Practical use of the central venous access port for contrast-enhanced CT: comparison with peripheral intravenous access regarding enhancement and safety.

AIM: To evaluate the efficacy of using the central venous (CV) port compared with peripheral intravenous access for contrast-material injection for contrast enhancement during the portal venous phase. MATERIALS AND METHODS: Patients were divided into three groups: CV delay, CV routine, and peripheral access (PA) groups. Patients in the CV delay group underwent injection in the arm-down position with an additional delay, while those in the CV routine and PA groups underwent injections with the routine injection protocol for portal venous phase imaging. Contrast enhancement was evaluated by measuring the mean radiodensity (Hounsfield units) values for the aortic arch, abdominal aorta, inferior vena cava, portal vein, and spleen. The peak injection pressure was recorded and compared among the three groups. RESULTS: No complications related to power injection were observed during 119 contrast-material injections performed using the CV port device. The CV delay group showed significantly lower radiodensity values than the PA group (165.7 ± 20.1 versus 181 ± 19 HU [p<0.01] for the portal vein); however, no significant differences in mean radiodensity values were observed between the CV routine and PA groups (p>0.05). The median peak injection pressure was 73.5, 67, and 47 psi in the CV delay, CV routine, and PA groups, respectively (p<0.01). CONCLUSION: The CV port can be used for safe contrast-material injection while maintaining contrast enhancement on portal venous phase comparable to that achieved with peripheral intravenous access.

Adenosine and adenosine uptake inhibitors potentiate the neuromuscular blocking action of rocuronium mediated by adenosine A(1) receptors in isolated rat diaphragms.

BACKGROUND: Adenosine, which pre-junctionally modulates neuromuscular transmission, and adenosine uptake inhibitors, which increase extracellular adenosine, have been used clinically. We investigated the effects of adenosine, dipyridamole and midazolam on the neuromuscular blocking action of rocuronium. METHODS: Isometric twitch tensions of rat nerve-hemidiaphragm preparations elicited by indirect (phrenic nerve) supra-maximal stimulation at 0.1 Hz were evaluated (n=6 in all data). RESULTS: Pre-treatments with adenosine (0.1 and 1 microM) and CCPA (1 microM, adenosine A(1) receptor agonist), but not that with CGS21680 (0.5 microM, A(2) receptor agonist), shifted the rocuronium concentration-twitch tension curves to the left and decreased the rocuronium concentration for 50% twitch depression (IC(50)) compared with the control (P<0.01). The leftward shift induced by 1 microM adenosine was inhibited by pre-treatments with theophylline (50 microM, non-selective adenosine receptor antagonist) and DPCPX (0.2 microM, A(1) receptor antagonist) but not by that with DPMA (5 microM, A(2) receptor antagonist). Pre-treatments with dipyridamole and midazolam, adenosine uptake inhibitors, shifted the curve to the left and decreased IC(50) at supra-therapeutic concentrations (10 and 2.5 microM, respectively) but not at clinical concentrations (2 and 0.5 microM, respectively), and the leftward shifts were inhibited by pre-treatment with DPCPX (0.2 microM). CONCLUSION: The results indicate that adenosine potentiates the neuromuscular blocking action of rocuronium mediated by adenosine A(1) receptors and that supra-therapeutic concentrations of dipyridamole and midazolam also potentiate the action of rocuronium by increasing endogenous adenosine concentration.

Male-specific function of Dmrt7 by sexually dimorphic translation in mouse testis.

Dmrt7 is known to be an essential gene for spermatogenesis but not for oogenesis despite mRNA expression in both testis and ovary. In this study, we examined further expression of Dmrt7 transcript and protein. Northern blot and RT-PCR analysis revealed that there was an alternative splicing variant possessing the entire sequence of intron 1 in adult testis (intron 1 variant), in addition to the mature form of mRNA. In fetal ovary, the intron 1 variant was not expressed whereas the fully spliced form of mRNA was expressed. Immunohistochemical analyses demonstrated that DMRT7 protein was present only in spermatocytes of adult testis but not in fetal ovary. In situ hybridization analyses revealed that the fully spliced form of Dmrt7 mRNA as well as the intron 1 variant were expressed in spermatogonia, spermatids and Sertoli cells in addition to spermatocytes. We also found that poly(A) tails of Dmrt7 mRNA underwent modification of its length from 70 to 440 bp long. Unlike Arbp mRNA, the size variation of poly(A) tails was observed in immature testis in which spermatids were absent. In this study, we demonstrated that Dmrt7 had unique sexually dimorphic expression patterns in transcripts that associated with spermatocyte-specific translation, but not in ovary.

A woman who required long-term mechanical ventilation to treat limbic encephalitis during pregnancy.

We describe our experience with a woman who had severe non-herpetic acute limbic encephalitis at 20 weeks' gestation. Despite receiving mechanical ventilation for about 3 months because of impaired consciousness and frequent convulsions, she had a normal delivery and an uneventful recovery with no sequelae. The patient did not respond to treatment with antiviral agents. Anticonvulsant agents were given while monitoring plasma drug concentrations. Early treatment and the prevention of complications apparently contributed to good outcomes in the mother and child.

5,6-Dichloro-1-methylgramine, a non-toxic antifoulant derived from a marine natural product.

The laboratory culture of the barnacle, Balanus amphitrite has made it possible to supply cypris larvae for antifouling assays all year round. The settlement of cyprids obtained from cultured B. amphitrite was indistinguishable from cyprids reared from field-collected barnacles. In laboratory cyprid settlement assays of extracts from marine sessile organisms, antifouling activity was expressed as the 99% inhibitory concentration (IC99), and toxicity as the 30% lethal concentration (LC30). The lipophilic extract of the marine bryozoan, Zoobotryon pellucidum, which showed promising antifouling activity, yielded 2,5,6-tribromo-1-methylgramine (TBG) by bioassay-guided isolation. The inhibitory activity of TBG was 6 times as strong as that of bis-(n-butyltin)oxide (TBTO), while its toxicity to cypris larvae was one-tenth that of TBTO. A structure-activity relationship study with 155 indole derivatives led to the discovery of the non-toxic antifoulant candidates 5,6-dichlorogramine, 5-chloro-2-methylgramine, and 5,6-dichrolo-1-methylgramine (DCMG), the latter being selected as the antifouling paint ingredient for performance evaluation tests (panel tests) following the results of a preliminary safety tests. A silicone-based antifouling paint containing 5-10% of DCMG was prepared and tested in the field; the painted surfaces remained almost barnacle-free for 1.5 years similar to silicone coatings such as Biox. Since the leaching rate of DCMG from the paint surface could be controlled by the addition of an acrylic acid-styrene copolymer (ASP), the life of the antifouling performance is expected to be improved. Thus, an extremely non-toxic silicone-based antifouling paint containing DCMG is under development.

Left ventricular mechanical performance in elderly patients after induction of anaesthesia. A comparison of inhalational induction with sevoflurane and intravenous induction with fentanyl and propofol.

We investigated changes in left ventricular mechanical performance in 40 patients aged > 70 years in whom anaesthesia had been induced with sevoflurane or with fentanyl and propofol. The ratio of ventricular contractility to arterial properties, which reflects left ventricular performance, was estimated from the ratio of ventricular end-systolic elastance to effective arterial elastance. This ratio decreased after induction in both groups, the magnitude of the decrease being significantly greater in the fentanyl/propofol group than in the sevoflurane group. Decreases in mean arterial pressure after induction of anaesthesia in the two groups were similar, whereas the magnitude of the decrease in heart rate in the sevoflurane group was greater than that in the fentanyl/propofol group. Sevoflurane may therefore be preferable to fentanyl and propofol for induction of anaesthesia in elderly patients because of its lesser effect on left ventricular performance.

Severe paradoxical intracranial embolism and pulmonary emboli during hip hemiarthroplasty.

Both paradoxical intracranial embolism, an intracranial arterial embolism caused by venous embolic material that has passed through a right-to-left shunt, and pulmonary arterial embolism are life-threatening complications of joint arthroplasty. We report a case of severe paradoxical intracranial embolism and pulmonary embolism that occurred during hip hemiarthroplasty.

Lightwand intubation is associated with less hemodynamic changes than fibreoptic intubation in normotensive, but not in hypertensive patients over the age of 60.

PURPOSE: To compare the effects of the lightwand and fibreoptic techniques for intubation, neither of which require laryngoscopy, on hemodynamic responses associated with tracheal intubation in normotensive and hypertensive elderly patients. METHODS: Eighty-eight normotensive and hypertensive patients aged more than 60 yr were randomly allocated to either the lightwand (LN and LH group, n=22 in both) or the fibreoptic group (FN and FH group, n=22 in both). All intubations were performed after induction of anesthesia with fentanyl and propofol and muscle relaxation with vecuronium. Systolic and mean arterial pressures (SAP and MAP) and heart rate (HR) were recorded, and rate-pressure product (RPP) and the change from "before intubation" to "immediately after intubation" of each variable (triangle upMAP triangle up,HR and triangle upRPP) were calculated. RESULTS: In normotensive patients, significantly smaller triangle upMAP, triangle upHR and triangle upRPP were observed in the LN group than in the FN group (P <0.05). In hypertensive patients, no significant differences between the LH group and the FH group were found in triangle upMAP or triangle upHR, while values of mean RPP in both groups were less than 20,000. CONCLUSION: We conclude that the lightwand technique significantly attenuates hemodynamic changes following intubation in comparison with fibreoptic intubation in normotensive patients over the age of 60. Hemodynamic changes following intubation using the lightwand technique and the fibreoptic technique in hypertensive elderly patients are similar. However, both techniques are useful for intubation in hypertensive elderly patients in terms of RPP.

Involvement of capsaicin-sensitive fibers in spinal NMDA-induced glutamate release.

The activation of spinal NMDA receptors can evoke glutamate release through the production of nitric oxide (NO) within the spinal cord, resulting in pain-relating behavior. In this study, we investigated the involvement of capsaicin-sensitive primary afferents in this phenomenon using in vivo intrathecal microdialysis. Intrathecal NMDA perfusion evoked increases in the concentrations of NO metabolises and glutamate and in pain-related behavior in both neonatal capsaicin and vehicle-treated rats. Although the degrees of increase in NO metabolises in capsaicin- and vehicle-treated rats were not significantly different, capsaicin-treated rats showed significantly smaller increases in glutamate concentration and pain-related behavior than did vehicle-treated rats. Our results showed that glutamate release from capsaicin-sensitive primary afferent terminals is involved in spinal NMDA-induced pain.

Peripheral nitric oxide in carrageenan-induced inflammation.

Recent studies have suggested that nitric oxide (NO) peripherally produced by different nitric oxide synthase (NOS) isoforms contributes to edema formation and development of hyperalgesia. The present study was designed to examine the effects of NOS isoforms on NO release in carrageenan-induced inflammation at various time points. A microdialysis probe was implanted subcutaneously into the glabrous skin of hindpaws of Sprague-Dawley rats under pentobarbital anesthesia. After sample collection to obtain the basal level of the total amount of nitrite and nitrate (NO2-/NO3-), modified Ringer solution, a non-selective NOS inhibitor, NG monomethyl-L-arginine acetate (L-NMMA), or an iNOS inhibitor, aminoguanidine hemisulfate (AG) was perfused through the microdialysis probe. 2 mg of carrageenan was injected into the plantar surface of the probe-implanted hindpaw. Carrageenan was also injected in rats that had undergone sciatic nerve sectioning. Carrageenan significantly increased the dialysate concentrations of NO2-/NO3- for more than 8 h. L-NMMA suppressed the carrageenan-induced increase in NO2-/NO3- concentration. Although AG did not suppress the increase in NO2-/NO3- for the first 2 h after carrageenan injection, significant suppression of the increase in NO2-/NO3- was observed from 2.5 h after carrageenan injection. In the rats in which the sciatic nerves had been denervated, the increases in concentrations of NO2-/NO3- were completely suppressed up to 3 h and partially suppressed 4.5-8 h after carrageenan injection. The results of the current study show that carrageenan induces peripheral release of NO, the production of which is mediated by nNOS in the early phase and by both nNOS and iNOS in the late phase of carrageenan-induced inflammation.

[Anesthesia for tricuspid valve replacement after heart transplantation].

A 41 year old male patient had received heart transplantation in U.S. in 1993. When myocardial biopsy was performed in 1998, tendinous cords of the tricuspid valve were injured. Tricuspid regurgitation developed along with right heart insufficiency, and the patient was scheduled for tricuspid replacement. For induction of anesthesia, midazolam and fentanyl were used. After induction, both blood pressure and pulse rate were stable. During extracorporeal circulation, perfusion pressure was controlled at 70-80 mmHg, and the duration of cardio-pulmonary perfusion was about 90 minutes. For withdrawal from extracorporeal circulation, dopamine and dobutamine were used. The course was steady and normal after the withdrawal. In tricuspid valve replacement after heart transplantation, stabilized anesthetic course could be maintained using midazolam and fentanyl.

Analysis of T cell receptor V(beta) gene expression and clonality in bronchoalveolar fluid lymphocytes from a patient with chronic eosinophilic pneumonitis.

Chronic eosinophilic pneumonitis (CEP) is characterized by longstanding respiratory symptoms accompanied by a massive pulmonary eosinophil infiltration. T lymphocytes in bronchoalveolar lavage (BAL) from patients with chronic eosinophilic pneumonitis are considered to recognize unknown antigens. To analyze the pathogenesis of CEP, we examined the T cell receptor (TCR) repertoire and T cell clonotype of BAL lymphocytes and peripheral blood lymphocytes (PBLs) in a 66-year-old woman patient with CEP. The expression of TCR BV gene was analyzed by the family PCR method using specific primers for 20 TCR BV genes and BC gene. The clonotype of BAL and peripheral T cells was examined by the PCR-single-strand conformation polymorphism (SSCP) method. Functional sequences of some T cell clones were also carried out. A TCR repertoire of BAL T cells was heterogeneous as well as PBLs. However, SSCP analysis showed that distinct T cell clonotypes were detected in BAL T cells, TCR BV3, BV4, BV6, BV8, BV9, BV14, and BV18-positive T cell clones especially, expanded clonally in BAL from the patient. Sequencing analysis showed that GVD, LGG, RDXS, and SSG amino acid sequence motif were found in the CDR3 in lung-specific T cells. BAL-specific T cell clones accumulated in the patient with CEP. Thus, we can conclude that BAL T cells are induced by the antigen-driven stimulation and these cells might play a crucial role in the generation of CEP.

The effects of peripheral administration of a novel selective antagonist for prostaglandin E receptor subtype EP(1), ONO-8711, in a rat model of postoperative pain.

UNLABELLED: Mechanically evoked pain, also known as incident pain, induced by coughing or deep breathing after surgery leads to potentially devastating consequences. It is generally thought that the prostaglandin receptor- (especially, the receptor for prostaglandin E(2), EP receptor) mediated sensitization of sensory nerve fibers is a key contributor to the generation of hyperalgesia. We examined whether a peripherally administered novel selective EP(1) antagonist, ONO-8711, would be a potential analgesic for incision-induced mechanical hyperalgesia. We used a rat model of postoperative pain introduced by Brennan et al. (1). Withdrawal thresholds to punctate stimulation and response frequencies to nonpunctate mechanical stimulation were determined by using von Frey filaments applied adjacent to the wound and directly to the incision site of the hind paw, respectively. Mechanical hyperalgesia to punctate and nonpunctate stimuli was observed 2 and 24 h after the incision. ONO-8711 (2, 10, or 50 microg) or saline was administered subcutaneously into the hind paw on the ipsilateral side to the incision. ONO-8711 significantly (P < 0.01) increased the withdrawal thresholds to punctate mechanical stimulation and significantly (P < 0.01) decreased the response frequencies to nonpunctate mechanical stimulation in a dose- and time-dependent manner 2 and 24 h after the incision. We conclude that EP(1) receptor-mediated sensitization of sensory nerve fibers may contribute to the generation of mechanical hyperalgesia produced by incisional surgery, and that the EP(1) receptor antagonist ONO-8711 may be an option for treatment of postoperative pain, especially incident pain. IMPLICATIONS: The peripheral administration of an antagonist for EP(1) receptor that is a subtype of prostaglandin E receptors can inhibit the mechanical hyperalgesia induced by a surgical incision.

The involvement of adenosine neuromodulation in pentobarbital-induced field excitatory postsynaptic potentials depression in rat hippocampal slices.

We investigated the contribution of adenosine neuromodulation to mechanisms of pentobarbital-induced depression of excitatory synaptic transmission in vitro. Transverse hippocampal slices were prepared from brains removed from isoflurane-anesthetized male Wistar rats. Field excitatory postsynaptic potentials (fEPSPs), elicited by orthodromic electrical stimulation of Schaffer collateral at 0.05 Hz, were recorded from the CA1 region in oxygenated artificial cerebrospinal fluid. Amplitude of fEPSP was analyzed for assessing drug effects. Pentobarbital (100 microM) transiently depressed fEPSPs (P<0.01); i.e., fEPSP was initially depressed to approximately 60% of control and then recovered to approximately 80% of control. The fEPSP depression was partially suppressed by pretreatment with 50 microM aminophylline, a nonselective adenosine receptor antagonist, and 0.2 microM 3, 7-Dimethyl-1-propagylxanthine, an adenosine A(1) receptor antagonist (P<0.01 each). However, the fEPSP depression was not affected by pretreatment with 10 microM 8-cyclopentyl-1, 3-dipropylxanthine, an A(2) receptor antagonist, or 10 microM bicuculline, a gamma-aminobutyric acid (GABA) A receptor antagonist. The results indicate that adenosine neuromodulation through A(1) receptors and other undefined mechanisms, which are independent from GABAergic mechanisms, are involved in pentobarbital-induced depression of excitatory synaptic transmission.

Analgesic mechanisms of ketamine in the presence and absence of peripheral inflammation.

BACKGROUND: The studies on the mechanisms of ketamine antinociception have led to conflicting results. In this study, the authors investigated the contribution of supraspinal monoaminergic descending inhibitory system to ketamine analgesia for acute nociception and inflammation-induced hyperalgesia. METHODS: Male Sprague-Dawley rats were used. The paw withdrawal latencies to radiant heat stimuli were measured to assess the thermal nociceptive threshold. The analgesic effects of intrathecal or intraperitoneal ketamine were examined in the rats that received unilateral intraplantar carrageenan and in those that were untreated. In addition, it was examined whether pretreatment with intrathecal yohimbine or methysergide inhibited the analgesic effects of ketamine. Using an intrathecal microdialysis method, noradrenaline and 5-hydroxytryptamine concentrations in lumbar cerebrospinal fluid were measured after intraperitoneal ketamine in both saline- and carrageenan-treated rats. RESULTS: In the untreated rats, intraperitoneal but not intrathecal ketamine produced antinociceptive effects in a dose-dependent manner. Pretreatment with intrathecal yohimbine or methysergide inhibited these antinociceptive effects. Intraplantar carrageenan significantly reduced paw withdrawal latencies on the injected paw but not on the contralateral paw. Both intraperitoneal and intrathecal ketamine reversed the shortened paw withdrawal latencies on the injected side in a dose-dependent manner without any effects on the contralateral side. Neither yohimbine nor methysergide inhibited these antihyperalgesic effects. In analyses of monoamines, the magnitude of increase in monoamines after intraperitoneal ketamine was significantly smaller in the carrageenan-treated rats than in the saline-treated rats. CONCLUSION: These results demonstrated that ketamine produced antinociceptive effects through an activation of the monoaminergic descending inhibitory system, whereas, in a unilateral peripheral inflammation-induced hyperalgesic state, the monoaminergic system did not contribute to the antihyperalgesic effects of ketamine. The mechanisms of the antinociceptive and antihyperalgesic properties of ketamine are different.

Activation of peripheral NMDA-nitric oxide cascade in formalin test.

BACKGROUND: It has been suggested that peripheral glutamate and nitric oxide (NO) released by tissue-damaging stimuli play an important role in peripheral nociceptive transmission. This study was conducted to determine whether NO was released in the periphery after subcutaneous injection of formalin and whether the peripheral N-methyl-d-aspartate (NMDA)-NO cascade was activated. METHODS: During pentobarbital anesthesia, a microdialysis probe was implanted subcutaneously into the glabrous skin of both hind paws of Sprague-Dawley rats. After sample collection to obtain the basal level of NO metabolites (total amount of nitrite [NO2-] and nitrate [NO3-] [NO2--NO3-]), 5% formalin was injected into the plantar surface of the right hind paw during perfusion of the dialysis catheters with artificial cerebrospinal fluid (ACSF), the NO synthase inhibitor NG-monomethyl-L-arginine acetate, or the NMDA antagonist D,l-2-amino-5-phosphonovaleric acid through a microdialysis probe. Formalin also was injected in the animals that underwent sciatic nerve sectioning. In another series of experiments, NMDA was perfused through one probe. Samples for measurement of NO2--NO3- were collected and immediately analyzed using high-performance liquid chromatography. RESULTS: Subcutaneous formalin significantly increased the dialysate concentrations of NO2--NO3- (maximum increase 144 +/- 12% of baseline value 30 min after formalin administration; P < 0.05) on the side ipsilateral to the injection. Both NG-monomethyl-l-arginine acetate and D, l-2-amino-5-phosphonovaleric acid significantly (P < 0.05) suppressed the formalin-induced increases in NO2--NO3- concentration. In the rats with denervation of the sensory nerves, formalin did not change the NO2--NO3- concentration. In addition, NMDA perfusion significantly (P < 0.05) increased the concentrations of NO2--NO3-. CONCLUSION: The results of the current study show that subcutaneous formalin injection induces peripheral release of NO, the production of which is mediated by activation of NMDA receptors in the peripheral nervous system.

The effects of midazolam and ketamine on D-tubocurarine-induced twitch depression in septic rat diaphragm.

The aim of this study was to elucidate the effects of midazolam and ketamine on neuromuscular blockade induced by non-depolarizing muscle relaxants (NDMRs) under the condition of sepsis induced by panperitonitis. A CLP operation (laparotomy, cecal ligation, and puncture of the cecum; septic group) or sham laparotomy (sham group) was performed on rats under O2-isoflurane anesthesia. At 18 hours after the operation, isometric twitch tensions of rat nerve-hemidiaphragm preparations elicited by indirect or direct stimulation at 0.1 Hz were measured. Midazolam enhanced the dTc (1 microM)-induced twitch depression (p < 0.05) at a high concentration (10 microM) in the septic group but not in the sham group. Ketamine enhanced the dTc (1 microM)-induced twitch depression in the sham group (p < 0.01) but not in the septic group. Midazolam and ketamine had no effect on directly elicited twitch tensions in either group. The results indicate that sepsis facilitates the midazolam-induced enhancement of the neuromuscular blocking effect of dTc but, conversely, inhibits the ketamine-induced enhancement. Sepsis elicits manifold alterations in the influence of intravenous anesthetics and sedatives on NDMR-induced neuromuscular blockade.

Prevention by methylprednisolone of increased circulating tumor necrosis factor-alpha levels and lung injury associated with systemic inflammatory response syndrome due to intraperitoneal hyperthermia.

UNLABELLED: We previously demonstrated that intraperitoneal hyperthermic perfusion (IPHP), which is performed clinically as a treatment for patients with advanced gastrointestinal cancer, can lead to increased serum tumor necrosis factor-alpha (TNF-alpha), systemic inflammatory response syndrome (SIRS), and acute lung injury. Glucocorticoids inhibit the production and actions of TNF-alpha. We investigated whether pretreatment with methylprednisolone (MPS) may modulate serum TNF-alpha and lung injury in patients subjected to IPHP. Serum TNF-alpha was not detected in the patients pretreated with MPS, whereas serum TNF-alpha increased in the control patients (45.7 +/- 8.3 pg/mL, mean +/- SEM) after IPHP. Postoperative lung injury scores were significantly lower in patients pretreated with MPS than in the control patients (P < 0.001). IMPLICATIONS: Pretreatment with methylprednisolone attenuates the increase in circulating tumor necrosis factor-alpha and prevents lung injury in this systemic inflammatory syndrome due to intraperitoneal hyperthermic perfusion.