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PubMedDate not supplied

[A comparison of the two schemes of protection of the electrocardiograph against defibrillator impulse].

Two typical scheme of protection of the input cascade of the electrocardiograph against defibrillator impulses are under consideration. It is concluded that the conditions of check-up and testing as envisaged in State Standard R 50267.25 (MEK 601-2-25-93), is not in line with the real operation conditions, therefore, appropriate changes are suggested to be made in the above Standard. The offered scheme is shown to ensure a decrease of the electrodes' polarization potential by 100 times.

Electric Countershock↗
PubMed1993

Antibiotic cost control measures in a hospital pharmacy.

Faced with rising drug costs and an increase in type-1 beta-lactamase resistance, hospitals have been looking for ways to contain antibiotic costs while continuing to provide quality medical care. The hospital pharmacy at Montefiore Medical Center, Moses Division, has developed a number of programs aimed at identifying antibiotic prescribing trends and minimizing costs. An antimicrobial susceptibility cascade reporting (ASCR) system is used to consolidate and target antimicrobial susceptibility information available to the staff physicians. All antibiotics are tested in the microbiology laboratory for susceptibility; however, physicians receive susceptibility reports only for the more cost-effective, conventional antibiotics. Broader-spectrum, more powerful, and usually more expensive antibiotics are not reported with the ASCR system unless resistance to the more cost-effective antibiotics is noted. Two other reforms initiated are expansion of the pharmacy-based intravenous additive program to include antibiotics and the implementation of a drug therapy enhancement program authorizing automatic conversion by the pharmacist of targeted drug regimens to more clinically rational, cost-effective regimens.

Anti-Bacterial Agents↗
PubMed1997

L-selectin shedding does not regulate human neutrophil attachment, rolling, or transmigration across human vascular endothelium in vitro.

Current models of the multistep adhesion cascade for leukocyte-endothelial interactions predict loss of L-selectin from the leukocyte surface before transendothelial migration. We have tested this hypothesis using in vitro adhesion and transendothelial migration assays and a zinc-dependent metalloproteinase inhibitor, Ro 31-9790 (N-2-((2s)-[(hydroxycarbamoyl)methyl)-4-methylvaleryl]-N-1,3 -dimethyl-L-valinamide), which prevents chemoattractant-induced (e.g., IL-8, FMLP, C5a, platelet-activating factor) L-selectin endoproteolytic cleavage from isolated human neutrophils. Inhibitor and vehicle-treated neutrophils exhibited identical behavior during both adhesive interactions with 4- and 24-h TNF-alpha-activated HUVEC monolayers under flow, (including rate of initial attachment, rolling velocities, stable adhesion, and transmigration) and in static adhesion assays. Flow cytometric analysis of transmigrated neutrophils with mAb to L-selectin revealed that vehicle treated neutrophils had minimal detectable surface L-selectin, whereas inhibitor-treated neutrophils retained comparable levels of L-selectin on their surface as neutrophils maintained at 37 degrees C. In addition, mAb to L-selectin that induce rapid shape change and homotypic adhesion (LAM1-116) did not enhance the rate or extent of neutrophil transmigration under flow or static conditions. Neutrophils preincubated with LAM 1-116 displayed similar behavior to neutrophils preincubated with the control anti-L-selectin mAb, LAM1-101. In summary, these results demonstrate that there is no requirement for L-selectin to be shed from the surface of neutrophils before, or during, their migration across endothelial monolayers, and that prevention of surface L-selectin proteolytic cleavage does not enhance or inhibit neutrophil-endothelial cell adhesive interactions.

Cell Adhesion↗
PubMed1996

Effect of dipyrone, L-NAME and L-arginine on endotoxin-induced rat paw edema.

Paw edema was induced in male Wistar rats (200-250 g) by intraplantar (ipl) administration of 2.5 micrograms endotoxin (Etx). Etx, like carrageenin, produced two distinct edema formation phases, an early phase (75 min) followed by a late phase (7 h). We showed that the edema formation in the early phase was antagonized by dipyrone (80 mg/kg, i.p.) and indomethacin (1 mg/kg, i.p.) by 52% and 55%, respectively, and that the late phase was resistant to these drugs. These results suggest that in the early phase prostaglandins appear to be involved in the process. However, the activation of the kinin cascade leading to the release of other mediators may be involved in the increase of edema in the late phase. To test this hypothesis, we investigated whether the release of nitric oxide (NO) is involved in the mechanism of endotoxin-induced rat paw edema during the late phase, using N omega-nitro-L-arginine methyl ester (L-NAME) (50 micrograms, ipl) as inhibitor of NO synthase and L-arginine (1 mg, ipl) as substrate of NO synthase. The paw edema induced by Etx was inhibited by L-NAME by 56% and increased by L-arginine by 81%. Furthermore, L-arginine given in combination with L-NAME completely reversed the inhibition of Etx-induced edema produced by L-NAME. These results support the hypothesis that in the late phase NO production is associated with the edema evoked by Etx.

Animals↗
PubMedDate not supplied

[Changes in blood coagulation in HIV infection].

The human immunodeficiency virus (HIV) infection is becoming more complex. Hemostatic abnormalities occur frequently in the patient with HIV. HIV-related thrombocytopenia (Tr-HIV) is the most common hemostatic disorder with a high morbidity and affects patients from every risk group independently of age, sex, or stage of infection. Two mechanisms are responsible for the Tr-HIV: bone marrow failure and immunological disorders, namely, circulating immune complex deposited on the platelet membrane and the production of autoantibodies directed against platelets. The treatment of choice is zidovudine; other available options are not as effective as zidovudine. In addition, there are some abnormalities in the fluid phase of the coagulation cascade which can produce bleeding or thrombosis in the HIV patient. The most common are a prolonged partially activated thromboplastin time test, the production of a lupic anticoagulant and anticardiolipin antibodies, and several abnormalities in the natural-occurring anticoagulants. The thrombotic thrombocytopenic purpura recently associated with HIV has a clinical presentation and treatment alternatives that closely resemble those for the classical disease. The knowledge of these hemostatic abnormalities in the HIV seropositive patient allows a more rational care of these patients.

Blood Coagulation Disorders↗
PubMed2006

Cascade PSI-BLAST web server: a remote homology search tool for relating protein domains.

Owing to high evolutionary divergence, it is not always possible to identify distantly related protein domains by sequence search techniques. Intermediate sequences possess sequence features of more than one protein and facilitate detection of remotely related proteins. We have demonstrated recently the employment of Cascade PSI-BLAST where we perform PSI-BLAST for many 'generations', initiating searches from new homologues as well. Such a rigorous propagation through generations of PSI-BLAST employs effectively the role of intermediates in detecting distant similarities between proteins. This approach has been tested on a large number of folds and its performance in detecting superfamily level relationships is approximately 35% better than simple PSI-BLAST searches. We present a web server for this search method that permits users to perform Cascade PSI-BLAST searches against the Pfam, SCOP and SwissProt databases. The URL for this server is http://crick.mbu.iisc.ernet.in/~CASCADE/CascadeBlast.html.

Internet↗
PubMed2004

Amphetamine-evoked gene expression in striatopallidal neurons: regulation by corticostriatal afferents and the ERK/MAPK signaling cascade.

The environmental context in which psychostimulant drugs are experienced influences their ability to induce immediate early genes (IEGs) in the striatum. When given in the home cage amphetamine induces IEGs predominately in striatonigral neurons, but when given in a novel test environment amphetamine also induces IEGs in striatopallidal neurons. The source of the striatopetal projections that regulate the ability of amphetamine to differentially engage these two striatofugal circuits has never been described. We report that transection of corticostriatal afferents selectively blocks, whereas enhancement of cortical activity with an ampakine selectively augments, the number of amphetamine-evoked c-fos-positive striatopallidal (but not striatonigral) neurons. In addition, blockade of the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) signaling cascade preferentially inhibits the number of amphetamine-evoked c-fos-positive striatopallidal neurons. These results suggest that glutamate released from corticostriatal afferents modulates the ability of amphetamine to engage striatopallidal neurons through an ERK/MAPK signaling-dependent mechanism. We speculate that this may be one mechanism by which environmental context facilitates some forms of drug experience-dependent plasticity, such as psychomotor sensitization.

Afferent Pathways↗
PubMed2002

Genetic testing for HFE hemochromatosis in Australia: the value of testing relatives of simple heterozygotes.

BACKGROUND: It is unclear whether screening of relatives of C282Y and H63D heterozygotes (other than compound heterozygotes) for hemochromatosis will detect sufficient numbers of cases to justify introduction of this screening strategy. METHODS: Conditional probabilities were determined using published Australian allele frequencies and penetrance data to determine the detection rate of hemochromatosis by testing the siblings and offspring of heterozygotes (subjects with only one HFE mutation). RESULTS: The number of individuals who are at risk of developing increased body iron stores because of HFE mutations is substantially higher (1 in 80) than previously estimated. In addition, 33% of the Australian population are heterozygous for either C282Y or H63D. Based on population estimates, the relative risk to the offspring of C282Y and H63D heterozygotes of developing increased iron stores is 4.1 and 1.5, respectively, while the relative risk to each sibling is 2.3 and 1, respectively. The risk of developing clinical features of hemochromatosis or hepatic fibrosis is likely to be substantially lower. CONCLUSIONS: Although the detection rate from testing the families of unaffected heterozygotes is low, this can be justified as a clinically useful screening strategy. At the present time this strategy should be restricted to first-degree relatives of heterozygotes. Further studies are recommended to determine if cascade genetic screening is a cost-effective alternative to general population screening.

Australia↗
PubMed2001

Observation of the Askaryan effect: coherent microwave Cherenkov emission from charge asymmetry in high-energy particle cascades.

We present the first direct experimental evidence for the charge excess in high-energy particle showers and corresponding radio emission predicted nearly 40 years ago by Askaryan. We directed picosecond pulses of GeV bremsstrahlung photons at the SLAC Final Focus Test Beam into a 3.5 ton silica sand target, producing electromagnetic showers several meters long. A series of antennas spanning 0.3 to 6 GHz detected strong, subnanosecond radio-frequency pulses produced by the showers. Measurements of the polarization, coherence, timing, field strength vs shower depth, and field strength vs frequency are completely consistent with predictions. These measurements thus provide strong support for experiments designed to detect high-energy cosmic rays such as neutrinos via coherent radio emission from their cascades.

Journal Article↗
PubMed1998

Prolonged discordant xenograft survival by inhibition of the intrinsic coagulation pathway in complement C6-deficient recipients.

BACKGROUND: Xenotransplantation of vascularized organs between unmodified discordant species results in hyperacute graft rejection within minutes to hours after graft reperfusion. This process is due to the presence of natural xenoreactive antibodies and complement activation, which lead to vessel injury, thrombosis, and hemorrhage. Because multiple components of the coagulation and complement cascades interact with each other, we have investigated the effects of inhibiting these systems together. The recombinant Kunitz type serine protease inhibitor (KPI-BG022) tested in these experiments inhibits factor XIIa, kallikrein, and plasmin. METHODS: Cardiac xenografts from male Hartley guinea pigs were heterotopically grafted into male PVG rats that were either sufficient (C6[+]) or deficient (C6[-]) for the complement component C6 and thus formation of the membrane attack complex. Experimental animals received KPI 5 mg/kg intravenously before reperfusion, and control animals received saline placebo. RESULTS: C6(+) recipients rejected their grafts hyperacutely, without a significant difference between KPI-treated (0.12+/-0.05 hours) and placebo-treated (0.13+/-0.06 hours) recipients (n = 10). As expected, C6(-) recipients showed prolonged graft survival (17.65+/-3.45 hours, n = 5). However, a single intravenous bolus of KPI before releasing the clamps further delayed graft rejection in C6(-) recipients (46.2+/-3.3 hours; n = 5). Histologic examination at 2, 6, and 12 hours after transplantation showed platelet aggregation and inflammatory infiltrates were significantly decreased in KPI-treated (C6[-]) recipients. However, intragraft hemorrhage was apparent at 6 and 12 hours. CONCLUSIONS: We conclude that in vivo inhibition of the intrinsic clotting cascade by functional inactivation of factor XIIa has a synergistic effect with inhibition of membrane attack complex formation in preventing hyperacute discordant xenograft rejection.

Animals↗
PubMed1993

Fast axonal diffusion of 3000 molecular weight dextran amines.

The distances of anterograde and retrograde axonal movement per hour were examined for dextran amines of 3000, 10,000 and 40,000 molecular weights (MW) conjugated to different fluorochromes (Cascade blue, fluorescein, tetramethylrhodamine, Texas red) or to biotin. Lateral line nerves of Xenopus laevis tadpoles were used as an easily accessible test system. Only 10,000 and 3000 MW dextran amines underwent significant anterograde and retrograde movement. Dextrans of 3000 MW progressed about twice as far (2 mm/h at 22 degrees C) than 10,000 MW dextrans. Dextrans conjugated to different fluorochromes or to biotin did not show differences in their distance covered. Tracers traveled over the same distance in amphibians pre-treated with either 1 microM colchicine for 2-6 h or 10 micrograms/ml nocodazole for 5 h prior to the application to depolymerize microtubules needed for active transport. This suggests that diffusion is the major mechanism of movement for dextran amines over short distances. In the developing Xenopus retina, 3000 MW dextrans traveled from the optic disc as far away as the ora serrata within 1 h. In mouse embryos, chicken embryos and larval lampreys dextran amines progress within 1 h from cut peripheral nerves through efferent and afferent tracts. These data show that 3000 MW dextrans can be used in much the same way as 10,000 MW dextrans, but label neuronal profiles in a shorter time in a wide variety of species.

Ambystoma↗
PubMed1999

Oxytocin activates mitogen-activated protein kinase and up-regulates cyclooxygenase-2 and prostaglandin production in human myometrial cells.

OBJECTIVE: The objective of our study was to test the hypothesis that oxytocin promotes prostaglandin production by up-regulating cyclooxygenase-2 via activation of mitogen-activated protein kinase cascade in human myometrial cells. STUDY DESIGN: Confluent cultures of human myometrial cells obtained from uterine specimens of premenopausal women undergoing hysterectomy were serum starved for 48 hours before oxytocin stimulation. Prostacyclin levels, as 6-keto-prostaglandin F(1) (alpha), were measured by radioimmunoassay, and the cellular cyclooxygenase-2 protein content was determined by Western blot. Mitogen-activated protein kinase activity was assessed by measuring the phosphorylation of myelin basic protein. RESULTS: In a time- and dose-dependent manner oxytocin promoted prostacyclin production in human myometrial cells. Maximal responses were observed after 8 hours of stimulation at a dose of 100 nmol/L. This effect was mainly due to the expression of cyclooxygenase-2 protein. Within 5 minutes oxytocin significantly stimulated mitogen-activated protein kinase, as compared with the expression in untreated controls. The maximal increase in enzyme activity (2.5-fold) was obtained at 45 minutes. A selective inhibitor of mitogen-activated protein kinase activation (PD98059), as well as herbimycin, a tyrosine kinase inhibitor, and the transcriptional blocker actinomycin D, suppressed oxytocin-induced cyclooxygenase-2 expression and prostacyclin production. The stimulatory action of oxytocin was also sensitive to inhibition by pertussis toxin but appeared to be independent of protein kinase C activation. CONCLUSION: Our data indicate a largely unrecognized signal transduction mechanism for oxytocin, involving G-protein-coupled activation of mitogen-activated protein kinase and cyclooxygenase-2 gene expression, leading to increased prostaglandin production in human myometrial cells. This signaling pathway complements the rapid activation of the phosphoinositide cycle and may be responsible for sustained release of prostaglandins in uterine tissues, promoting labor and parturition.

Blotting, Western↗
PubMed2003

Anti-HuD-induced neuronal apoptosis underlying paraneoplastic gut dysmotility.

BACKGROUND & AIMS: The role of autoimmunity underlying paraneoplastic gut dysmotility remains unsettled. Because anti-Hu antibodies may impair enteric neuronal function, we tested whether anti-HuD-positive sera from patients with paraneoplastic gut dysmotility or commercial anti-HuD antibodies activated the apoptotic cascade in a neuroblastoma cell line and cultured myenteric neurons. METHODS: Anti-HuD antibodies from patients with severe paraneoplastic gut dysmotility were characterized by immunofluorescence and immunoblot. SH-Sy5Y neuroblasts and cultured myenteric neurons were exposed to sera containing anti-HuD antibodies or 2 commercial anti-HuD antibodies. Cells were processed for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) technique to evaluate apoptosis. Immunofluorescence was used to identify activated caspase-3 and apaf-1, along with microtubule-associated protein 2. RESULTS: In SH-Sy5Y cells, the percentage of TUNEL-positive nuclei observed after exposure to anti-HuD-positive sera (32% +/- 7%) or anti-HuD antibodies (23% +/- 2%) was significantly greater than that of control sera or fetal calf serum (P < 0.001). The time-course analysis showed a significantly greater number of apoptotic neuroblastoma cells evoked by the 2 commercial anti-HuD antibodies at 24, 48, and 72 hours versus controls. The number of TUNEL-positive myenteric neurons exposed to anti-HuD antibodies (60% +/- 14%) was significantly greater than that of fetal calf serum (7% +/- 2%; P < 0.001). Apaf-1 and caspase-3 immunolabeling showed intense cytoplasmic staining in a significantly greater proportion of cells exposed to anti-HuD-positive sera or to commercial anti-HuD antibodies compared with controls. CONCLUSIONS: Anti-HuD antibodies evoked neuronal apoptosis that may contribute to enteric nervous system impairment underlying paraneoplastic gut dysmotility. Apaf-1 activation suggests participation of a mitochondria-dependent apoptotic pathway.

Apoptosis↗
PubMed1998

Fluorescent tracers as potential candidates for double labeling of descending brain neurons in larval lamprey.

In larval lamprey, seven fluorescent tracers were tested as potential candidates for retrograde double labeling of descending brain neurons: Fluoro Gold (FG); fluorescein dextran amine (FDA); True Blue (TB); cascade blue dextran amine (CBDA); Fast Blue (FB); Texas red dextran amine (TRDA); and tetramethylrhodamine dextran amine (RDA). The first tracer (FG, TB, FB, or CBDA) was applied to the spinal cord at 40% body length (BL). In separate experiments, the second tracer (TRDA or RDA) was applied to the spinal cord at 20% BL. The tracer combination FG/TRDA was found to have the best optical properties for double labeling. However, application of FG to the spinal cord with the method used for the other tracers resulted in labeling of 'lateral cells' along the sides of the rhombencephalon that were presumed to be non-neuronal and that obscured some of the descending brain neurons. Control experiments suggested that FG was transported in the circulation to the brain, where the tracer was taken up by lateral cells. Therefore, a special technique was developed for applying FG to the spinal cord without allowing the tracer to enter the circulation. In larval lamprey, this important double-labeling technique that was developed for TRDA and FG is being used to examine axonal regeneration and projection patterns of descending brain neurons.

Animals↗
PubMed2000

Stress-induced mitogen-activated protein kinase signaling in the corpus luteum.

Current evidence suggests that stress-induced apoptosis is mediated through the activation of the mitogen-activated protein kinase (MAPK) signaling cascade. We hypothesize that stress-related signaling events documented in other cell lines may also occur in the corpus luteum. To test this, cultured bovine luteal cells were exposed to UV irradiation and harvested at different intervals (0, 30, 120, 240 and 360 min) for analysis of protein or apoptotic cell death. In response to UV treatment cellular levels of phosphorylated p38MAPK and jun-n-terminal kinase (JNK) were increased within 30 min and remained elevated over controls for the duration of the experiment. In contrast, the levels of the phosphorylated forms of p42MAPK and p44MAPK were dramatically reduced. The changes in MAPK signaling were similar to those observed in response to tumor necrosis factor alpha, a cytokine implicated in luteal regression. The UV-induced changes in MAPK phosphorylation were associated with an increase in caspase 3 activity and apoptotic cell death. Taken together, these data demonstrate that stress-induced signaling events in the corpus luteum are similar to those observed in unrelated cell types. Thus, stress-related signaling events may play a role in luteal regression.

Animals↗
PubMed1997

Effects of inhibitors of serine protease, phenoloxidase and dopa decarboxylase on the melanization of Dirofilaria immitis microfilariae with Armigeres subalbatus haemolymph in vitro.

The melanization of Dirofilaria immitis microfilariae in Armigeres subalbatus haemolymph in vitro is a two-step process. Firstly, the microfilariae are encased in a transparent capsule, then the capsule material is melanized later. Benzamadine HC1 and p-amidinophenylmethanesulfonyl fluoride, both serine protease inhibitors, inhibited the deposition of the transparent capsule material and melanization. Diethyldithiocarbamate, a phenoloxidase inhibitor, did not prevent the deposition of the transparent capsule material but it did inhibit melanization. m-Hydroxybenzylhydrazine, a dopa decarboxylase inhibitor, had no inhibitory action on the deposition of the transparent capsule material. However, the time for the transparent capsule to become melanized was delayed due to the presence of m-hydroxybenzylhydrazine in the test system. Immmunocytochemical localization showed that propheoloxidase and/or phenoloxidase was present in the transparent capsule material. These results suggest (1) that prophenoloxidase cascade is essential in the melanization of microfilariae in mosquitoes and its putative activation behaviour is similar to that of other insects and (2) that the deposition of transparent capsule material is the result of the activation of prophenoloxidase by serine proteases and the melanization of the transparent capsule material is due to the presence of active phenoloxidase in capsule.

Animals↗
PubMed1998

Differentiating and proliferative effects of HGF in renal proximal tubular cells are mediated via different signalling pathways.

BACKGROUND: As a renotropic cytokine, hepatocyte growth factor (HGF) prevents acute renal failure and accelerates renal regeneration. HGF initiates its biological effects by interaction with specific transmembrane receptors, the c-Met proto-oncogene, possessing an intracellular tyrosine kinase domain. We tested the hypothesis of whether the complex biological effects of HGF in renal proximal tubular cells are mediated by different intracellular signalling cascades and/or different receptors. METHODS: PT-1 cells, a proximal tubular cell line derived from rabbit kidney, were cultured under defined serum-free conditions to examine the biological effects of exogenously added HGF. By specific assays, we determined HGF binding and its effects on cell proliferation, migration, scattering and tubulogenic differentiation. To investigate whether HGF action could be inhibited by protein tyrosine kinase inhibitors (PTKIs), cells were incubated with HGF and different concentrations of herbimycin A, genestein, methyl-2,5-dihydroxycinnamate (MDC) and geldanamycin. All PTKIs are known inhibitors of pp60(c-src), a non-receptor tyrosine kinase involved in cell growth control. RESULTS: HGF bound with high affinity to cell membrane receptors and displayed multiple biological effects. Compared with serum-free controls, HGF increased the number of microvilli 1.5-fold, enhanced cell proliferation and migration 1.8-fold, and stimulated the formation of tubular structures 2.3-fold. Consistent with the known tyrosine kinase activity of the c-Met receptor, the mitogenic and motogenic effects of HGF were inhibited by PTKIs in a dose-dependent manner with the following order of potency: geldanamycin > herbimycin A > genestein > MDC. In contrast, however, the HGF-induced tubulogenic cell differentiation was not inhibited specifically by PTKIs. CONCLUSIONS: The finding that PTKIs inhibited the mitogenic response but not the tubulogenic differentiation induced by HGF indicates different intracellular signal transduction pathways. We suggest that pp60(c-src) plays a key role in mediating the mitogenic and motogenic action of HGF, whereas tubulogenic cell differentiation induced by HGF is transduced by a pp60(c-src)-independent signalling pathway.

Animals↗
PubMed2004

Moderate increase in intraabdominal pressure attenuates gastric mucosal oxygen saturation in patients undergoing laparoscopy.

BACKGROUND: Perioperative disturbances of microvascular blood flow and oxygenation in the intestinal tract have been hypothesized to play an important role in development of the multiple organ dysfunction syndrome. Herein, increased intra-abdominal pressure (IAP) has been identified as a key factor in the initiation of the pathophysiologic cascade. The authors hypothesized that increasing the IAP by intraperitoneal insufflation of carbon dioxide attenuates microvascular oxygen saturation in gastric mucosa. They tested this hypothesis in a prospective, observational study in 16 patients scheduled to undergo elective diagnostic laparoscopy. METHODS: The authors continuously assessed microvascular oxygen saturation in gastric mucosa by reflectance spectrophotometry. Simultaneously systemic oxygen saturation, heart rate, arterial blood pressure, and ventilation-derived variables were measured noninvasively. During general anesthesia and controlled mechanical ventilation, baseline values were obtained. Thereafter, the IAP was increased to 8 and 12 mmHg, respectively, followed by a control period after desufflation. RESULTS: The increase in IAP from baseline to 8 mmHg decreased microvascular oxygen saturation in gastric mucosa from 69+/-7% (mean +/- SD) to 63+/-8% at 8 mmHg IAP (P <0.05), with a further significant reduction to 54+/-13% at 12 mmHg IAP (P <0.01). Microvascular oxygen saturation in gastric mucosa recovered rapidly to baseline level (66 +/- 10%) after release of increased IAP. In striking contrast to regional mucosal oxygen saturation, systemic oxygenation did not change with either of the interventions. CONCLUSIONS: The results suggest that increasing intraabdominal pressure to moderate levels, commonly applied to induce a surgical pneumoperitoneum, decreases gastric mucosal oxygen saturation.

Abdominal Cavity↗