations were determined. The amplitudes of peristaltic pressure waves, resting LOS pressure and the percentage LOS relaxations were diminished by LPS. AG attenuated the decrease in amplitude of oesophageal pressure waves, LOS pressure, and percentage relaxation of LOS brought about by LPS. LPS decreased electrical field stimulation (EFS)-induced relaxation of LOS muscle. AG attenuated this decrease in LOS relaxation. The off-response of transverse oesophageal muscle strips was decreased, and AG antagonized this effect. Plasma concentrations of nitrite/nitrate were increased. The increase in plasma nitrite/nitrate was attenuated by AG. These studies support the hypothesis that endotoxin modulates oesophageal motor function by increasing NO production and suggest that this results from the induction of iNOS.
Animals↗
Effect of endotoxin on opossum gallbladder motility: a model of acalculous cholecystitis.
OBJECTIVE: To determine whether endotoxin causes histologic changes in the gallbladder consistent with acalculous cholecystitis, and to determine the effects of endotoxin on gallbladder motility. SUMMARY BACKGROUND DATA: Acute acalculous cholecystitis is frequently seen in critically ill, septic patients, after prolonged fasting and gallbladder stasis. The pathogenesis of acalculous cholecystitis is unknown; however, previous studies have suggested that ischemia may play a role. METHODS: Adult opossums received Escherichia coli lipopolysaccharide. The gallbladder was removed for histologic examination or for physiologic studies 4 hours to 2 weeks later. For histologic examination, gallbladder strips underwent standard hematoxylin-and-eosin processing. For physiologic studies, they were mounted in a tissue bath to determine responses to cholecystokinin octapeptide or electrical field stimulation. RESULTS: Intravenous endotoxin at a dose of 0.005 mg/kg resulted in disrupted mucosal surfaces and areas of hemorrhage; higher doses of endotoxin resulted in coagulation necrosis, hemorrhage, areas of fibrin deposition, and extensive mucosal loss, consistent with an acute ischemic insult. Endotoxin abolished the contractile response to cholecystokinin octapeptide in gallbladder strips 4 hours after endotoxin administration. The 0.005-mg/kg dose of endotoxin decreased the contractile response to cholecystokinin octapeptide for up to 96 hours after endotoxin administration and decreased the contractile response to electrical field stimulation for 48 hours after administration. Inhibition of nitric oxide synthase reversed the decreased contractile response to cholecystokinin octapeptide. CONCLUSIONS: Endotoxin causes an ischemic insult to the gallbladder similar to that seen in acalculous cholecystitis. Also, endotoxin may lead to gallbladder stasis by decreasing gallbladder contractile responses to hormonal and neural stimuli.
Animals↗
Damage to DNA in bacterioplankton: a model of damage by ultraviolet radiation and its repair as influenced by vertical mixing.
A model of UV-induced DNA damage in oceanic bacterioplankton was developed and tested against previously published and novel measurements of cyclobutane pyrimidine dimers (CPD) in surface layers of the ocean. The model describes the effects of solar irradiance, wind-forced mixing of bacterioplankton and optical properties of the water on net DNA damage in the water column. The biological part includes the induction of CPD by UV radiation and repair of this damage through photoreactivation and excision. The modeled damage is compared with measured variability of CPD in the ocean: diel variation in natural bacterioplankton communities at the surface and in vertical profiles under different wind conditions (net damage as influenced by repair and mixing); in situ incubation of natural assemblages of bacterioplankton (damage and repair, no mixing); and in situ incubation of DNA solutions (no repair, no mixing). The model predictions are generally consistent with the measurements, showing similar patterns with depth, time and wind speed. A sensitivity analysis assesses the effect on net DNA damage of varying ozone thickness, colored dissolved organic matter concentration, chlorophyll concentration, wind speed and mixed layer depth. Ozone thickness and mixed layer depth are the most important factors affecting net DNA damage in the mixed layer. From the model, the total amplification factor (TAF; a relative measure of the increase of damage associated with a decrease in ozone thickness) for net DNA damage in the euphotic zone is 1.7, as compared with 2.1-2.2 for irradiance weighted for damage to DNA at the surface.
Animals↗
The effect of peroxynitrite on sphincter of Oddi motility.
BACKGROUND: Nitric oxide (NO*) is an inhibitory neurotransmitter that induces sphincter of Oddi relaxation. Superoxide (O*-2)-scavenging enzymes are present in enteric plexuses of the sphincter of Oddi and O*-2 alters sphincter of Oddi motor function. O*-2 rapidly oxidizes nitric oxide (NO*) to form peroxynitrite (ONOO-), thus terminating the biological activity of NO*. The aim of our study was to determine the effects of ONOO- on sphincter of Oddi motility in vitro. MATERIALS AND METHODS: Adult opossums were sacrificed and the sphincter of Oddi was removed and placed in a tissue bath containing oxygenated Krebs solution at 37 degreesC. In the first series of experiments, force transducers recorded tension in a transverse orientation at two sites along the spontaneously contracting sphincter of Oddi. In a second series of experiments, circular muscle strips were precontracted with carbachol and stimulated by an electrical field. RESULTS: ONOO-, superoxide dismutase (SOD), Nomega-nitro-l-arginine (l-NNA), or oxyhemoglobin were added to the tissue baths. ONOO- decreased the frequency of contractions in the spontaneously contracting sphincter of Oddi. Adding hemoglobin increased the frequency of contractions. ONOO- also increased the stimulation-induced relaxation compared to controls. The increase in relaxation induced by ONOO- was inhibited by oxyhemoglobin and l-NNA but not SOD. Pretreatment with oxyhemoglobin prevented the increase in the stimulation-induced relaxation caused by ONOO-. CONCLUSION: These results suggest that hemoglobin binds ONOO- or that ONOO- generates NO.
Animals↗
Changes in intestinal transit and absorption during endotoxemia are dose dependent.
BACKGROUND: Septic patients are often intolerant of enteral feedings due to a combination of motility disturbances and impaired absorptive function. Our laboratory has previously demonstrated that endotoxemia results in rapid intestinal transit and decreased jejunal absorption of water, electrolytes, and glucose. We hypothesized that the changes in jejunal transit and absorption during endotoxemia may be dependent on the dose of endotoxin. MATERIALS AND METHODS: Under general anesthesia, rats underwent placement of an internal jugular line, a femoral arterial line, and a 20-cm jejunal Thiry-Vella loop. The jejunal segment was perfused with an isotonic solution containing polyethylene glycol. For 90 min, baseline measurements of blood pressure, heart rate, jejunal absorption of water, electrolytes, and glucose, and jejunal transit were made. Following this baseline period I, rats were given 0.9% NaCl (1 ml/kg) or one of three doses of Escherichia coli lipopolysaccharide (0.5, 1.0, or 5.0 mg/kg). Studies were then repeated for an additional 90 min. RESULTS: Changes in blood pressure and heart rate were similar among the four groups of animals. Endotoxin decreased water and glucose flux, increased potassium flux, and quickened intestinal transit in a dose-dependent fashion. CONCLUSIONS: We conclude that endotoxemia causes dose-dependent changes in jejunal transit and absorption. The effects of increasing doses of endotoxin on jejunal absorptive and motor function do not appear to be mediated by changes in blood pressure or heart rate.
Animals↗
The role of antioxidant enzymes in the control of opossum gallbladder motility.
BACKGROUND: Superoxide rapidly oxidizes nitric oxide (NO) to form peroxynitrite, thus terminating the biological activity of NO. The aims of our study were to determine if superoxide alters the motor function of the gallbladder and to localize the antioxidant enzymes in the gallbladder. MATERIALS AND METHODS: Immunostaining and immunoblots were performed and enzyme activities were measured in the gallbladder. In physiologic experiments, force-displacement transducers recorded tension in gallbladder muscle strips. Superoxide was generated by the addition of xanthine with xanthine oxidase, while superoxide radicals were scavenged by the addition of superoxide dismutase (SOD) and catalase. SOD was inhibited by deithyldithiocarbamate. RESULTS: Immunostaining demonstrated superoxide dismutase and catalase immunoreactivity in ganglia situated throughout the smooth muscle. Total superoxide dismutase activity was 115 +/- 12 U/mg. Western blots detected expression of proteins of 19.4 kDa for copper/zinc SOD and 25.0 kDa for manganese SOD. Generation of superoxide increased isometric tension, while pretreatment with SOD prevented the increase in isometric tension induced by superoxide. Inhibition of SOD diminished the EFS-induced off response. CONCLUSIONS: We conclude that superoxide alters gallbladder motor function, and the presence of superoxide scavenging enzymes in enteric plexuses suggests that they may regulate gallbladder neuromuscular function by clearing endogenous superoxide.
Animals↗
The cup is half full.
BACKGROUND: The clinical outcomes following feeding tube procedures are infrequently studied because most patients have other incurable conditions. METHODS: Multiple electronic databases were used to track clinical outcomes following all gastrostomies and jejunostomies performed at a single institution from October 1, 1992, through December 31, 1995. Preoperative risk factors and postoperative morbidity were available for all 104 cases; long-term status was available for all but 2 of 104. RESULTS: The in-hospital mortality was 11.4%. Mortality was lower in those receiving feeding tubes as primary procedures (7.4%) than in those who had a feeding tube placed during other major procedures (24%, P <0.05). Postoperative pneumonia was frequent (24.7%), and was associated with preoperative gastroesophageal reflux (odds ratio 4.2, P = 0.01) and history of aspiration (odds ratio 3.9, P = 0.01). Although 14.5% of the patients were newly discharged to care facilities, the majority (74%) returned to their previous residence. Median survival was just over 6 months, with 18% surviving more than 2 years. Survival was inversely related to do-not-resuscitate status (odds ratio 4.6, P <0.001), metastatic tumor (odds ratio 2.7, P <0.001), dementia (odds ratio 2.3, P = 0.005), and unresectable tumor (odds ratio 2.1, P <0.001), but was unrelated to type of feeding tube. CONCLUSIONS: Significant morbidity and mortality follow feeding enterostomies, but the majority of patients benefit and can return to their previous residence. Am J Surg. 1999;178:406-410. 1999 by Excerpta Medica, Inc.
Adult↗
Gastric emptying of liquids and postprandial pancreatobiliary secretion are temporarily impaired during endotoxemia.
The aims of our study were to determine mechanisms by which pancreatobiliary secretion is altered during endotoxemia. Dogs underwent placement of duodenal perfusion and aspiration catheters and antral manometry catheters. Gastric emptying of liquids, antral motility, output of bile acids and amylase, and serum levels of enteric hormones were determined after ingestion of a 360-kcal mixed-nutrient liquid meal. Each dog was then given a single dose of E. coli lipopolysaccharide (200 microg/kg, intravenously) and the studies repeated for the next three days. Endotoxin slowed gastric emptying of liquids and decreased amylase output for two days. Bile acid output was decreased on postendotoxin day 1. Pancreatic polypeptide alone was decreased on postendotoxin day 1. We conclude that the decrease in pancreatobiliary output is probably due to decreased nutrient flow into the duodenum and not due to decreased production of hormones that influence pancreatobiliary secretion. The delayed gastric emptying, decreased pancreatobiliary output, and decreased postprandial levels of pancreatic polypeptide suggest diminished vagal output as a possible explanation for the effects of endotoxin on upper gut function.
Amylases↗
Effects of endotoxin on regulation of intestinal smooth muscle nitric oxide synthase and intestinal transit.
BACKGROUND: The disrupted intestinal transit during endotoxemia may be mediated by nitric oxide (NO). We hypothesized that the isoforms of nitric oxide synthase (NOS) are up-regulated in intestinal smooth muscle during endotoxemia and that the scavenging of NO will normalize transit. METHODS: Rats were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg intravenously and were killed 4 hours later. To determine the activity of NOS isoforms in the jejunum and ileum, the conversion of tritiated L-arginine to tritiated L-citrulline was measured. Western immunoblots were performed by incubating the extracted protein with specific polyclonal antibodies. To determine intestinal transit, rats were divided into 4 groups: 0.9% sodium chloride 1 mL/h intravenously for 5 hours, LPS 10 mg/kg intravenous bolus plus 1 mL/h 0.9% sodium chloride intravenously, LPS plus oxyhemoglobin 0.5 g/kg/h intravenously, and oxyhemoglobin 0.5 g/kg/h intravenously. RESULTS: LPS increased the constitutive and inducible NOS enzyme activities in the jejunum and ileum. Western blots demonstrated that LPS up-regulates both the NOS1 and NOS2 isoforms in jejunal and ileal smooth muscle. Oxyhemoglobin alone increased intestinal transit compared with controls, whereas endotoxemia increased intestinal transit, which was ameliorated with infusions of oxyhemoglobin. CONCLUSIONS: NO may play a major role in mediating the rapid intestinal transit induced by endotoxemia.
Animals↗
Endotoxin temporarily impairs canine colonic absorption of water and sodium.
Diarrhea is a common manifestation of sepsis. We hypothesized that endotoxin may impair colonic absorption of water and electrolytes, an effect which may be related to altered liquid transit in the colon. Five dogs underwent construction of 50-cm colonic Thiry-Vella fistulas (TVF). Following recovery, absorption studies were performed by perfusing the TVF with an isotonic solution at 2.9 ml/min containing polyethylene glycol (5 g/L). Fasting and postprandial colonic absorption of water, electrolytes, and glucose were determined. Liquid transit was assessed by bolus of a nonabsorbable marker (PSP) instilled into the proximal end of the TVF. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide 200 micrograms/kg i.v. and the studies were repeated daily for the next 3 days. Following endotoxin bolus, colonic absorption of water and sodium were decreased during fasting, while postprandial colonic absorption of water was also decreased. Colonic absorption of water and sodium returned to baseline values on postendotoxin day 2. Colonic secretion of potassium was decreased on postendotoxin days 1 and 3 in both the fasting and the fed periods. Fasting and postprandial liquid transit was also rapid on postendotoxin day 1, which correlated with the decreased absorption seen on that day. Liquid transit returned to baseline values on postendotoxin day 2. We conclude that endotoxin temporarily impairs postprandial colonic absorption, which may be due to the rapid liquid transit that occurs. These effects may contribute to the diarrhea seen during and after septic episodes.
Animals↗
Vertical gastroplasty: evolution of vertical banded gastroplasty.
The objective of this paper is to summarize the goals, technical requirements, advantages, and potential risks of gastroplasty for treatment of severe obesity. Gastroplasty is preferred to more complex operations, as it preserves normal digestion and absorption and avoids complications that are peculiar to exclusion operations. The medical literature and a 30-year experience at the University of Iowa Hospitals and Clinics (UIHC) provides an overview of vertical banded gastroplasty (VBG) evolution. Preliminary 10-year results with the VBG technique currently used at UIHC are included. At UIHC the VBG is preferred to other gastroplasties because it provides weight control that extends for at least 10 years and the required objective, intraoperative quality control required for a low rate of reoperation. It is recommended that modifications of the operative technique not be attempted until a surgeon has had experience with the standardized operation--and then only under a carefully designed protocol. Realistic goals for surgery and criteria of success influence the choice of operation and the optimum, lifelong risk/benefit ratio. In conclusion, VBG is a safe, long-term effective operation for severe obesity with advantages over complex operations and more restrictive simple operations.
Gastroplasty↗
Gastric mucosal protection from enteral nutrients: role of motility.
BACKGROUND: Cold restraint stress increases the force of gastric contractions and produces gastric mucosal injury in rats. The aim of our study was to determine whether enteral glucose or hyperglycemia alone would alter the stress-induced gastric motility pattern and ameliorate the associated gastric mucosal injury. METHODS: Adult male rats underwent surgical placement of gastric catheters, jugular venous catheters, and gastric strain gauge transducers 5 days before cold restraint. Three groups of rats received different substances during the same cold restraint stress protocol. Group 1 received 0.9% NaCl, 2 mL/h infused both intravenously (i.v.) and intragastrically (i.g.); group 2 received 0.9% NaCl, 2 mL/h i.g. plus 25% glucose, 2 mL/h i.v.; and group 3 received 0.9% NaCl, 2 mL/h i.v. plus 25% glucose i.g. Following baseline gastric motility measurements, all rats were restrained for 2 hours at 20 degrees C followed by 2 hours at 4 degrees C. RESULTS: Restraint even at room temperature increased the force of gastric contractions; the cold environment gradually prolonged gastric contractions. Enteral glucose blunted the effects of stress on gastric motility, increased gastric residual volume, decreased gastric acidity, and prevented gastric mucosal injury. Parenteral glucose had little effect on any gastric parameters. CONCLUSIONS: Enteral glucose prevents the abnormal gastric motility pattern that is necessary to produce the gastric mucosal injury associated with cold restraint stress, but hyperglycemia alone has little effect on the pathophysiology of cold restraint.
Animals↗
Metabolism of superoxide dismutase during the adynamic ileus of endotoxemia.
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Animals↗
The effect of endotoxin on canine jejunal motility and transit.
Intestinal transit is rapid during endotoxemia; however, little is known regarding the small intestinal motility changes which produce this rapid intestinal transit. The aim of our study was to determine the degree and duration of disrupted jejunal transit, and changes in jejunal motility following a sublethal dose of endotoxin. Eight dogs underwent construction of jejunal Thiry-Vella fistulas (TVF) with manometry catheters to record motility along the TVF. Following recovery, a 240-kcal liquid meal was given and the TVF was perfused with an isotonic solution. Liquid transit was assessed by bolus of a nonabsorbable marker instilled into the proximal end of the TVF. Recordings of gastrointestinal contractile activity were made digitally to determine postpandial motility. Following completion of the baseline studies, each dog was given a single dose of Escherichia coli lipopolysaccharide (200 micrograms/kg, iv) and the postprandial studies were repeated for the next 3 days. Endotoxin decreased the frequency of jejunal contractions for 2 days while the strength of jejunal contractions was diminished for 1 day. Jejunal transit of liquids was rapid on Postendotoxin Day 1. The rapid transit was associated with a greater percentage of single pressure waves propagating aborally on Postendotoxin Day 1 than the baseline percentages established prior to endotoxin. We conclude that endotoxemia temporarily disrupts postprandial jejunal motility and transit. The rapid liquid intestinal transit seen with endotoxemia may be due to changes in contractile propagation.
Animals↗