Association of the time to first epinephrine administration and outcomes in out-of-hospital cardiac arrest: SOS-KANTO 2012 study

Objective

This study assessed the association between the timing of first epinephrine administration (EA) and the neurological outcomes following out-of-hospital cardiac arrests (OHCAs) with both initial shockable and non-shockable rhythms.

MRI and ultrasonography of atherosclerosis of the thoracic aorta and carotid arteries in elderly hypercholesterolemic patients]

In 53 elderly participants aged more than 60 the thoracic aorta and bilateral carotid arteries were observed with noninvasive techniques, MRI and ultra-sonography, in order to elucidate the relationship between hypercholesterolemia and atherosclerosis in the elderly. Hypercholesterolemic subjects were classified as group H (serum total cholesterol (TC) greater than 220 mg/dl), group H-I (220 mg/dl less than TC less than 250 mg/dl) and group H-II (TC greater than or equal to 250 mg/dl). Atherosclerotic changes of the thoracic aorta were observed in 46% of group H, 27% of group H-I, 60% of group H-II and 37% of normolipidemic subjects (group NL). Carotid atherosclerotic changes were observed in 19% of group H, 9% of group H-I, 27% of group H-II and 18% of group NL. In group H-I, the percentages of atherosclerotic changes in both thoracic aorta and carotid arteries were lower than those in group NL. However, atherosclerotic changes of thoracic aorta and carotid arteries were detected in 43% and 29% of the subjects showing higher apo B/Apo Al ratio than 1.0 among group H-I + NL (TC less than 250 mg/dl). These changes occurred in 32% and 13% of the subjects showing lower apo B/Apo Al ratio than 1.0 among the same groups. Namely, atherosclerotic changes of the thoracic aorta and carotid arteries were observed more frequently in the subjects showing a higher apo B/Apo Al ratio than 1.0 even if their serum cholesterol values were not higher than 250 mg/dl. We should use not only the serum cholesterol value but also the apo B/Apo Al ratio as an indicator to evaluate the roles of lipids in the development of atherosclerosis.     

CROMAKALIM SUPPRESSES HYPERTONIC SALINE-INDUCED RENAL VASOCONSTRICTION IN ANAESTHETIZED DOGS

1. Intrarenal arterial infusion of hypertonic saline (HS) transiently increased and then gradually reduced renal blood flow (RBF) in anaesthetized dogs. Glomerular filtration rate (GFR) but not filtration fraction decreased at the end of the infusion. 2. In the presence of a potassium channel opener cromakalim (0.3 μg/kg per min), HS infusion failed to reduce RBF; the initial increase in RBF was maintained throughout the infusion. Since cromakalim also prevented the decrease in GFR, HS infusion lowered filtration fraction. 3. The results suggest that cromakalim inhibits both pre-and postglomerular vasoconstriction induced by HS infusion.     

A case of heparin-induced thrombocytopenia that worsened preexisting cerebral infarction]

A 75-year-old man was admitted to our hospital with dysesthesia of the right lip, dysphagia and gait disturbance. He presented with right Wallenberg syndrome and brain MR image showed a fresh infarction in the right lateral medulla. Therapy with heparin and ozagrel sodium was started. For a time his symptom improved a little, but after 8 days he developed re-infarction, thrombocytopenia and DIC, while being treated with heparin for cerebral infarction. Heparin was discontinued, and these symptoms improved quickly. The clinical course and the positive anti-platelet factor 4-heparin complex antibody suggested that these symptoms were caused by heparin-induced thrombocytopenia (HIT). HIT should be included as a differential diagnosis for progression of ischemic stroke under heparin therapy.     

Malacoplakia of the bladder: Efficacy of enoxacine therapy

Malacoplakia of the urinary bladder was seen in a 69-year-old woman with haematuria. We firstly treated her with distigmine bromide, ascorbic acid and trimethroprim-sulfamethoxazole. Haematuria subsided but the lesion did not change after 6 weeks. Thereafter we tried enoxacine therapy. Eight weeks after the medication the tumorous leson disappeared. Bladder biopsy performed 4 months after the initiation of the treatment revealed predominantly granulation tissue. We can find no previous case treated successfully with long-term enoxacine.     

A case of adenocarcinoma of the nasal cavity associated with syndrome of inappropriate secretion of antidiuretic hormone(SIADH)

An inappropriate antidiuretic hormone secretion (SIADH) has been recognized as the cause of hypotonic hyponatremia, and the occurrence of this syndrome, accompanied by an ADH-producing adenocarcinoma in the nasal cavity, is reported. In February, 1987, a 50-year-old male, showing sights of delirium, disorientation, and irritability was admitted to the hospital. The patient was observed to be healthy, except for a neck lymphnode metastasis that was present up to the time of his hospitalization. The hyponatremia was incidentally found, although dehydration or intravascular volume depletion were not noted. These neuropsychiatric symptoms were considered to be associated with hyponatremia due to SIADH. He had had a partial maxillectomy, a neck dissection, and irradiation to the nose and nasal cavity 32 months earlier, and then underwent a surgical resection of the neck metastasis; he had a total of 10 other operations before the onset of the symptoms. Upon initial inspection, since neither an intracranial invasion nor a brain metastasis was found, we diagnosed that his symptoms were due to an autonomic disturbance caused by surgical and mental "stress". When he died of cardiac failure due to a mediastinal invasion 8 months after the onset of SIADH, tumor tissues was extirpated in an autopsy and was then cultured. In this manner, it was proved that the tumor cells had been producing ADH. This procedure clarified that the syndrome had resulted from an ADH-producing tumor of the nasal cavity.     

Relationship between the intestinal permeability to macromolecules and invasion of septicemia-inducing Escherichia coli in neonatal piglets.

The influence of age and diet on the invasion of septicemia-inducing Escherichia coli and the endocytotic activity of the small intestinal epithelium were examined in colostrum-deprived conventional and gnotobiotic piglets orally infected with E. coli 078. The piglets infected at birth and the animals fed glucose-amino acids solution and infected at 3 days after birth soon suffered from septicemia caused by the invasion of E. coli 378. The piglets fed artifical milk and infected at 3 days after birth, however, showed resistance to the invasion of E. coli in the absence of passively acquired serum gamma globulin. The endocytotic activity of the small intestinal epithelium was more intense in the former than in the latter piglets. Some of the ileal epithelial cells of the piglets infected at birth contained organisms, although these cells were morphologically intact and showed intense endocytosis. The present results suggest that the intestinal permeability to macromolecules, which depends on the endocytotic activity of the small intestinal epithelium, might predispose neonatal piglets to colisepticemia.     

Cytotoxic effects of 2,6-di-tert-butyl-4-methylphenyl N-methylcarbamate (terbutol) herbicide on hepatocytes and mitochondria isolated from male rats

The cytotoxic effects of 2,6-di-tert-butyl-4-methylphenyl N-methylcarbamate (terbutol) and its major metabolites were investigated in freshly isolated rat hepatocytes. Terbutol and its metabolite, especially 2,6-di-tert-butyl-4-methylphenyl carbamate (N-demethylterbutol), at a concentration of 1.0 mM resulted in a time dependent cell killing accompanied by losses of intracellular ATP, protein thiols, and glutathione (GSH) and the accumulation of oxidized GSH. Supplementation of the hepatocyte suspension with 5 mM N-acetylcysteine, a precursor of intracellular GSH, inhibited the cytotoxicity of N-demethylterbutol. In mitochondria isolated from rat liver, terbutol and its metabolites impaired respiration related to oxidative phosphorylation and the potency of their toxicity is associated with impairment of mitochondrial respiration. These results indicate that N-demethylterbutol is the most cytotoxic followed by terbutol and other metabolites, and that both the mitochondrial respiratory system and protein thiols are important targets for these compounds.     

Extraosseous metastases of hepatocellular carcinoma detection and therapeutic assessment with Tc-99m PMT SPECT

Owing to recent advances in imaging technology and radiologic intervention, survival rates in patients with hepatocellular carcinoma have improved markedly. However, such prolonged survival has resulted in an increase in extrahepatic metastases. Tc-99m (Sn)-N-pyridoxyl-5-methyltryptophan (Tc-99m PMT), developed for hepatobiliary scintigraphy, has been used to visualize extrahepatic metastases, with most related reports limited to osseous metastases. The authors report two cases of hepatocellular cancer presenting as a hypopharyngeal metastasis and intraperitoneal dissemination along the tract of a fine-needle biopsy. Lesions undetectable on planar imaging could be visualized by Tc-99m PMT SPECT.     

Haemodynamic responses to the intubating laryngeal mask and timing of removal

We determined (a) the haemodynamic responses to intubating laryngeal mask (ILM) airway insertion/intubation and removal in anaesthetized patients, and (b) whether the timing of ILM removal influences these responses. One-hundred and twenty patients without cardiovascular disease were studied. ILM airway insertion/intubation was 5 min after induction with propofol 2 mg kg(-1) and maintenance of anaesthesia with sevoflurane 2% in oxygen 33% and nitrous oxide. Patients were randomly assigned for removal of the intubating laryngeal mask airway at 1, 3 and 5 min after successful intubation. Systolic and diastolic arterial pressures and heart rate were recorded preinduction (baseline), before ILM airway insertion/intubation, at 1-min intervals after insertion/intubation, and at 1-min intervals for 5 min after ILM removal. ILM insertion was successful at the first attempt in all patients, but 46 patients required more than one intubation attempt. Compared with baseline values, there were no increases in systolic or diastolic arterial pressure, but there was an increase in heart rate 1 min after ILM insertion/intubation (9%, P<0.001) and 1 min after ILM removal (8%, P<0.01). There was a significant increase in systolic and diastolic pressures and heart rate 1 min after ILM insertion/intubation (30%, 31% and 15%; all: P<0.002) compared with before ILM insertion/intubation values and 1 min after ILM removal (9%, 8% and 7%; all P<0.05) compared with 1 min after ILM insertion/intubation values. Removal of the ILM 1 min after successful intubation resulted in higher arterial pressure compared with removal at 3 min (systolic arterial pressure 10% higher for 1 min, P = 0.01) and 5 min (systolic arterial pressure 10-23% higher for 3 min, P<0.01; diastolic arterial pressure 10-20% higher for 4 min, P>0.02), but there were no differences in heart rate between groups. Systolic and diastolic arterial pressures were greater if more than one intubation attempt was required. Early removal or multiple intubation attempts did not exceed baseline haemodynamic values. We conclude that ILM insertion/intubation and removal in anaesthetized patients produces little or no haemodynamic response, even if multiple intubation attempts are required. The timing of removal exerts a small, but clinically unimportant influence on these responses.