[Evaluation of efficiency of ACD-CPR and STD-CPR; a multi-institutional study].

We compared the efficacy of ACD-CPR and STD-CPR based on 64 multi-institutional reports. No significant differences were observed in the rate of restoration of spontaneous circulation (ROSC) and in cardiopulmonary parameters during CPR using the two methods. There were 5 cases in which cardiopulmonary parameters improved after switching from STD-CPR to ACD-CPR and, eventually, in two of them spontaneous circulation was restored. In the ROSC cases of both groups, ETCO2 and values of SpO2, PaO2, and systolic BP at 30 minutes were higher than those of non-ROSC cases. ETCO2 never exceeded 20 mmHg in the non-ROSC cases, but it was higher in the ROSC cases. ACD-CPR is a good choice when trained persons are present or when extra hands are available to continue the CPR.

Activation of alveolar phospholipase A2 after hydrochloric acid aspiration in rats.

PURPOSE: The present study was carried out to determine phospholipase A2 (PLA2) activity in the bronchoalveolar lavage fluid (BALF) in rats subjected to HCI aspiration. MATERIALS AND METHODS: Rats were allocated into one of five groups. Groups H-1 and H-3 received instillation of HCI into lungs. Groups S-1 and S-3 received saline instead of HCI. Group C received no instillation. BAL was performed according to the protocol, that is, 1 hour after the instillation in groups H-1 and S-1, 3 hours after the instillation in groups H-3 and S-3, and arbitrarily in group C. Obtain BALF was analyzed for the protein concentration, PLA2 activity, and the molecular mass of PLA2. RESULTS: The protein concentration in BALF showed an increase in groups H-1 and H-3. PLA2 activity decreased in group H-1, but increased in group H-3, compared with groups S-1 and S-3, respectively. PLA2 in groups C and H-1 revealed a high molecular mass (HM), but that in group H-3 revealed a low molecular mass (LM). CONCLUSIONS: There is an increase in the alveolar LM-PLA2 at inflammatory phase after HCI aspiration, suggesting the pathophysiologic role of LM-PLA2 in the acute lung injury.

Hyperbaric nitrogen prolongs breath-holding time in humans.

UNLABELLED: Either an increase in PaCO(2) or a decrease in PaO(2), can affect respiratory stimulation through respiratory centers, thus influencing breath-holding time (BHT). This study was designed to determine whether and how hyperbaric air could influence BHT in comparison with hyperbaric oxygen in humans. We studied 36 healthy volunteers in a multiplace hyperbaric chamber. BHT, pulse oximeter, and transcutaneous carbon dioxide tension were measured at 1 and 2.8 atmosphere absolute (ATA) in two groups. Group A (n = 20) breathed air. Group O (n = 16) breathed oxygen with a face mask (5 L/min). BHTs were 108 +/- 28 s at 1.0 ATA and 230 +/- 71 s at 2.8 ATA in Group A, and 137 +/- 48 s at 1.0 ATA and 180 +/- 52 s at 2.8 ATA in Group O. Transcutaneous carbon dioxide tension in Group A (59 +/- 2 mm Hg) was higher than that in Group O (54 +/- 2 mm Hg) at the end of maximal breath-holding at 2.8 ATA. The prolongation of BHT in hyperbaric air is significantly greater than that in hyperbaric oxygen. IMPLICATIONS: Breath-holding time is significantly prolonged in hyperbaric air than it is in hyperbaric oxygen. The mechanism involves the anesthetic effect of nitrogen suppressing the suffocating feeling during breath-holding.

Effects of sevoflurane compared with those of isoflurane on arterial oxygenation and hemodynamics during one-lung ventilation.

PURPOSE: This study was designed to compare the effects of sevoflurane and isoflurane on Pao(2) and hemodynamic variables during one-lung ventilation (OLV) in surgical patients. METHODS: Twelve patients undergoing an esophageal procedure with thoracotomy for which a long period of OLV was required were studied using a randomized crossover design. Group 1 received 1.2% isoflurane from the induction of anesthesia until 30 min after starting OLV, and then received 1.7% sevoflurane during the remaining period. In group 2, the order of the anesthetics was reversed. All experimental procedures were performed in the left lateral decubitus position with the chest opened. Arterial and mixed venous blood gases and cardiac outputs were analyzed immediately before OLV, during OLV, and after resumption of two-lung ventilation (TLV). RESULTS: OLV produced lower PaO(2) and higher venous admixture (Q(s)/Q(t)) values than TLV. However, there was no significant difference between sevoflurane and isoflurane in PaO(2) or Q(s)/Q(t) during OLV. Other hemodynamic variables except for PVO(2) showed no significant differences between the anesthetics. CONCLUSION: The effects of sevoflurane on PaO(2) and the hemodynamic variables were similar to those of isoflurane during TLV and OLV in the lateral decubitus position.

Role of reactive oxygen in phospholipase A2 activation by ischemia/reperfusion of the rat kidney.

PURPOSE: To investigate the role of phospholipase A(2) (PLA(2)) in reperfusion injury of the kidney in an in vivo animal model, renal mitochondrial PLA(2) activity was measured under three different conditions. METHODS: Male Wistar rats (n = 72) anesthetized with pentobarbital underwent renal ischemia surgically for 45 min and were reperfused for the indicated time (renal ischemia/reperfusion). Treatments included reperfusion for various predetermined periods (phase 1), exposure to hyperbaric oxygen (phase 2), and administration of reactive oxygen species (ROS) scavenger (phase 3). Thereafter, each kidney was harvested, and mitochondrial PLA(2) activity was measured by a radioisotope technique. RESULTS: Ischemia/reperfusion resulted in time-related PLA(2) activation in the renal mitochondria up to 48 h of reperfusion after renal ischemia. Renal mitochondrial PLA(2) activity was further augmented by hyperbaric oxygen exposure prior to reperfusion, whereas administration of the ROS scavengers suppressed mitochondrial PLA(2) activity. CONCLUSION: These data suggest that ROS may play an important role in the in vivo activation of PLA(2) associated with renal ischemia/reperfusion.

Role of potassium channels in halothane-epinephrine arrhythmias.

It has been reported that antiarrhythmic drugs possessing the property of potassium channel blockade were most effective in preventing halothane-epinephrine induced arrhythmias. Recent attention has focused on ATP-sensitive potassium (K(ATP)) channels because of their contribution to the cardiovascular actions of volatile anesthetics. The present study was designed to evaluate whether K(ATP) channels or transient outward potassium channels (Ito) were involved in the mechanism of halothane-epinephrine arrhythmias in rat. Rats were anesthetized with halothane (1.5%), and the lungs were mechanically ventilated. The arrhythmogenic thresholds of epinephrine during halothane anesthesia were determined in 74 rats receiving saline or one of tested agents. The arrhythmogenic dose of epinephrine (ADE) was significantly increased by a K(ATP) channel opener, JTV506 (P < 0.01), and had a tendency to be increased by other K(ATP) channel openers, cromakalim, nicorandil, KRN2391 and Y 26763, but were not affected by a K(ATP) channel blocker, glibenclamide. The Ito blocker, 4-aminopyridine, also significantly increased the ADE. Epinephrine produced second-degree or complete atrioventricular block in 4 out of 7 rats receiving glibenclamide. These results suggest that Ito but not K(ATP) channels might be involved in the mechanism in producing halothane-epinephrine arrhythmias.

Phospholipase A2 is activated in the kidney, but not in the liver during ischemia-reperfusion.

Phospholipase A2 (PLA2) has been demonstrated to play an important role in the reperfusion injury of the kidney, gut, brain, heart and pancreas. This study was carried out to clarify whether PLA2 was involved in the ischemia-reperfusion injury of the liver. Rats were anesthetized and underwent laparotomy. They were allocated into one of 4 groups, i.e., the groups of renal ischemia (group RI), renal control (group RC), hepatic ischemia (group HI), and hepatic control (group HC). In group RI, the left renal pedicle was occluded for 1 hr, and the left kidney was removed after 1-hr reperfusion. In group HI, the portal and the hepatic artery supplying the left and middle lobes were clamped for 1 hr, followed by reperfusion. After predetermined periods of reperfusion up to 24 hr, the ischemic lobes were removed, homogenized and centrifuged. PLA2 activities in the mitochondrial fraction and the cytosolic fraction were measured with 14C-phosphatidylcholine (PC) and 14C-phosphatidylethanolamine (PE) as exogenous substrates. PLA2 activities of the both fractions in the kidney were significantly enhanced after 1-hr ischemia followed by 1-hr reperfusion. However, there was no enhancement of PLA2 activity of the either fraction in the group HI compared with the group HC. The results indicate that PLA2 is activated in the kidney but not in the liver during ischemia-reperfusion.

Anticholinesterase drugs stimulate phosphatidylinositol response in rat tracheal slices.

Some anticholinesterase (anti-ChE) drugs induce airway smooth muscle contraction. Whether anti-ChE drugs stimulate muscarinic receptors in airway smooth muscle as well as nicotinic receptors in neuromuscular junction is unknown. Since there is a direct relationship between phosphatidylinositol (PI) response and airway smooth muscle contraction induced by muscarinic agonists, we examined the effects of neostigmine, physostigmine, pyridostigmine, and edrophonium on PI response in the airway smooth muscle. The rat tracheal slices were incubated in Krebs-Henseleit solution containing LiCl and [3H]myo-inositol in the presence of carbachol, anti-ChE, or none of them. [3H]inositol monophosphate (IP1), which is a degradation product of PI response, was counted with a liquid scintillation counter. Inositol monophosphate accumulation was stimulated by neostigmine, physostigmine, and pyridostigmine in a dose-dependent manner, but was not affected by edrophonium. These increases were completely inhibited by atropine. The results suggest that neostigmine, physostigmine, and pyridostigmine stimulate PI response in the airway smooth muscle, which would cause bronchoconstriction, while edrophonium does not affect PI response.

Ischemia and reperfusion enhance ATF-2 and c-Jun binding to cAMP response elements and to an AP-1 binding site from the c-jun promoter.

The transcription factors controlling the complex genetic response to ischemia and their modes of regulation are poorly understood. We found that ATF-2 and c-Jun DNA binding activity is markedly enhanced in post-ischemic kidney or in LLC-PK1 renal tubular epithelial cells exposed to reversible ATP depletion. After 40 min of renal ischemia followed by reperfusion for as little as 5 min, binding of ATF-2 and c-Jun, but not ATF-3 or CREB (cAMP response element binding protein), to oligonucleotides containing either an ATF/cAMP response element (ATF/CRE) or the jun2TRE from the c-jun promoter, was significantly increased. Binding to jun2TRE and ATF/CRE oligonucleotides occurred with an identical time course. In contrast, nuclear protein binding to an oligonucleotide containing a canonical AP-1 element was not detected until 40 min of reperfusion, and although c-Jun was present in the complex, ATF-2 was not. Incubating nuclear extracts from reperfused kidney with protein phosphatase 2A markedly reduced binding to both the ATF/CRE and jun2TRE oligonucleotides, compatible with regulation by an ATF-2 kinase. An ATF-2 kinase, which phosphorylated both the transactivation and DNA binding domains of ATF-2, was activated by reversible ATP depletion. This kinase coeluted on Mono Q column chromatography with a c-Jun amino-terminal kinase and with the peak of stress-activated protein kinase, but not p38, immunoreactivity. In conclusion, DNA binding activity of ATF-2 directed at both ATF/CRE and jun2TRE motifs is modulated in response to the extreme cellular stress of ischemia and reperfusion or reversible ATP depletion. Phosphorylation-dependent activation of the DNA binding activity of ATF-2, which appears to be regulated by the stress-activated protein kinases, may play an important role in the earliest stages of the genetic response to ischemia/reperfusion by targeting ATF-2 and c-Jun to specific promoters, including the c-jun promoter and those containing ATF/CREs.

Histochemical demonstration of free radicals (H2O2) in ischemic brain edema and protective effects of human recombinant superoxide dismutase on ischemic neuronal damage.

A new histofluorescence method by HPAA (p-hydroxyphenyl acetic acid) for free radicals in the brain tissue was devised to study neuronal damage induced by ischemia. Cerebral ischemia was produced in rats by injection of plastic microspheres and arachidonic acid (AA) into the right carotid artery. The concentration of malondialdehyde (MDA; free radical) in cerebral cortex of aminotriazol (an H2O2-dependent inhibitor of catalase) treated rats 2 h after stroke was 6.33 times the level before infarction, while the concentration of MDA in h-r SOD (free radical-scavenging enzyme) treated rats 2 h after stroke was significantly lower than in untreated rats. The histochemical findings demonstrated marked H2O2 production around blood vessels occluded by microspheres in the cerebral cortex of the aminotriazole treated rats 2 h after stroke together with disruption of the BBB. Light microscopical findings demonstrated extensive edematous changes in the aminotriazole treated rats 2 h after stroke, while pathological damage in SOD treated rat brains was absent or minimal. We conclude that free radicals are formed during ischemia, and that AA appears to be a major source of activated oxygen radicals. The findings indicate that SOD is protective against ischemia-induced neuronal damage.

[Adrenal catecholamine releases during hypotension with continuous administration of calcium entry blockers and nitroglycerin].

We investigated the effect of nicardipine and diltiazem on adrenal catecholamine releases, and compared it with the effect of nitroglycerin in dogs. A 35% reduction in mean arterial pressure was achieved and maintained for 45 minutes. The dogs were observed until 60 minutes after the discontinuation of drug infusions. Adrenal catecholamine releases increased during hypotension with continuous administration of nicardipine, diltiazem and nitroglycerin, but they showed no significant differences between each drug. There was no more increase in adrenal catecholamine releases in spite of additional nicardipine administration. These results suggest that Ca2+ antagonist such as nicardipine directly inhibits the catecholamine releases from the adrenal glands.

[Long-term observation of individual erythrocyte sedimentation rate and its relation to other tests variation].

We have studied individual changes of erythrocyte sedimentation rate (ESR) in 30 so-called healthy subjects by examining them 2-4 times a year for 14-20 years. The results showed big differences in the same subjects during these period, and clearly different values were obtained between male and female groups. Furthermore, increased values were seen in accordance with aging in all except 3 cases. Even this aging effect showed remarkable individual differences, which, however, lead to a better correlation to aging than increase of gamma-globulin. In many cases with ESR values out of +/- 2 SD of their mean values, their other laboratory findings such as general peripheral blood tests and plasma protein tests etc., showed also the results out of +/- 2 SD of their mean values. These results show that ESR can be a useful tool as one of screening parameters.

[Intercostal nerve cross-anastomosis and DREZ-tomy in a patient with brachial plexus avulsion].

An 18-year-old male with a right brachial plexus injury caused by a motorcycle accident was admitted on October 13, 1988. A detailed examination revealed that the brachial plexus was totally injured. The axon reflex test suggested that the lesion sites were postganglionic in the C5 and C6 nerves, and preganglionic in the C7, C8 and Th1. On December 14, 1988, intercostal nerve cross-anastomosis was performed in the hope that a lost motor function of the right upper extremity could be restored as a first step. An electromyogram 6 months after this anastomotic operation demonstrated synkinesis between the biceps brachialis and the intercostal muscles during deep inspiration. Fifteen months after this operation, active voluntary muscle discharges which were higher than before in amplitude, were provoked. The right elbow flexion was gradually restored independently of respiration. On the other hand, intractable pain with a persistent severe tingling sensation appeared approximately one week after the injury on the lesioned upper extremity. The pain rapidly increased in severity. The DREZ-tomy from C5 to Th1 was performed on March 7, 1989. This has brought complete relief of the intractable pain. A brief discussion was given concerning some aspects of the brachial plexus avulsion and DREZ-tomy.

[Free and conjugated catecholamines in gastric and bile juice during surgical operations].

From 40 patients under surgical operation, gastric or bile juice was obtained to determine the possible excretion of free and conjugated catecholamine (CA) into the two kinds of juice. The patients were divided into normal renal function group and chronic renal failure group and former group was further divided into the dopamine (DA)-administered group and the non-DA-administered group. In the non-DA group with normal renal function, the gastric juice contained 0.30 +/- 0.11ng.ml-1 of free and 0.12 +/- 0.06ng.ml-1 of conjugated norepinephrine (NE) and also 0.09 +/- 0.07ng.ml-1 of free and 0.40 +/- 0.10ng.ml-1 of conjugated DA. In DA group, the gastric juice contained 2.01 +/- 0.41ng.ml-1 of free and 3.66 +/- 0.84ng.ml-1 of conjugated DA respectively. Significant differences in DA were observed between two groups. In the bile juice, the conjugated NE increased significantly from 0.15 +/- 0.05 ng.ml-1 to 1.24 +/- 0.34ng.ml-1 and also the conjugated DA increased significantly from 2.17 +/- 0.77ng.ml-1 to 21.33 +/- 5.23ng.ml-1 by infusion of DA at the rate of 2 micrograms.kg-1.min-1 for 197 +/- 48min. In chronic renal failure group, the conjugated NE and DA increased significantly to 1.04 +/- 0.27ng.ml-1 and 1.64 +/- 0.61ng.ml-1 respectively compared to that of normal renal group. It was confirmed that gastric juice and bile juice contain the free and conjugated CA during surgical operation and by the infusion of DA, free and conjugated DA are excreted into gastric juice and bile juice and also conjugated CA in the gastric juice from chronic renal failure group is increased.

[Effect of monoamine oxidase inhibitors on the concentrations of free and conjugated dopamine in rat small intestine and liver following exogenous dopamine administration].

In rats treated with MAO inhibitors, free and conjugated catecholamine concentrations in small intestine and liver following exogenous free dopamine (DA) administration at the rate of 2 micrograms.kg-1.min-1 for two hours were measured. Free and conjugated DA concentrations increased in both small intestine and liver following exogenous free DA administration. Free and conjugated DA concentrations of the tissue of the rat treated with MAO inhibitors were higher than that of the control group. These results suggest that transformation of free DA into conjugated DA is activated in the small intestine and liver of the rat treated with MAO inhibitors when exogenous DA is given.