Effects of temperature gradient reduction in three different carbon dioxide absorbents.

BACKGROUND AND OBJECTIVE: Temperature gradients in CO2 absorbents may locally increase the water content by condensation. We hypothesized that temperature gradient reduction (TGR) would prevent increased water content, thus preserving the reactivity of the CO2 absorbent and thereby increasing its time to exhaustion (longevity). The purpose of this study was to compare the effects of TGR on the longevity of CO2 absorbent with three different types of CO2 absorbents. METHODS: We constructed a novel TGR canister. Experiments were conducted using three different types of CO2 absorbents: Drägersorb 800 Plus (D800), Drägersorb Free and Amsorb Plus. One kilogram of fresh CO2 absorbent of each type was placed into two types of canister: the conventional control canister (n = 6) and the TGR canister (n = 6). RESULTS: In the case of Drägersorb Free, the TGR canister most effectively and specifically prevented local increase in water content of the CO2 absorbent and markedly increased the longevity (30% increase) compared with the control canister. In the case of Amsorb Plus, the TGR canister also prevented local excessive water content, but the increase in longevity was smaller (17% increase). In the case of D800, the TGR canister markedly increased the longevity (27% increase), but its prevention of local excessive water content was smaller. CONCLUSIONS: TGR is a useful method to prevent local increase in water content and improve the longevity of CO2 absorbent. The effectiveness of TGR on longevity and water content changes varied in the different types of CO2 absorbent.

Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation.

Cerebral injury is a critical aspect of the management of patients in intensive care. Pathological conditions induced by cerebral ischemia, hypoxia, head trauma, and seizure activity can result in marked residual impairment of cerebral function. We have investigated the potential mechanisms leading to neuronal cell death in pathological conditions, with the aim of discovering therapeutic targets and methods to minimize neuronal damage resulting from insults directed at the central nervous system (CNS). Over the years, deeper understanding of the mechanisms of neuronal cell death has indeed evolved, enabling clinical critical care management to salvage neurons that are at the brink of degeneration and to support recovery of brain function. However, no substantial breakthrough has been achieved in the quest to develop effective pharmacological neuroprotective therapy directed at tissues of the CNS. The current situation is unacceptable, and preservation of function and protection of the brain from terminal impairment will be a vital medical issue in the twenty-first century. To achieve this goal, it is critical to clarify the key mechanisms leading to neuronal cell death. Here, we discuss the importance of the calcineurin/immunophilin signal transduction pathway and mitochondrial involvement in the detrimental chain of events leading to neuronal degeneration.

Calcium-induced generation of reactive oxygen species in brain mitochondria is mediated by permeability transition.

Mitochondrial uptake of calcium in excitotoxicity is associated with subsequent increase in reactive oxygen species (ROS) generation and delayed cellular calcium deregulation in ischemic and neurodegenerative insults. The mechanisms linking mitochondrial calcium uptake and ROS production remain unknown but activation of the mitochondrial permeability transition (mPT) may be one such mechanism. In the present study, calcium increased ROS generation in isolated rodent brain and human liver mitochondria undergoing mPT despite an associated loss of membrane potential, NADH and respiration. Unspecific permeabilization of the inner mitochondrial membrane by alamethicin likewise increased ROS independently of calcium, and the ROS increase was further potentiated if NAD(H) was added to the system. Importantly, calcium per se did not induce a ROS increase unless mPT was triggered. Twenty-one cyclosporin A analogs were evaluated for inhibition of calcium-induced ROS and their efficacy clearly paralleled their potency of inhibiting mPT-mediated mitochondrial swelling. We conclude that while intact respiring mitochondria possess powerful antioxidant capability, mPT induces a dysregulated oxidative state with loss of GSH- and NADPH-dependent ROS detoxification. We propose that mPT is a significant cause of pathological ROS generation in excitotoxic cell death.

Spinal cord mitochondria display lower calcium retention capacity compared with brain mitochondria without inherent differences in sensitivity to cyclophilin D inhibition.

The mitochondrial permeability transition (mPT) is a potential pathogenic mechanism in neurodegeneration. Varying sensitivity to calcium-induced mPT has been demonstrated for regions within the CNS possibly correlating with vulnerability following insults. The spinal cord is selectively vulnerable in e.g. amyotrophic lateral sclerosis and increased mPT sensitivity of mitochondria derived from the spinal cord has previously been demonstrated. In this study, we introduce whole-body hypothermia prior to removal of CNS tissue to minimize the effects of differential tissue extraction prior to isolation of spinal cord and cortical brain mitochondria. Spinal cord mitochondria were able to retain considerably less calcium when administered as continuous infusion, which was not related to a general increased sensitivity of the mPT to calcium, its desensitization to calcium by the cyclophilin D inhibitor cyclosporin-A, or to differences in respiratory parameters. Spinal cord mitochondria maintained a higher concentration of extramitochondrial calcium during infusion than brain mitochondria possibly related to an increased set-point concentration for calcium uptake. A hampered transport and retention capacity of calcium may translate into an increased susceptibility of the spinal cord to neurodegenerative processes involving calcium-mediated damage.

Usefulness of galvanic skin reflex monitor in CT-guided thoracic sympathetic blockade for palmar hyperhidrosis.

Computed tomography (CT)-guided thoracic sympathetic blockade with ethanol was performed while monitoring sympathetic nerve activity, with an alternating current (AC) galvanic skin reflex (GSR) monitor, in a patient with palmar hyperhidrosis in whom endoscopic thoracic sympathectomy was impossible because of pleural adhesion. Sweating was suppressed after the thoracic sympathetic blockade, and the monitor showed a significant increase in skin resistance. The effect of sympathetic blockade could be evaluated directly and in real time using a GSR monitor.

[Molecular mechanism of ischemic brain injuries and perspectives of drug therapies for neuroprotection].

Ischemic brain injury is a critical condition in the management of patients during anesthesia and intensive care. It is not rare that pathological conditions such as cerebral ischemia, head trauma and low oxygen result in marked impairment of cerebral function, even if the patient's life is saved. We sometimes encounter sudden changes in a patient's condition not only during anesthesia, but also in intensive care unit with transient low-oxygen and ischemic conditions accompanying serious shock. We have been studying the mechanisms to counteract pathological conditions leading to neuronal cell death that have been exposed to such emergency conditions, and to discover therapeutic methods to minimize the brain damage after insult. With advances in the understanding of the mechanism of neuronal cell death, technology in intensive care for salvaging neuronal cell that are at the brink of death and for recovery of brain function has progressed. However, a breakthrough has not been achieved in the development of effective therapy. Protection of the brain from terminal impairment and preservation of function will be an important issue. To achieve this goal, it is critical to clarify the susceptible mechanisms causing ischemic brain damage. This report discusses the importance of the calcineurin/immunophilin signal transduction mechanism as a new mechanism that is involved in the induction of ischemic brain damage and refers the status-quo of cerebral protection by drug therapy.

[Evaluation of cancer pain--possibility of biomarkers].

The accurate assessment of pain is needed to control cancer pain and its treatment. Pain itself is subjective experience and is difficult to estimate quantitatively. Until now, there is no precise method to quantitate the cancer pain objectively. First, we show the tools to assess cancer pain by patient's description, including visual analogue scales, verval rating scales and numerical rating scales and so on. These scales have been used to evaluate the intensity of clinical pain, however they cannot assess the quality of cancer pain and only McGill Pain Questionnaire (MPQ) has specificity for the qualitative and quantitative properties of clinical pain. Molecular biological approach has been advanced in the neuroscience field to find the candidate of neuropathic pain. In this article, we would like to show the results of the proteomics research for neuropathic pain. We also tried to discuss about the biomarker and its possibility whether it can reflect cancer pain and effect of cancer treatment.

[General anesthesia for thyroplasty employing voice test].

BACKGROUND: We reported an anesthetic technique for thyroplasty employing voice test. Thyroplasty is performed to improve voice quality in patients with unilateral vocal cord paralysis. Correct displacement of the vocal cord is assessed by asking the patient to phonate. At this point all patients should have recovered from general anesthesia and cooperate to phonation, facilitating correct displacement of the vocal cords. METHODS: Anesthesia was induced with i.v. pentazocine 15-30 mg and continuous propofol infusion 10 mg x kg(-1) x hr(-1). The patients received propofol infusion 4-6 mg x kg(-1) x hr(-1) with spontaneous ventilation. At the point of correct displacement of the vocal cords, we stopped propofol infusion and all the patients woke up immediately and cooperated. After determining the voice propofol was given at a rate of 4-6 mg x kg(-1) x hr(-1). RESULTS: The average times of surgery and anesthesia were 98 +/- 23 min and 139 +/- 22 min, respectively. At the point of correct displacement of the vocal cords, the average time from the end of propofol infusion until awakening with good quality of recovery was 313 +/- 93 sec. No patients complained of pain during or after CONCLUSIONS: This anesthetic technique provided both optimal operating conditions and patient comfort without serious complications.

A comparison of frontal and occipital bispectral index values obtained during neurosurgical procedures.

UNLABELLED: We placed bispectral index (BIS) sensors on the frontal and occipital areas of neurosurgical patients and compared BIS values obtained from both areas during propofol/fentanyl anesthesia. BIS showed a strong correlation between frontal and occipital montages (r(2) = 0.96; P = 0.03). It may be valid to measure BIS with the sensor on the occipital area if required during frontal neurosurgical procedures. IMPLICATIONS: Bispectral values were positively correlated when recorded from frontal and occipital sensors in patients undergoing clipping of unruptured cerebral aneurysms while anesthetized with propofol and fentanyl.