Biology of the neonate最新文献

{"title":"Consistent expression of HGF and c-met in the perinatal lung.","authors":"P Lassus,&nbsp;J Janer,&nbsp;C Haglund,&nbsp;R Karikoski,&nbsp;L C Andersson,&nbsp;S Andersson","doi":"10.1159/000091663","DOIUrl":"https://doi.org/10.1159/000091663","url":null,"abstract":"<p><strong>Background: </strong>Hepatocyte growth factor (HGF), an epithelial cell mitogen, has been shown to participate in normal lung development and in regeneration after lung injury. In human preterm infants, lower pulmonary HGF has been associated with more severe respiratory disease.</p><p><strong>Objectives: </strong>We studied the protein expression of HGF and its receptor c-met during the perinatal period in the human lung.</p><p><strong>Methods: </strong>Immunohistochemistry for HGF and c-met was performed on lung tissues from autopsies of 4 fetuses, 5 preterm infants, 5 term infants, and 4 infants with bronchopulmonary dysplasia.</p><p><strong>Results: </strong>Immunohistochemistry for HGF showed staining in all cases in mesenchymal cells (fibroblasts and cartilage cells). Additional staining was found in bronchial and distal airway epithelium. Immunohistochemistry for c-met showed staining in bronchial and distal airway epithelium, and in most cases in neutrophils.</p><p><strong>Conclusions: </strong>The consistent expression of HGF and c-met during the perinatal period supports a physiological role for HGF in human lung development.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"90 1","pages":"28-33"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000091663","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25871199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stopping a randomized trial early: from protocol to publication. Commentary to Thome at al.: outcome of extremely preterm infants randomized at birth to different PaCO2 targets during the first seven days of life (Biol Neonate 2006;90:218-225).","authors":"Pollyanna Hardy,&nbsp;Felicity Clemens","doi":"10.1159/000092724","DOIUrl":"https://doi.org/10.1159/000092724","url":null,"abstract":"even reverse itself, and so fi xed stopping rules dictated by predetermined signifi cance levels for differences in outcome are increasingly discouraged [3] . Additional information such as the medical plausibility of the difference, ethical considerations both for the trial participants and for the wider target population, evidence from other relevant trials and the nature of the disease under consideration may also be important [2, 4–6] . The decision to stop a trial for harm can also be based on adverse events, although attribution of the cause of an adverse event may be diffi cult [3] . There is less guidance available on when and how trials should be stopped for futility. The 2005 DAMOCLES study [3] highlights a recognition in the literature that termination of a trial may be recommended where it is considered that there is no longer a reasonable chance of accumulating suffi cient evidence against the null hypothesis (usually due to poor recruitment or to external information becoming available [7] ). However, it is unclear whether trials should be stopped on these grounds [3, 4] . Another reason for stopping for futility is that the trial is unlikely to come to a sound conclusion [3] . This is illustrated in the trial by Thome et al. The diffi culty with this trial was that, at the time of the interim analysis, the majority of the patients randomized to the active arm (minimal ventilation to achieve higher PaCO 2 ) had not An important, often neglected element to planning a clinical trial is to consider the possibility of stopping the trial early, before either recruitment or follow-up is completed. A trial may be stopped for futility, harm or benefi t. A trial that is stopped on the grounds of benefi t is one that early on identifi es important treatment effects unlikely to be due to chance. A trial stopped for harm provides evidence that the treatment under investigation is unsafe for trial subjects. A trial stopped for futility requires a decision that the trial would not provide suffi ciently useful information to warrant continuation. Stopping a trial early is always a diffi cult decision to make and consideration must be given to who will be making these decisions and on what grounds they will be made. This issue of Biology in the Neonate publishes a trial by Thome et al. investigating the use of increased PaCO 2 targets on outcomes in extremely preterm neonates. It appears that this trial was stopped for futility on the grounds that the increased target levels of PaCO 2 were not being reached in the active arm of the trial. Guidance for stopping a trial for benefi t or harm is well documented [1] although approaches remain controversial. Statistical methods exist and may contribute to deciding whether the observed data imply that benefi t is very likely or, in the case of stopping for harm, very unlikely, or that the new treatment is harmful [2] . An early trend in the data under consideration may fl uctuate and Published online: Apr","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"90 4","pages":"226-8"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092724","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25991838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo dilatation of the fetal and postnatal ductus arteriosus by inhibition of phosphodiesterase 3 in rats.","authors":"Katsuaki Toyoshima,&nbsp;Kazuo Momma,&nbsp;Shinichiro Imamura,&nbsp;Toshio Nakanishi","doi":"10.1159/000089954","DOIUrl":"https://doi.org/10.1159/000089954","url":null,"abstract":"<p><strong>Background: </strong>Clinically, it appears that phosphodiesterase 3 (PDE 3) inhibitors, which are used for acute cardiac failure in premature infants, dilate the ductus arteriosus (DA).</p><p><strong>Objectives: </strong>To clarify the ductus-dilating effects of PDE 3 inhibitors in near-term rat pups and their differential effects in near-term and preterm fetal rats, in in vivo studies.</p><p><strong>Methods: </strong>The in vivo ductal diameter of rat pups and fetuses was measured using a rapid whole-body freezing method, by cutting on a freezing microtome and measuring with a microscope and micrometer. Eight to twenty pups and fetuses were studied in each group. Milrinone and amrinone (specific inhibitors of PDE 3) were injected into 1-hour-old pups and the DA was studied 0.5 and 1 h later. The differential effects of these PDE 3 inhibitors on the near-term and preterm ductus were studied by injecting indomethacin (10 mg/kg) and PDE 3 inhibitors into 21D (21st day of pregnancy: term-21.5 days) and 19D dams and studying the fetal ductus 4 and 8 h later.</p><p><strong>Results: </strong>Milrinone and amrinone dilated the postnatal ductus dose-dependently. Large doses of these drugs dilated it completely, and clinically equivalent doses dilated it minimally. Milrinone and amrinone prevented constriction of the fetal ductus by indomethacin. Their ductus-dilating effects were more potent in the preterm than in the near-term fetuses, and clinically equivalent doses of these PDE 3 inhibitors dilated preterm ductus completely.</p><p><strong>Conclusion: </strong>In rats, PDE 3 inhibitors reopen the constricted postnatal DA slightly. PDE 3 inhibitors dilate the fetal DA constricted with indomethacin effectively and more sensitively in preterm than in near-term fetuses.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"89 4","pages":"251-6"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000089954","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25718003","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of midazolam and morphine on cerebral oxygenation and hemodynamics in ventilated premature infants.","authors":"A A E M van Alfen-van der Velden,&nbsp;J C W Hopman,&nbsp;J H G M Klaessens,&nbsp;T Feuth,&nbsp;R C A Sengers,&nbsp;K D Liem","doi":"10.1159/000093489","DOIUrl":"https://doi.org/10.1159/000093489","url":null,"abstract":"<p><strong>Background: </strong>Midazolam sedation and morphine analgesia are commonly used in ventilated premature infants.</p><p><strong>Objectives: </strong>To evaluate the effects of midazolam versus morphine infusion on cerebral oxygenation and hemodynamics in ventilated premature infants.</p><p><strong>Methods: </strong>11 patients (GA 26.6-33.0 weeks, BW 780-2,335 g) were sedated with midazolam (loading dose 0.2 mg/kg, maintenance 0.2 mg/kg/h) and 10 patients (GA 26.4-33.3 weeks, BW 842-1,955 g) were sedated with morphine (loading dose 0.05 mg/kg, maintenance 0.01 mg/kg/h). Changes in oxyhemoglobin (Delta cO2Hb) and deoxyhemoglobin (Delta cHHb) were assessed using near infrared spectrophotometry. Changes in cHbD (= Delta cO(2)Hb - Delta cHHb) reflect changes in cerebral blood oxygenation and changes in concentration of total hemoglobin (Delta ctHb = Delta cO2Hb + Delta cHHb) represent changes in cerebral blood volume (DeltaCBV). Changes in cerebral blood flow velocity (DeltaCBFV) were intermittently measured using Doppler ultrasound. Heart rate (HR), mean arterial blood pressure (MABP), arterial oxygen saturation (saO2) and transcutaneous measured pO2 (tcpO2) and pCO2 (tcpCO2) were continuously registered. Statistical analyses were carried out using linear mixed models to account for the longitudinal character study design.</p><p><strong>Results: </strong>Within 15 min after the loading dose of midazolam, a decrease in saO2, tcpO2 and cHbD was observed in 5/11 infants. In addition, a fall in MABP and CBFV was observed 15 min after midazolam administration. Immediately after morphine infusion a decrease in saO2, tcpO2 and cHbD was observed in 6/10 infants. Furthermore, morphine infusion resulted in a persistent increase in CBV.</p><p><strong>Conclusions: </strong>Administration of midazolam and morphine in ventilated premature infants causes significant changes in cerebral oxygenation and hemodynamics, which might be harmful.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"90 3","pages":"197-202"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000093489","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26038238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progress in discovery and evaluation of treatments to prevent bronchopulmonary dysplasia.","authors":"Linda J Van Marter","doi":"10.1159/000092867","DOIUrl":"https://doi.org/10.1159/000092867","url":null,"abstract":"<p><strong>Background: </strong>Recent improvements in the survival of extremely preterm infants have been accompanied by evolution in the pathogenesis and histopathology of bronchopulmonary dysplasia (BPD). Although oxygen and barotrauma-induced injury remain important contributing factors, pulmonary developmental arrest appears to play an equally important causal role in prolonged respiratory illness, especially among the most immature surviving preterm newborns. To date, clinical trials have failed to demonstrate a substantial benefit of a single treatment or preventive strategy for BPD.</p><p><strong>Objectives: </strong>To evaluate the current evidence in favor of treatments that might prevent BPD.</p><p><strong>Methods: </strong>Review of clinical studies of preventive treatment strategies for BPD.</p><p><strong>Results: </strong>High frequency oscillatory ventilation, permissive hypercapnea, and inhaled nitric oxide might offer benefit to infants at risk of BPD. These and other potential preventive therapies for BPD, such as superoxide dismutase, inositol, and alpha(1)-proteinase inhibitor, deserve further study.</p><p><strong>Conclusions: </strong>Although some current treatments offer promise, no preventive therapy for BPD has proven safe and effective, except for intramuscular vitamin A. Additional studies of respiratory technologies, management strategies, and protective molecules are needed.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"89 4","pages":"303-12"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092867","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26085526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of body warming on regional blood flow distribution in conscious hypoxic one-month-old rabbits.","authors":"Erin L Seifert,&nbsp;Guilherme M Sant Anna,&nbsp;Charles V Rohlicek","doi":"10.1159/000092069","DOIUrl":"https://doi.org/10.1159/000092069","url":null,"abstract":"<p><strong>Background: </strong>Previous experiments have shown that warming hypoxic infants reduces total peripheral vascular resistance. This suggests that the usual vasoconstriction of less essential vascular beds during hypoxia may be reduced and that the normal redistribution of blood flow to more vital organs may be compromised.</p><p><strong>Objective: </strong>Evaluate the effect of body warming during hypoxia on the distribution of blood flow.</p><p><strong>Methods: </strong>The fluorescent microsphere technique was used to compare regional blood flow in 1-month-old rabbits during systemic hypoxia (10% inspired O2) with (n = 9) and without (n = 10) body warming. Blood flow was measured in brain, stomach, small intestine, hindlimb muscle, skin, and kidneys. Arterial blood pressure, whole-body O2 consumption, arterial blood O2 saturation and blood gases were also measured.</p><p><strong>Measurements and main results: </strong>In hypoxia all animals decreased body temperature (-2 degrees C). With hypoxia blood flow increased to brain and hindlimb muscle; decreased to stomach, small intestine, and kidneys, and was unchanged in skin. The increase in brain-blood flow maintained O2 delivery at normoxic levels. Rewarming to the normoxic body temperature significantly changed blood flow in hypoxia. Brain blood flow increased by 102 +/- 30% (mean +/- SEM) thereby increasing O2 delivery by 50 +/- 23% above normoxic values. Blood flow also increased to skin, stomach, and small intestine. However, O2 delivery to these tissues remained below normoxic levels.</p><p><strong>Conclusions: </strong>Warming during hypoxia may impose an additional cardiovascular demand. The changes in the pattern of blood flow distribution with mild warming during hypoxia support the hypothesis that warming represents a significant heat stress.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"90 2","pages":"104-12"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092069","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25915586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glucocorticoid metabolism in the human fetal lung: implications for lung development and the pulmonary surfactant system.","authors":"Mark R Garbrecht,&nbsp;Jonathan M Klein,&nbsp;Thomas J Schmidt,&nbsp;Jeanne M Snyder","doi":"10.1159/000088653","DOIUrl":"https://doi.org/10.1159/000088653","url":null,"abstract":"<p><p>It has been nearly 35 years since Liggins and Howie first reported the benefits of antenatal glucocorticoid (GC) treatment to promote the maturation of the human fetal lung, and nearly that long since Pasqualini and colleagues demonstrated that the human fetal lung actively metabolizes GCs. Since that time, our understanding of the effects of GCs on fetal lung maturation and pulmonary surfactant production has increased dramatically. Similarly, characterization of the enzymes involved in GC metabolism has greatly expanded our understanding of GC signaling in target tissues. In man, the biologically active GC (cortisol) and the biologically inactive GC (cortisone) are interconverted by the tissue-specific expression of the type 1 and type 2 11beta-hydroxysteroid dehydrogenase enzymes (HSD1 and HSD2). Much of the research on GC metabolism in peripheral target tissues has focused on the role of HSD1 in amplifying the effects of GCs in liver and adipose tissue or on the role of HSD2 in blocking the effects of GCs in the kidney and placenta. In contrast, the role of GC metabolism in modulating the effects of GCs on fetal lung maturation and the pulmonary surfactant system in humans is less understood. The goal of this review article is to present a brief overview of the role of GCs in human fetal lung maturation and pulmonary surfactant production, and to familiarize the reader with the biochemistry of the metabolism of natural and synthetic GCs by the HSD enzymes. In addition, we will review data concerning the expression and activity of the HSD enzymes in the human fetal lung and contrast this to what is known about the HSD enzymes in the fetal rodent lung. Although rodents, rabbits, sheep, and several primates have been invaluable model systems for the study of fetal lung development, we have chosen to largely focus this review on human lung, since there are significant differences in GC metabolism between humans and other species.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"89 2","pages":"109-19"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000088653","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25610270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary insulin affects leucine aminopeptidase, growth hormone, insulin-like growth factor I and insulin receptors in the intestinal mucosa of neonatal pigs.","authors":"Yong Jiu Huo,&nbsp;Tian Wang,&nbsp;Ruo Jun Xu,&nbsp;Scot Macdonald,&nbsp;Gentao Liu,&nbsp;Fangxiong Shi","doi":"10.1159/000091482","DOIUrl":"https://doi.org/10.1159/000091482","url":null,"abstract":"<p><strong>Background: </strong>Recent studies suggest that milk-borne insulin may regulate the development of the gastrointestinal tract in neonatal mammals.</p><p><strong>Objectives: </strong>To explore the mechanism by which milk-borne insulin affects gastrointestinal tract development, we examined the effect of dietary insulin on the expression levels of leucine aminopeptidase (LAP) and insulin-like growth factor I (IGF-I), as well as its effect on growth hormone (GH), IGF-I and insulin receptors in the small intestinal mucosa of neonatal pigs.</p><p><strong>Methods: </strong>Five piglets were anesthetized and sampled within 2-4 h after birth. They were not allowed to suckle and were used as newborn controls (group N). Ten other piglets from 5 litters were randomly divided into group M (n=5), which was fed cow's milk, and group MI (n=5), which was fed cow's milk and insulin (2.5 mg/l). Piglets in groups M and MI were artificially fed for 3 days and then sampled. Total RNA in their intestinal mucosa was extracted with Tripure reagents (Roche, USA). Reverse transcription PCR (RT-PCR) was used to semi-quantify mRNA levels of target genes and 18S rRNA was used in an RT-PCR system as an internal control. PCR products were loaded onto a 9% nondenaturing polyacrylamide gel. The gel was stained by silver staining agents. Digital photos were taken and the strength of the band areas was quantified using software.</p><p><strong>Results: </strong>The results showed that the DNA contents and LAP activity in the small intestines of the piglets in group MI were higher (p<0.05) than in the piglets in group N. Compared with group M, piglets in group MI exhibited significantly increased expression levels of both insulin and GH receptor in the ileum, and LAP in the jejunum (p<0.05); IGF-I receptor expression levels in both the jejunum and ileum were significantly decreased (p<0.01 and p<0.05, respectively), while IGF-I expression was unchanged (p>0.05).</p><p><strong>Conclusion: </strong>Collectively, dietary insulin increased mRNA levels of insulin and GH receptor, which could help explain the effect of dietary insulin on receptor-mediated postnatal development of the small intestine. Dietary insulin suppressed IGF-I receptor expression, which may be the result of negative feedback caused when insulin binds to IGF-I receptors.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"89 4","pages":"265-73"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000091482","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25856179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surfactant proteins in innate host defense of the lung.","authors":"Jeffrey A Whitsett","doi":"10.1159/000087580","DOIUrl":"https://doi.org/10.1159/000087580","url":null,"abstract":"<p><p>Surfactant proteins A and D (SP-A and SP-D) are members of the collectin family of host defense proteins that are expressed in epithelial cells lining the lung. SP-A and SP-D interact with surfactant lipids in complex ways to determine the structure of tubular myelin, and the ratio of surfactant subfractions that, in turn, influences surfactant uptake and metabolism, respectively. SP-A and SP-D play critical roles in host defense of the lung against diverse viral, fungal, and bacterial pathogens. The collectins bind to the surfaces of microbes via carbohydrate-dependent interaction, aggregating, opsonizing, and enhancing clearance of the organisms by alveolar macrophages in the lung. Pulmonary surfactant proteins A and D play dual roles in pulmonary homeostasis, determining the structure of alveolar lipids and mediating the innate host defense system of the lung.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"88 3","pages":"175-80"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000087580","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25626190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Three-day enteral exposure to a red kidney bean lectin preparation enhances the pancreatic response to CCK stimulation in suckling pigs.","authors":"L Evilevitch,&nbsp;S G Pierzynowski,&nbsp;A Linderoth,&nbsp;B Ahrén,&nbsp;Ch Erlanson-Albertsson,&nbsp;M Podgurniak,&nbsp;B R Weström","doi":"10.1159/000080896","DOIUrl":"https://doi.org/10.1159/000080896","url":null,"abstract":"<p><strong>Background: </strong>A reason for the digestive problems that often occur around early weaning in piglets could be that the pancreas is not yet fully developed and the enzymes required for degradation of the solid food are not secreted in enough amounts.</p><p><strong>Objectives: </strong>The aim of the study was to investigate the possibility of inducing pancreas maturation with enhanced enzyme secretion.</p><p><strong>Methods: </strong>10-day-old suckling pigs were gavage fed with a red kidney bean lectin preparation for 3 days, and the pancreatic response to intravenous infusion of CCK-33 was measured in the anaesthetized animals fitted with pancreatic duct catheters.</p><p><strong>Results: </strong>The pancreatic fluid secretion, protein output, and the trypsin and amylase outputs were significantly increased in response to CCK stimulation after the lectin treatment, as compared to those of the control littermates (p < or = 0.05). In addition, the plasma insulin basal levels and those observed during CCK-33 stimulation were lower in the lectin-treated piglets.</p><p><strong>Conclusion: </strong>The results suggested that the lectin treatment led to an increase in the capacity for pancreatic enzyme secretion in the suckling piglets. An enhanced pancreatic function might help to ameliorate the problems that may appear in modern pig production which are associated with weaning.</p>","PeriodicalId":9091,"journal":{"name":"Biology of the neonate","volume":"87 1","pages":"20-5"},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000080896","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24689801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}