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Biomedical subjects

S Roth

Publications and source records attributed to S Roth.

At least 127 records · Page 7Linked to original sources
PubMed1999

Effects of low-dose dopexamine on splanchnic oxygenation during major abdominal surgery.

OBJECTIVE: To study the influence of low-dose dopexamine on splanchnic oxygenation during major abdominal surgery. DESIGN: Prospective, randomized, placebo-controlled study. SETTING: University hospital. PATIENTS: Eighteen adult patients undergoing elective major abdominal surgery. INTERVENTIONS: The patients received either dopexamine at 1 microg/kg/min (group A, n = 9) or 0.90% saline as control (group B, n = 9). MEASUREMENTS AND RESULTS: To assess the splanchnic oxygenation, intestinal tissue PO2 (PtissO2) and gastric intramucosal Pco2 (PmucCO2) were measured, and the PCO2 gap (PmucCO2 - PaCO2) was calculated at baseline (T1) and after an infusion period of 60 mins (T2). There was no difference between the groups in the global oxygen transport parameters. Low-dose dopexamine increases PtissO2 on the serosal side of the small bowel (deltaPtissO2, 17+/-24 mm Hg in group A vs. -5+/-10 in group B). The changes in PtissO2 at the serosal side of the colon after dopexamine demonstrated a nonsignificant increase (deltaPtissO2, 7+/-11 mm Hg in group A vs. -11+/-23 mm Hg in group B). In both groups, the Pco2 gap (group A, 6+/-7 mm Hg [T1] and 5+/-6 mm Hg [T2], vs. group B, 9+/-10 mm Hg [T1] and 12+/-10 mm Hg [T2]) remained unchanged compared with the baseline. CONCLUSION: It is concluded that low-dose dopexamine improves PtissO2 at the serosal side of the gut, preferably at the small bowel. However, low-dose dopexamine did not improve gastric PmucCO2.

Abdomen↗
PubMed1999

Sevoflurane induced suppression of inhibitory synaptic transmission between soma-soma paired Lymnaea neurons.

The cellular and synaptic mechanisms by which general anesthetics affect cell-cell communications in the nervous system remain poorly defined. In this study, we sought to determine how clinically relevant concentrations of sevoflurane affected inhibitory synaptic transmission between identified Lymnaea neurons in vitro. Inhibitory synapses were reconstructed in cell culture, between the somata of two functionally well-characterized neurons, right pedal dorsal 1 (RPeD1, the giant dopaminergic neuron) and visceral dorsal 4 (VD4). Clinically relevant concentrations of sevoflurane (1-4%) were tested for their effects on synaptic transmission and the intrinsic membrane properties of soma-soma paired cells. RPeD1- induced inhibitory postsynaptic potentials (IPSPs) in VD4 were completely and reversibly blocked by sevoflurane (4%). Sevoflurane also suppressed action potentials in both RPeD1 and VD4 cells. To determine whether the anesthetic-induced synaptic depression involved postsynaptic transmitter receptors, dopamine was pressure applied to VD4, either in the presence or absence of sevoflurane. Dopamine (10(-]5) M) activated a voltage-insensitive K(+) current in VD4. The same K(+) current was also altered by sevoflurane; however, the effects of two compounds were nonadditive. Because transmitter release from RPeD1 requires Ca(2+) influx through voltage-gated Ca(2+) channels, we next tested whether the anesthetic-induced synaptic depression involved these channels. Individually isolated RPeD1 somata were whole cell voltage clamped, and Ca(2+) currents were analyzed in control and various anesthetic conditions. Clinically relevant concentrations of sevoflurane did not significantly affect voltage-activated Ca(2+) channels in RPeD1. Taken together, this study provides the first direct evidence that sevoflurane-induced synaptic depression involves both pre- and postsynaptic ion channels.

Action Potentials↗
PubMed1999

The role of brinker in mediating the graded response to Dpp in early Drosophila embryos.

Brinker (Brk), a novel protein with features of a transcriptional repressor, regulates the graded response to Decapentaplegic (Dpp) in appendage primordia of Drosophila. Here, we show that in the embryo brk also has differential effects on Dpp target genes, depending on the level of Dpp activity required for their activation. Low-level target genes, like dpp itself, tolloid and early zerknüllt, show strong ectopic expression in ventrolateral regions of brk mutant embryos; intermediate-level target genes like pannier show weak ectopic expression, while high-level target genes like u-shaped and rhomboid are not affected. Ectopic target gene activation in the absence of brk is independent of Dpp, Tkv and Medea, indicating that Dpp signaling normally antagonizes brk's repression of these target genes. brk is expressed like short gastrulation (sog) in ventrolateral regions of the embryo abutting the dpp domain. Here, both brk and sog antagonize the antineurogenic activity of Dpp so that only in brk sog double mutants is the neuroectoderm completely deleted.

Animals↗
PubMed1999

Binuclear Drosophila oocytes: consequences and implications for dorsal-ventral patterning in oogenesis and embryogenesis.

The position of the nucleus along the anterior rim of stage 8 Drosophila oocytes presages the dorsal side of the egg and the developing embryo. In this paper, we address the question of whether the oocyte has a previously determined dorsal side to which the nucleus is drawn, or whether nuclear position randomly determines the dorsal side. To do so, we have taken advantage of a genetic system in which Drosophila oocytes occasionally become binuclear. We find that (i) the two nuclei migrate independently to their respective positions on the anterior rim, sometimes selecting the same site, sometimes not, (ii) the two nuclei are equivalent in their ability to induce a dorsal-ventral pattern in the overlying follicular epithelium, and (iii) at any position around the anterior circumference of the egg chamber the follicle cell sheet is equally responsive to the Gurken signal associated with the oocyte nuclei. These results argue that the dorsal-ventral axis is determined arbitrarily by the randomly selected position of the nucleus on the anterior rim of the oocyte. Some of the binuclear eggs support embryonic development. However, despite the duplication of dorsal chorion structures, the majority of such embryos show normal dorsal-ventral patterning. Thus, processes exist in the ventral follicular epithelium or in the perivitelline space that compensate for the expansion of dorsal follicle cell fates and consequently allow the formation of a normal embryonic axis.

Animals↗
PubMed1999

Retinal ischemic preconditioning in the rat: requirement for adenosine and repetitive induction.

PURPOSE: A brief period of ischemia can induce a remarkably complete state of ischemic tolerance in the retina, a phenomenon known as ischemic preconditioning (IPC). The mechanisms of IPC were studied in the rat retina by examining the role of adenosine as a possible mediator and determining whether IPC protection could be induced more than once in the same rat. METHODS: Retinal ischemia was produced for 60 minutes in ketamine-xylazine-anesthetized Sprague-Dawley rats, and recovery was measured using electroretinography. Twenty-four hours earlier, the IPC stimulus of 5 minutes of ischemia was applied. To test the role of adenosine as a mediator of IPC, the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 0.45 mg/kg, 2.25 mg/kg, or 4.5 mg/kg), the A2a antagonist 8-(3-chlorostyryl)caffeine (CSC; 0.1 mg/kg or 1.0 mg/kg), or their cyclodextrin vehicle were administered 15 minutes before IPC. To examine whether exogenous adenosine administration could mimic IPC, animals received intravitreal injections of the adenosine A1 receptor stimulant adenosine amine congener (ADAC) or the A2a stimulant CGS21680, followed by ischemia 24 hours later. To test the hypothesis that IPC could be induced repeatedly without loss of protection, rats were divided to receive IPC or sham IPC, followed 10 days later by IPC or a sham procedure, and 24 hours later by 60 minutes of ischemia. RESULTS: Adenosine A1 receptor blockade with 4.5 mg/kg DPCPX administered intraperitoneally (IP) before or immediately after 5 minutes of ischemia completely blocked IPC protection, whereas lower doses resulted in partial blockade. CSC at the lowest dose (0.1 mg/kg) had no significant effect on IPC's protective effect, whereas partial blockade was found with 1.0 mg/kg CSC. A1 or A2a receptor stimulation produced partial but significant mimicking of IPC protection, effects that were antagonized by DPCPX or CSC. Ischemic preconditioning applied twice, separated by 10 days, and followed by 60 minutes of ischemia 24 hours after the second IPC stimulus, resulted in nearly identical recovery of function after ischemia compared with IPC performed one time. CONCLUSIONS: Adenosine, acting through the A1 and A2a receptors, is a critical component in the induction of ischemic tolerance after preconditioning in the retina. The neuroprotective effects of IPC in the retina are lost over time but may be reinduced by subsequent application of the IPC stimulus.

Adenosine↗
PubMed1999

Ileal ureteral substitution in reconstructive urological surgery: is an antireflux procedure necessary?

PURPOSE: Whether antireflux implantation techniques are necessary in adults who undergo ileal ureteral substitution is controversial. We prospectively evaluated the correlation between reflux and renal function in 19 patients who underwent ileal ureteral substitution with no antireflux implantation technique. MATERIALS AND METHODS: Followup included clinical evaluation, serum creatinine, blood gasses, excretory urogram, cystogram and dynamic selective renographic clearance on technetium mercaptotriglycine renal scans. All patients were followed for a minimum of 4 years except 2 who died 26 and 43 months postoperatively. Mean followup was 57 months (range 48 to 72). RESULTS: Despite reflux, renal scans indicated a significant increase in renal function in all patients. Vesico-ileal reflux was present in 9 cases and reflux in the renal pelvis occurred in only 3. Reflux occurred in only 3 of 10 patients with ileal segments longer than 15 cm., and did not reach the renal pelvis. CONCLUSIONS: Reflux appears to have no detrimental effect on renal function in adults with ileal ureters and, therefore, an antireflux procedure is unnecessary. In addition, an ileal segment longer than 15 cm. appears to safeguard the renal pelvis against visible reflux stemming from pro-grade intestinal peristalsis.

Adult↗
PubMed1999

Ischemic preconditioning attenuates hypoperfusion after retinal ischemia in rats.

PURPOSE: Retinal blood flow (RBF) was measured in rats to test the hypotheses that hypoperfusion follows severe ischemia in the retina and that ischemic preconditioning (IPC) attenuates this change in blood flow. METHODS: Male Sprague-Dawley rats were anesthetized with halothane and mechanically ventilated by tracheostomy to maintain normocarbia and normoxia. Retinal ischemia was induced for 0, 5, 30, 60, 75, or 90 minutes. RBF was measured 60 and 150 minutes after the end of ischemia using the radioactive microsphere blood flow method, and electroretinography was performed during the first 120 minutes after ischemia to quantitate the extent of functional recovery. Additional groups received IPC (5 minutes of ischemia) 24 hours before 30, 60, or 75 minutes of ischemia. RESULTS: Control (0 minutes' ischemia) RBF was 22+/-3 ml/100 g per minute (mean +/- SE). At 60 minutes after 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 15+/-2 (NS), 11+/-1, 8+/-2, 8+/-1, and 10+/-1 ml/100 g per minute, respectively (significance, P<0.05 versus control). At 150 minutes after 5, 30, 60, 75, or 90 minutes of ischemia, RBF was 18+/-3 (NS), 13+/-1, 12+/-3, 12+/-2, and 11+/-1 ml/100 g per minute respectively (significance, p<0.05 versus control). With prior IPC, RBF after 30 and 60 minutes of ischemia was 21+/-1 and 19+/-3 ml/100 g per minute (both NS compared with control; P<0.05 compared with 30 or 60 minutes of ischemia without IPC). When ischemia was 75 minutes in duration, IPC did not prevent postischemic hypoperfusion. The extent of recovery of the electroretinogram b wave was inversely related to the length of ischemia. CONCLUSIONS: Postischemic hypoperfusion is present in the rat retina 60 minutes after ischemia, does not resolve by 150 minutes after ischemia, and is attenuated by IPC when ischemia is 60 minutes or less in duration. Maintenance of postischemic perfusion in the retina may be one of the mechanisms involved in the neuroprotection afforded by IPC.

Animals↗
PubMed1998

Mutations in the SMAD4/DPC4 gene in juvenile polyposis.

Familial juvenile polyposis is an autosomal dominant disease characterized by a predisposition to hamartomatous polyps and gastrointestinal cancer. Here it is shown that a subset of juvenile polyposis families carry germ line mutations in the gene SMAD4 (also known as DPC4), located on chromosome 18q21.1, that encodes a critical cytoplasmic mediator in the transforming growth factor-beta signaling pathway. The mutant SMAD4 proteins are predicted to be truncated at the carboxyl-terminus and lack sequences required for normal function. These results confirm an important role for SMAD4 in the development of gastrointestinal tumors.

Cell Membrane↗
PubMed1998

Somatic mutations in LKB1 are rare in sporadic colorectal and testicular tumors.

Germ-line mutations in a serine/threonine kinase gene, LKB1, were recently shown to underlie Peutz-Jeghers syndrome (PJS), a hereditary disorder that predisposes to benign and malignant tumors of multiple organ systems. Most mutations that have been described thus far dramatically change the predicted protein and are likely to be of an inactivating nature. This observation and a previous observation that the LKB1 locus is often deleted in PJS polyps suggest that the gene may function as a tumor suppressor. We examined whether somatic mutations in this gene are present in sporadic carcinomas of the colon and testis, tumors that are characteristic of PJS. First, 20 randomly selected colorectal and 28 testicular tumors were analyzed by single-strand conformation polymorphism analysis. No mutations in LKB1 were found in colorectal tumors. One testicular tumor displayed a heterozygous missense type variant, in which glycine 163 was changed to aspartic acid. This change was absent in the DNA of normal tissue. To better focus our efforts, we tested 75 additional colon carcinomas for loss of heterozygosity at 19p, where LKB1 is localized. Of 75 samples analyzed, 50 were informative with a closely linked marker, D19S886, and 13 (26%) of these displayed loss of heterozygosity. The 13 tumors were scrutinized for LKB1 mutations by genomic sequencing. This analysis revealed no changes. Together, these findings suggest that somatic mutations of LKB1 are not frequent in colorectal and testicular cancer.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

Thrombin generation, inhibition and clinical outcomes in patients with acute myocardial infarction treated with thrombolytic therapy and heparin: results from the GUSTO-I Trial. GUSTO-I Hemostasis Substudy Group. Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries.

OBJECTIVES: We sought to assess the effects of antithrombotic therapy after thrombolysis for acute myocardial infarction on markers of thrombin generation and activity and to determine the relation of these markers with clinical outcomes. BACKGROUND: Thrombin activation and generation often occur with thrombolysis for acute myocardial infarction. Antithrombotic regimens have been developed to reduce the resulting thrombotic complications. METHODS: We sampled plasma markers of thrombin generation and activity after thrombolysis in 292 patients. We assessed the relations of these markers with clinical outcomes at 30 days. RESULTS: Fibrinopeptide A (FPA), a marker of thrombin activity toward fibrinogen, was elevated at baseline (12.3 ng/ml) and increased to 18.4 ng/ml by 90 min after streptokinase and subcutaneous heparin treatment. With intravenous heparin, this increase was attenuated, but intravenous heparin did not prevent thrombin generation, as measured by prothrombin fragment 1.2 (F1.2). Heparin level, measured by anti-Xa activity, correlated with activated partial thromboplastin time (aPTT, r = 0.62 to 0.67). Thrombin activity, measured by FPA, was as closely related to aPTT as to the heparin level. Baseline levels of F1.2 were significantly related to the risk of death or reinfarction at 30 days (p = 0.008); values 12 h after enrollment also were related to 30-day mortality (p = 0.05). CONCLUSIONS: Although intravenous heparin partly suppresses the increased thrombin activity associated with thrombolysis, it does not inhibit thrombin generation. The aPTT was as good a measure of suppression of thrombin activity as the heparin level itself. Hematologic markers of thrombin generation were found to be related to the subsequent risk of thrombotic events.

Aged↗
PubMed1998

A serine/threonine kinase gene defective in Peutz-Jeghers syndrome.

Studies of hereditary cancer syndromes have contributed greatly to our understanding of molecular events involved in tumorigenesis. Here we investigate the molecular background of the Peutz-Jeghers syndrome (PJS), a rare hereditary disease in which there is predisposition to benign and malignant tumours of many organ systems. A locus for this condition was recently assigned to chromosome 19p. We have identified truncating germline mutations in a gene residing on chromosome 19p in multiple individuals affected by PJS. This previously identified but unmapped gene, LKB1, has strong homology to a cytoplasmic Xenopus serine/threonine protein kinase XEEK1, and weaker similarity to many other protein kinases. Peutz-Jeghers syndrome is therefore the first cancer-susceptibility syndrome to be identified that is due to inactivating mutations in a protein kinase.

AMP-Activated Protein Kinase Kinases↗
PubMed1998

An examination of individual differences in the relationship between interpersonal stress and disease activity among women with rheumatoid arthritis.

OBJECTIVE: The effects of interpersonal stress on disease activity were examined for married women with rheumatoid arthritis (RA) who differ in the quality of their relationships with their spouses. METHODS: Measures of interpersonal events were collected weekly for 12 weeks and related to disease activity through a comparison of clinician ratings and immune markers taken at baseline and during a highly stressful week for 20 RA patients. Individual differences in marital relationship variables and illness characteristics were used to predict group differences in how stress affected disease activity. RESULTS: Significant elevations in total T cell activation (DR + CD3 cells), soluble interleukin-2 receptor (sIL-2R), and clinician's global ratings of disease activity were found during a week of significant interpersonal stress. However, women with better spousal relationships did not show increases in disease activity following an episode of interpersonal stress. In addition, patients taking low-dose prednisone showed greater reactivity to stress than patients not currently using glucocorticoid treatment. CONCLUSION: The results are consistent with the hypothesis that disease activity in RA increases following increases in interpersonal stress and that women with stronger marital relationships were less vulnerable to those stressors.

Adult↗
PubMed1998

(Latent) transforming growth factor beta in liver parenchymal cells, its injury-dependent release, and paracrine effects on rat hepatic stellate cells.

Cultured parenchymal liver cells (PC) were recently recognized to contain (latent) transforming growth factor beta (TGF-beta) while the expression of TGF-beta mRNA remains controversial. This study was designed to analyze PC in different microenvironments (liver in situ, highly purified, isolated, and cultured PC) regarding the qualitative and quantitative content of mature and latent TGF-beta protein (immunostainings, enzyme-linked immunosorbent assay [ELISA], and enzyme-labeled fluorescence [ELF] technique). The results were compared with its gene expression (reverse-transcription polymerase chain reaction [RT-PCR]). In all microenvironments, PC contained latent TGF-beta, which was partially activated after cell isolation and culture. The amount of total TGF-beta (mature plus latent) of latency-associated peptide (LAP) and of latent TGF-beta binding protein (LTBP) were shown to decrease during culture. In contrast, TGF-beta2 and TGF-beta3 mRNA and LTBP-1 and -3 mRNA expression were first detectable after culture. Permeabilization of cell membranes in whole liver and of isolated PC with streptolysin O or carbon tetrachloride, respectively, released TGF-beta, a part of which was integrated in the large latent complex as estimated by analytical gel filtration chromatography. The TGF-beta released by damaged PC induces paracrine effects on hepatic stellate cell cultures. It stimulates hyaluronan synthesis and antagonizes the effect of mitogenic factor(s) of PC on [3H]thymidine incorporation. The results strongly suggest that the main part of hepatocellular TGF-beta is not generated by de novo synthesis but from uptake into the liver in vivo. The immunodetection of preexisting mature TGF-beta after isolation of the cells is probably caused by intracellular activation of latent TGF-beta. The injury-dependent discharge of TGF-beta from PC might be an important mechanism for initiation and perpetuation of various forms of chronic human liver diseases.

Animals↗
PubMed1998

Analysis of the expression pattern of the latent transforming growth factor beta binding protein isoforms in normal and diseased human liver reveals a new splice variant missing the proteinase-sensitive hinge region.

Latent transforming growth factor beta binding protein (LTBP), a component of the extracellular matrix (ECM) of various tissues, is important for the secretion of TGF-beta and, furthermore, for the storage of TGF-beta in ECM. The proteolytic cleavage of LTBP is assumed to be the prerequisite for the activation of TGF-beta. We investigated the mRNA expression pattern of the three LTBP isoforms (LTBP-1, -2, -3) and the protein distribution of the components of the large latent TGF-beta complex, namely LTBP-1 and -2, latency-associated protein (LAP), and TGF-beta, in human liver using reverse-transcription polymerase chain reaction (RT-PCR) and immunohistochemical alkaline phosphatase anti-alkaline phosphatase (APAAP) staining. Parts of explanted livers diagnosed as hepatitis B, hepatitis C, primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC) and normal liver tissue were examined. LTBP transcripts were detected in the same manner in all liver specimens. Interestingly, we found a new splice variant of LTBP-1 (LTBP-1D), in which the sequence coding for the proteinase-sensitive hinge region is deleted. The corresponding parts of the human LTBP-2 and LTBP-3 cDNA coding for the hinge region were sequenced and show neither similar proteinase cleavage sites nor deleted cDNA sequences. The proposed proteinase cleavage site of mouse LTBP-3 seems not to be conserved in the human LTBP-3 gene. By immunohistochemistry, LTBP-1, -2, and LAP were detectable in normal and diseased livers and showed a different staining pattern for both LTBP isoforms. By contrast, TGF-beta showed a spotted staining pattern in diseased livers only, predominantly in the area of parenchymal cells that are close to fibrotic tissue. This strongly suggests the release of active TGF-beta from preexisting latent complexes. The LTBP-1D splice variant, which is probably less sensitive against proteolytic degradation and therefore may protect TGF-beta from activation, may have importance for modulating the biological activity of TGF-beta in normal and diseased liver.

Amino Acid Sequence↗
PubMed1998

Transformation-dependent susceptibility of rat hepatic stellate cells to apoptosis induced by soluble Fas ligand.

Cytokine-driven activation of hepatic stellate cells (HSC) in tissue injury and inflammation is a key pathogenetic event in liver fibrogenesis leading to an expanded pool of matrix producing myofibroblasts (MFB) which represent the transformed counterpart of HSC. We hypothesize that expansion of the pool of MFB might also be accomplished by modulation of apoptosis, which plays an opposite and complementary role to mitosis in the cellular homeostasis. We characterized the susceptibility of HSC in primary culture and of MFB in secondary culture to apoptosis induced by the soluble Fas ligand (sFasL) and related the effects to the expression levels of Fas (APO-1/CD95) and some major proapoptotic and contra-apoptotic protooncogenes. MFB showed a dose-dependent apoptotic reaction upon exposure to sFasL as evidenced by a strong increase of nucleosomal DNA fragments, loss of cellular DNA, positive TUNEL reaction, and annexin staining. The effect was found only if protein synthesis (cycloheximide) or RNA synthesis (actinomycin D) were arrested. HSC maintained for various times in primary culture were completely resistant to sFasL in combination with cycloheximide, but in late primary cultures (day 7 onward) an increasing susceptibility to sFasL-mediated apoptosis was developed. By semiquantitative reverse-transcriptase polymerase chain reaction (RT-PCR) analysis and alkaline phosphatase-anti-alkaline phosphatase staining Fas receptor was identified both in HSC and MFB at comparable expression levels. The expression of the contra-apoptotic protooncogenes bcl-2 and bcl-xl was found to be much stronger in early HSC than in late HSC and MFB as shown by ribonuclease protection assay. The expression of bcl-2 was additionally confirmed by semiquantitative RT-PCR and immunoblotting. Proapoptotic bax was found in comparable quantities at the RNA level in HSC and MFB but at the protein level MFB showed increased bax expression. It is concluded that transformation of HSC to MFB is paralleled by an increasing sensitivity to sFasL-mediated apoptosis, which might be related to a strong decrease of bcl-2 and bcl-xl expression, leading to a preponderance of proapoptotic gene expression in MFB. Modulation of apoptotic susceptibility of transforming HSC could be an important complementary pathway in the pathogenesis of fibrosis.

Animals↗
PubMed1998

Simultaneous continuous measurement of pO2, pCO2, pH and temperature in brain tissue and sagittal sinus in a porcine model.

INTRODUCTION: The clinical use of brain tissue oxygen measurement in patients with severe head injury is increasing. It is important to compare the findings in brain tissue with cerebrovenous blood oximetry, to obtain normal values and to find out limitations of the method. We evaluated a newly available multisensor probe simultaneously in the brain tissue and in the sagittal sinus in a porcine animal model. METHODS: We placed the Paratrend 7-probe (BSL, High Wycombe, UK) in the left frontoparietal white matter and measured pO2 (PtiO2), pCO2 (ptiCO2), pH and temperature while simultaneously measuring these parameters (pcvO2, pcvCO2) in the sagittal sinus in 7 pigs under general anaesthesia during oxygen enhancement. RESULTS: The relation between oxygen increase in brain tissue and in the sagittal sinus showed a coefficient of correlation (CCmean) rmean = 0.96. The quantitative response in brain tissue was much more sensitive than in the sinus. A close correlation between pCO2 in brain tissue and sagittal sinus and the increase of the inspired oxygen was seen: CC ptiCO2 to arterial oxygen pressure (paO2) - rmean = 0.67, CC pcvCO2 to paO2 - rmean = 0.88. CONCLUSIONS: Measuring partial oxygen pressure in brain tissue is more responsive to physiological variations, and the absolute values are more sensitive than oxygen measurement in the cerebrovenous compartment. This is important for interpreting measured values and introducing new coefficients for patient monitoring.

Acid-Base Equilibrium↗
PubMed1998

Validating of a transoesophageal ultrasonic-Doppler-probe to the detection of air in the venous blood.

OBJECTIVES: The aim of this study was to compare the sensitivity of a newly applied transoesophageal ultrasonic Doppler sensor for detection of air with the traditional precordial ultrasonic Doppler sensor in clinical use. METHODS: We studied 16 patients undergoing neurosurgical procedures in a sitting position. Two ultrasonic Doppler devices were compared as to their ability to detect venous air embolisms (VAE): transoesophageal (ODM II, co. Abbott) versus a precordial ultrasonic Doppler sensor (Parks Medical Electronics Inc.). After establishing general anaesthesia and endotracheal intubation, we applied an ultrasonic Doppler sensor to the right sternal border of the patient's chest and inserted an ultrasonic Doppler probe into the oesophagus. With the patient in the sitting position, microparticularly d-galactose was injected to verify the efficacy of both ultrasonic Doppler devices. RESULTS: Using ODM II by positioning the probe toward the azygos vein, a dosage of 1 ml microparticularly d-galactose was detected in every patient. When adjusting the ODM II-probe on the right myocardial wall or using the precordial ultrasonic Doppler sensor, the administration of microparticularly d-galactose was detected by the devices in only 11 patients. CONCLUSIONS: This study demonstrates that a transoesophageal ultrasonic Doppler sensor (ODM II) is more efficient than the precordial ultrasonic Doppler sensor for monitoring patients who are at risk of VAE by sonification of the azygos vein.

Air↗