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Biomedical subjects

C Gentili

Publications and source records attributed to C Gentili.

At least 19 recordsLinked to original sources
PubMed2006

Alcohol consumption and heavy drinking: a survey in three Italian villages.

AIMS: We investigated drinking habits, and heavy and problem drinking prevalence in a sample of individuals attending the consulting rooms of local General Practitioners in three Italian villages. METHODS: The samples were selected to be representative of the entire population of the three villages. Information on alcohol-drinking patterns was collected using a questionnaire that included a masked form of the CAGE rating scale. According to the frequency of alcohol intake, subjects were grouped in three categories: abstainers, occasional drinkers, and daily drinkers. In agreement with WHO guidelines, 40 g/day for males and 20 g/day for females were taken as cut-off for 'heavy drinking' and consumptions of > 80 g/day for males and 40 g/day for females were used to define 'problem drinking'. RESULTS: A total of 2972 individuals were included in the survey (19% of the population). Of these, 44% were abstinent, 20% occasional drinkers, and 36% daily drinkers. Daily drinking was found to be more common in males than in females but heavy drinking was significantly higher in females compared with males (P > or = 0.0001). The problem drinkers were 12% of the entire population and the CAGE-positive subjects (> or = 2 positive answers) were 3.5%. CONCLUSIONS: Our data indicate that alcohol drinking is widely diffused in the three communities. A large layer of the population drinks above the WHO-established cut-off. The incidence of heavy and problem drinking seems to have significant gender and regional differences that are important to consider when planning effective prevention programmes.

Adolescent↗
PubMed2005

Neural correlates of spatial working memory in humans: a functional magnetic resonance imaging study comparing visual and tactile processes.

Recent studies of neural correlates of working memory components have identified both low-level perceptual processes and higher-order supramodal mechanisms through which sensory information can be integrated and manipulated. In addition to the primary sensory cortices, working memory relies on a widely distributed neural system of higher-order association areas that includes posterior parietal and occipital areas, and on prefrontal cortex for maintaining and manipulating information. The present study was designed to determine brain patterns of neural response to the same spatial working memory task presented either visually or in a tactile format, and to evaluate the relationship between spatial processing in the visual and tactile sensory modalities. Brain activity during visual and tactile spatial working memory tasks was measured in six young right-handed healthy male volunteers by using functional magnetic resonance imaging. Results indicated that similar fronto-parietal networks were recruited during spatial information processing across the two sensory modalities-specifically the posterior parietal cortex, the dorsolateral prefrontal cortex and the anterior cingulate cortex. These findings provide a neurobiological support to behavioral observations by indicating that common cerebral regions subserve generation of higher order mental representations involved in working memory independently from a specific sensory modality.

Adult↗
PubMed2005

Cholesterol secretion and homeostasis in chondrocytes: a liver X receptor and retinoid X receptor heterodimer mediates apolipoprotein A1 expression.

Cholesterol is required for chondrocyte differentiation and bone formation. Apolipoprotein A1 (apoA-1) plays a major role in lipoprotein clearance and cholesterol redistribution. We report here that apoA-1 is expressed during chondrocyte differentiation in vitro and in vivo. In differentiating chondrocytes, the expression of the liver X receptor (LXR) is modulated and its expression correlates to the expression of apoA-1. The expression of other LXR target genes related to cholesterol homeostasis such as ABCA1 cholesterol transporter and sterol regulatory element-binding protein 1 (SREBP1) is similarly regulated. Small molecule ligands activating either LXR or retinoid X receptor (RXR) lead to a dramatic increase in apoA-1 mRNA and protein expression in cultured chondrocytes. These ligands strongly induce ABCA1 cholesterol transporter expression and effectively mediate cholesterol efflux from hypertrophic chondrocytes. In addition, we report that, in the same cells, the ligands down modulate Serum Amyloid A expression induced by bacterial lipopolysaccharide. Our studies provide evidence that LXR/RXR mediate a fine regulation of cholesterol homeostasis in differentiating chondrocytes.

Animals↗
PubMed2005

Acute phase lipocalin Ex-FABP is involved in heart development and cell survival.

Ex-FABP is an extracellular fatty acid binding protein, expressed during chicken embryo development in cartilage, muscle fibers, and blood granulocytes. Transfection of chondrocytes and myoblasts with anti-sense Ex-FABP cDNA results in inhibition of cell proliferation and apoptosis induction. Ex-FABP expression is dramatically enhanced by inflammatory stimuli and in pathological conditions. In this paper, by in situ whole mount and immunohistochemistry analysis we show that, at early developmental stage, Ex-FABP is diffuse in all tissues of chick embryos. Particularly high level of transcript and protein are expressed in the heart. During acute phase response (APR) induced by endotoxin LPS injection, a marked increase of Ex-FABP mRNA was observed in embryos, highest Ex-FABP expression being in heart and liver. To investigate in vivo the biological role of Ex-FABP, we have directly microinjected chicken embryos with antibody against Ex-FABP. Almost 70% of chicken embryos died and the target tissue was the heart. We detected in heart of the treated embryos a significant increase of apoptotic cells and high level of fatty acids. We propose that the accumulation of fatty acid, specific ligand of Ex-FABP, in the cell microenvironment is responsible of heart cell death, and we suggest that Ex-FABP may act as a survival protein by playing a role as scavenger for fatty acids.

Animals↗
PubMed2003

Runx2 expression and action in chondrocytes are regulated by retinoid signaling and parathyroid hormone-related peptide (PTHrP).

OBJECTIVE: Runx2 (also known as Cbfa1) is a transcription factor required for chondrocyte maturation and osteoblast differentiation. While there is information on the regulation of its expression during osteogenesis, much less is known about it during cartilage maturation. Here we asked whether Runx2 expression and function are affected by retinoic acid (RA) and parathyroid hormone-related peptide (PTHrP), which represent an important stimulator and inhibitor of chondrocyte maturation, respectively. DESIGN: We first cloned and characterized Runx2 expressed by chick chondrocytes (cRunx2). We then constructed expression vectors of cRunx2 and a dominant-negative form (DN-cRunx2) and determined their effects on chondrocyte maturation in culture before and during retinoid and PTHrP treatment. RESULTS: cRunx2 showed similar transactivation activity to that of its mammalian counterparts although it has a very short QA domain and lacks a small portion of the PST domain. cRunx2 over-expression stimulated chondrocyte maturation, as indicated by increases in alkaline phosphatase activity (APase), mineralization, and type X collagen and MMP-13 expression, and by maintenance of Indian hedgehog (Ihh) expression. RA treatment stimulated cRunx2 gene expression and boosted its pro-maturation effects. PTHrP treatment blocked Runx2 expression and its pro-maturation effects. Over-expression of DN-cRunx2 inhibited maturation and even prevented RA from exerting its pro-maturation role. CONCLUSIONS: As previously indicated by mammalian studies, cRunx2 has chondrocyte pro-maturation activity. Its expression and roles are favorably modulated by retinoid signaling but are completely inhibited by PTHrP. A model integrating cRunx2 with PTHrP, Ihh and retinoid signaling and operating during skeletogenesis is proposed.

Animals↗
PubMed2001

Parathyroid hormone activation of map kinase in rat duodenal cells is mediated by 3',5'-cyclic AMP and Ca(2+).

In a previous study, we demonstrated that parathyroid hormone (PTH) stimulates in rat duodenal cells (enterocytes) the phosphorylation and activity of extracellular signal-regulated mitogen-activated protein kinase (MAPK) isoforms ERK1 and ERK2. As PTH activates adenylyl cyclase (AC) and phospholipase C and increases intracellular Ca(2+) in these cells, in the present study we evaluated the involvement of cAMP, Ca(2+) and protein kinase C (PKC) on PTH-induced MAPK activation. We found that MAPK phosphorylation by the hormone did not depend on PKC activation. PTH response could, however, be mimicked by addition of forskolin (5-15 microM), an AC activator, or Sp-cAMP (50-100 microM), a cAMP agonist, and suppressed to a great extent by the AC inhibitor, compound Sq-22536 (0.2-0.4 mM) and the cAMP antagonist Rp-cAMP (0.2 mM). Removal of external Ca(2+) (EGTA 0.5 mM), chelation of intracellular Ca(2+) with BAPTA (5 microM), or blockade of L-type Ca(2+)-channels with verapamil (10 microM) significantly decreased PTH-activation of MAPK. Furthermore, a similar degree of phosphorylation of MAPK was elicited by the Ca(2+) mobilizing agent thapsigargin, the Ca(2+) ionophore A23187, ionomycin and membrane depolarization with high K(+). Inclusion of the calmodulin inhibitor fluphenazine (50 microM) did not prevent hormone effects on MAPK. Taken together, these results indicate that cAMP and Ca(2+) play a role upstream in the signaling mechanism leading to MAPK activation by PTH in rat enterocytes. As Ca(2+) and cAMP antagonists did not block totally PTH-induced MAPK phosphorylation, it is possible that linking of the hormone signal to the MAPK pathway may additionally involve Src, which has been previously shown to be rapidly activated by PTH. Of physiological significance, in agreement with the mitogenic role of the MAPK cascade, PTH increased enterocyte DNA synthesis, and this effect was blocked by the specific inhibitor of MAPK kinase (MEK) PD098059, indicating that hormone modulation of MAPK through these messenger systems stimulates duodenal cell proliferation.

Animals↗
PubMed2001

PTH stimulates PLCbeta and PLCgamma isoenzymes in rat enterocytes: influence of ageing.

We previously reported that in rat duodenal cells (enterocytes), parathyroid hormone (PTH [1-34]: PTH) stimulates the hydrolysis of polyphosphoinositides by phospholipase C (PLC), generating the second messengers inositol trisphosphate (IP(3)) and diacylglycerol (DAG) and that this mechanism is severely altered in old animals. In the present study, we show that PTH [1-34]-dependent IP(3) release in young rats was blocked to a great extent by an antibody against guanine nucleotide binding protein Galphaq/11, indicating that the hormone activates a beta isoform of PLC coupled to the alpha subunit of Gq/11. In addition, PTH rapidly (within 30 s, with maximal effects at 1 min) stimulated tyrosine phosphorylation of PLCgamma in a dose-dependent fashion (10(-10)-10(-7) M). The hormone response was specific as PTH [7-34] was without effects. The tyrosine kinase inhibitors, genistein (100 microM) and herbimycin (2 microM), suppressed PTH-dependent PLCgamma tyrosine phosphorylation. Stimulation of PLCgamma tyrosine phosphorylation by PTH [1-34] greatly decreased with ageing. PP1 (10 microM), a specific inhibitor of the Src family of tyrosine kinases, completely abolished PLCgamma phosphorylation. The hormone-induced Src tyrosine dephosphorylation, a major mechanism of Src activation, an effect that was blunted in old animals. These results indicate that in rat enterocytes PTH generates IP(3) mainly through G-protein-coupled PLCbeta and stimulates PLCgamma phosphorylation via the nonreceptor tyrosine kinase Src. Impairment of PTH activation of both PLC isoforms upon ageing may result in abnormal hormone regulation of cell Ca(2+) and proliferation in the duodenum.

Aging↗
PubMed2000

Age-related decline in mitogen-activated protein kinase phosphorylation in PTH-stimulated rat enterocytes.

In the present study we analyzed whether parathyroid hormone (rPTH[1-34]; PTH) stimulates the tyrosine phosphorylation of the growth-related protein mitogen-activated protein (MAP) kinases (p42/44-MAPK), also known as extracellular signal-regulated kinases (ERK1/2), in duodenal enterocytes isolated from young (3months) and aged (24months) rats. Western blot analysis revealed that PTH rapidly stimulates MAPK phosphorylation. The hormone effects on MAPK were evident within 30s, peaking at 1min (4-fold). PTH response was dose-dependent (10(-11)-10(-7) M) with maximal stimulation achieved at 10(-9)-10(-8) M. PTH-induced MAPK phosphorylation was effectively suppressed by the tyrosine-kinase inhibitors, genistein (100microM) and herbimycin (2microM). Moreover, the tyrosine phosphorylation and activation of MAPK was dependent on Src kinase, since PP1 (10 and 20microM), a specific Src family tyrosine-kinase inhibitor, blocked PTH-induced MAPK activation. With aging, the response to PTH was significantly reduced. However, The amount of basal protein expression determined by Western blot analysis for MAPK was not different in the enterocytes from young and aged rats. In conclusion, the results obtained in this work expand our knowledge on the mechanism of action of PTH in duodenal cells, revealing that protein tyrosine phosphorylation is linked to the PTH regulation of enterocyte MAPK activation, and that this mechanism is impaired with aging. Understanding the molecular mechanisms for the age-related differences in PTH signaling will require more information about the subtle mechanisms that modulate the PTH receptor-MAPK signaling pathway.

Aging↗
PubMed2000

Extracellular fatty acid binding protein (Ex-FABP) modulation by inflammatory agents: "physiological" acute phase response in endochondral bone formation.

Ex-FABP, extracellular fatty acid binding protein, is a 21 kDa lipocalin expressed in hypertrophic cartilage, muscle and heart during chick embryo development and in granulocytes. Ex-FABP synthesis was increased in chondrocyte and myoblast cultures by inflammatory agents (LPS; IL6) and repressed by antiinflammatory agents. Expression of Ex-FABP and specific gelatinases is paralleled in hypertrophic cartilage; LPS specifically induced high molecular weight gelatinase ( > 200 kDa). LPS-treated hypertrophic chondrocytes showed increased chemotactic activity for endothelial cells paralleled by increased expression of transferrin. A high amount of Ex-FABP was expressed in adult pathological cartilage both in dyschondroplastic and osteoarthritic chickens. Controls were negative. Ex-FABP could represent a stress protein physiologically expressed in tissues where active remodelling is taking place during development and in tissues characterized by an acute phase response due to pathological conditions. We also suggest that during endochondral bone formation other responses characteristic of a local inflammatory status, such as gelatinase production and angiogenic factor secretion, are "physiologically" activated.

Acute-Phase Reaction↗
PubMed2000

Development of articular cartilage: what do we know about it and how may it occur?

Articular cartilage has a fundamental role in joint function. While much is known about its structure, organization and biomechanical properties, there is a very poor understanding of how articular chondrocytes develop during embryogenesis and acquire the unique ability to organize and maintain the articular tissue. Given that articular cartilage forms in close juxtaposition with the joint, here we review past studies on limb joint determination and morphogenesis and more recent studies on a number of factors thought to have roles in joint and epiphysis development. These factors include: the homeobox gene Barx-1; the bone morphogenetic protein (BMP) family member GDF-5; the growth factors HGF and PTHrP; and the transcription factor ERG. We summarize current thinking on how these factors participate in joint development and how some of these factors may influence development and behavior of epiphyseal chondrocytes. We also describe pertinent recent studies from our laboratories on ERG and the newly-identified alternatively spliced variant C-1-1, and finally propose a sequela of events that may subtend the process of determination and emergence of articular chondrocytes during limb synovial joint development.

Animals↗
PubMed2000

[Peritoneal innervation and post-laparoscopic course. Role of CO2].

BACKGROUND: 30-67% of patients undergoing laparoscopic surgery reports shoulder pain. Besides, post-surgical course of patients undergoing converted laparoscopic procedures is similar to the course of patients who received a completely laparoscopic procedure. It is supposed that there is a temporary neurotoxic damage of the peritoneal sensitive nervous fibres defined by CO2. METHODS: A prospective review has been carried out by histologically analyzing 38 peritoneal biopsies from 10 selected patients, during different laparoscopic surgical procedures (6 cholecystectomies, 2 appendectomies, 1 selective bilateral ligature of the spermatic vessles) and at different times during each operation. Patients whom anamnesis, clinical or local conditions were suggestive for peritoneal flogosis were excluded from the study: therefore only 29 biopsies from 8 patients have been considered useful to the study. RESULTS: Histological analysis has been carried out with different methods of coloration (hematoxylin eosin, argentic staining) and at different magnifications (30x, 60x, 100x), without electronical microscopy or immunohistochemical studies. No biopsy showed signs of damage of the nervous structures. CONCLUSIONS: Certainly, the realization of a pneumoperitoneum at CO2 doesn't cause damages of the peritoneal sensitive fibres. It has been demonstrated that the abdominal introduction of CO2 causes a "relative peritoneal acidosis", directly depending from the percentage of CO2 employed: the peritoneal pH decreases to 6.9 after 15 min of pneumoperitoneum with CO2 at 100% and to 7.35% with CO2 at 5% of air. Probably this condition causes a temporary biochemical change that defines reduction of the nervous impulses and, therefore, the "peritoneization" of the patient subjected to laparoscopic procedure. The "biochemical hypoesthesia", based on a change of the peritoneal homeostasis, would translate itself in a beneficial effect for the patient, persisting also when converted to laparotomic operation due the impossibility to proceed under laparoscopy, held up by the residual pneumoperitoneum.

Adult↗
PubMed2000

[Microinvasive carcinoma of the uterine cervix. Risk factors and therapeutic options].

Aim of this study was to analyze the staging of disease according to correlation between depth of stromal invasion, lymph vascular space involvement, nodal metastases and recurrence and mortality rates in uterine cervical carcinoma. Data of 16 different surveys from 1980 to 1996 inclusive were collected through a Medline research; papers were selected according to available information about depth of invasion, lymph vascular invasion, nodal metastases, recurrence and mortality rate. Results of these surveys were pooled with the following aims: 1 correlation between depth of invasion and nodal metastases occurrence; 2 evolution of prognostic value of lymph vascular invasion; 3 best management according to biology of disease. Depth of stromal invasion seems to be the most important prognostic factor in early cervical cancer, with a critical cut-off of 3 mm of depth. Lymph vascular invasion correlates both with nodal metastases and with prognosis, which strictly depends only on depth of invasion; as a consequence, lymph vascular invasion would not represent an independent prognostic factor. Finally radical treatment (i.e. more aggressive therapies) does not add any curative advantage when compared with conservative treatment, which must be currently considered standard in stage IA cervical cancer.

Female↗
PubMed1998

Expression of the extracellular fatty acid binding protein (Ex-FABP) during muscle fiber formation in vivo and in vitro.

We report that Ex-FABP, an extracellular protein belonging to the lipocalin family and involved in the extracellular transport of long-chain fatty acids, is expressed in the forming myotubes both in vivo and in vitro. The presence of the protein and of the mRNA was observed in newly formed myotubes at early stages of chick embryo development by immunohistochemistry and by in situ hybridization. At later stages of development myofibers still expressed both the mRNA and the protein. Ex-FABP expression was observed also in the developing myocardium and the muscular layer of large blood vessels. In agreement with these findings, an initial expression of the mRNA and protein secretion by cultured chicken myoblasts were observed only after the onset of myoblast fusion. Double-immunofluorescence staining of these cultured cells revealed that multinucleate myotubes were stained by antibodies directed against both the Ex-FABP and the sarcomeric myosin, whereas immature myotubes and single myoblasts were not. When added to cultured myoblasts, antibodies against the Ex-FABP induced a strong enhancement of the production of the same protein. In all experiments some cell sufferance and a transient impairment of myotube formation were also observed. The finding that the continuous removal of the Ex-FABP from the culture medium of myoblasts, due to the formation of immune complexes, resulted in an overproduction of the protein suggests a feedback (autocrine) control during myotube differentiation and maturation. We propose that the requirement for increased transport and metabolism of free fatty acid released from the membrane phospholipids and storage lipids, mediated by Ex-FABP, may be essential during differentiation of multinucleated myotubes or that an increased local demand of fatty acids and metabolites may act as a local hormone in tissues differentiating and undergoing morphogenesis.

Animals↗
PubMed1998

Vis-à-vis cells and the priming of bone formation.

Bone formation throughout skeletal growth and remodeling always entails deposition of new bone onto a pre-existing mineralized surface. In contrast, the initial deposition of bone in development requires the formation, ex novo, of the first mineralized structure in a nonmineralized tissue. We investigated the cellular events associated with this initial bone formation, with specific reference to the respective role of cartilage and bone cells in bones which form via a cartilage model. The cellular architecture of initial osteogenic sites was investigated by light, confocal, and electron microscopy (EM) in the membranous ossification of fetal calvarial bones (not forming via a cartilage model) and in the membranous ossification of the bony collars of endochondral bones. Bone sialoprotein (BSP), which is expressed during early phases of bone deposition and has been proposed to be involved in the control of both mineral formation and bone cell-matrix interactions, was used as a marker of initial bone formation. We found that at all sites, BSP-producing cells (as identified by intracellular immunoreactivity) are arranged in a characteristic vis-à-vis (face to face) pattern prior to the appearance of the first mineralizing BSP-immunoreactive extracellular matrix. In perichondral osteogenesis, the vis-à-vis pattern comprises osteoblasts differentiating from the perichondrium/periosteum and early hypertrophic chondrocytes located at the lateral aspects of the rudiment. By EM, the first mineral and the first BSP-immunoreactive sites coincide temporally and spatially in the extracellular matrix at the boundary between cartilage and periosteum. We further showed that in an in vitro avian model of chondrocyte differentiation in vitro to osteoblast-like cells, early hypertrophic chondrocytes replated as adherent cells turned on the expression of high levels of BSP in conjunction with the switch to collagen type I synthesis and matrix mineralization. We propose a model for the priming of bone deposition, i.e., the formation of the first bone structure, in which the architectural layout of cells competent to deposit a mineralizing matrix (the vis-à-vis pattern) determines the polarized deposition of bone. For bones forming via a cartilage model, the priming of bone deposition involves and requires cells that differentiate from early hypertrophic chondrocytes.

Animals↗
PubMed1997

Transferrin promotes endothelial cell migration and invasion: implication in cartilage neovascularization.

During endochondral bone formation, avascular cartilage differentiates to hypertrophic cartilage that then undergoes erosion and vascularization leading to bone deposition. Resting cartilage produces inhibitors of angiogenesis, shifting to production of angiogenic stimulators in hypertrophic cartilage. A major protein synthesized by hypertrophic cartilage both in vivo and in vitro is transferrin. Here we show that transferrin is a major angiogenic molecule released by hypertrophic cartilage. Endothelial cell migration and invasion is stimulated by transferrins from a number of different sources, including hypertrophic cartilage. Checkerboard analysis demonstrates that transferrin is a chemotactic and chemokinetic molecule. Chondrocyte-conditioned media show similar properties. Polyclonal anti-transferrin antibodies completely block endothelial cell migration and invasion induced by purified transferrin and inhibit the activity produced by hypertrophic chondrocytes by 50-70% as compared with controls. Function-blocking mAbs directed against the transferrin receptor similarly reduce the endothelial migratory response. Chondrocytes differentiating in the presence of serum produce transferrin, whereas those that differentiate in the absence of serum do not. Conditioned media from differentiated chondrocytes not producing transferrin have only 30% of the endothelial cell migratory activity of parallel cultures that synthesize transferrin. The angiogenic activity of transferrins was confirmed by in vivo assays on chicken egg chorioallantoic membrane, showing promotion of neovascularization by transferrins purified from different sources including conditioned culture medium. Based on the above results, we suggest that transferrin is a major angiogenic molecule produced by hypertrophic chondrocytes during endochondral bone formation.

Allantois↗
PubMed1996

The developmentally regulated avian Ch21 lipocalin is an extracellular fatty acid-binding protein.

Ch21, a developmentally regulated extracellular protein expressed in chick embryos and in cultured chondrocytes, was expressed in the baculovirus system, and the recombinant protein was purified to homogeneity by gel-filtration chromatography. Separation of two isoforms was achieved on an ion-exchange column. Previous work had shown that Ch21 belongs to the superfamily of lipocalins, which are transport proteins for small hydrophobic molecules. Studies were performed to identify the Ch21 ligand. By analysis of recombinant Ch21 on native polyacrylamide gel electrophoresis and by Lipidex assay, the binding of fatty acid to the protein was shown and a preferential binding of long-chain unsaturated fatty acids was observed. Both isoforms had the same behavior. The binding was saturable. Stoichiometry was about 0.7 mol of ligand/mol of protein. The protein binds the ligand in its monomeric form. Calculated dissociation constants were 2 X 10(-7) M for unsaturated fatty acids and 5 X 10(-7) M for stearic acid. The binding was specific; other hydrophobic molecules, as retinoic acid, progesterone, prostaglandins, and long-chain alcohols and aldehydes did not bind to the protein. Short-chain fatty acids did not bind to the protein. Ch21, also present in chicken serum, represents the first extracellular protein able to selectively bind and transport fatty acid in extracellular fluids and serum. We propose to rename the Ch21 protein as extracellular fatty acid-binding protein (Ex-FABP).

Animals↗
PubMed1996

Respiratory dysfunction related to diaphragmatic shoulder pain after abdominal and pelvic laparoscopy.

Many recent studies registered respiratory dysfunction after laparoscopic surgery; it is well known that the stimulation of the diaphragmatic tendon centre produces a typical shoulder pain. We hypothesize that diaphragmatic tendon centre stress causes postlaparoscopic ventilatory alterations; the aim of this study was to verify whether clinically respiratory dysfunction and shoulder pain relationship exists, after laparascopy with or without contemporaneous stimulation of gallbladder area. So we evaluated, preoperatively and 24 hours after the operation, 20 patients undergoing laparoscopic cholecystectomy (CP), 20 gynaecological patients undergoing laparoscopic ovarian surgery (GP) and 20 control patients undergoing orthopaedic limbs operations (OP) by pulmonary function tests, using computerized spirometry. Diaphragm referred pain was assessed for location and intensity. No orthopaedic patient showed postoperatively pain or pulmonary dysfunction demonstrating that the typical postlaparoscopic restrictive pattern is independent of general anaesthesia. In the CP and GP groups postoperative pulmonary functions were significantly reduced if compared with the orthopaedic control group but not significantly different between them. Moreover, 8 patients from the CP group and 13 from the GP group referred diaphragmatic pain: they showed significantly greater reduction of pulmonary function in comparison with the patients without pain in the respective groups. We conclude that diaphragmatic dysfunction after pneumoperitoneum, and not gallbladder area stimulation, seems to play the most important role in the pathogenesis of both shoulder pain and respiratory restrictive abnormalities after laparoscopy.

Abdomen↗