Purpose: We compared the penetration force of eight brands of 18-gauge intravenous catheters using an original experimental device. Differences in penetration force were examined for 20 catheters for each brand.
Method: The inner needles of the intravenous catheters were inserted into a 0.08-mm polyethylene film at a 30- or 45-degree penetration angle by a push-pull gauge moved by a motor at 4.5 mm/sec. until the outer catheter penetrated the film. Each intravenous catheter consisted of an inner needle and an outer catheter. Inner needles were divided into two groups according to tip grinding method: Lancet or Backcut. Catheter tips were classified in two designs: acute- and obtuse-tapering. We studied the impact of these inner needle grinding methods and catheter tip designs on penetration forces, and catheter damage was observed under an electron microscope.
Result: At a 45-degree penetration angle, the penetration force of inner needles ranged from 25 to 45 grams, while the penetration force of catheters ranged from 35 to 58 grams, with no obvious influence of inner needle tip grinding method or catheter tip design on penetration force. At a 30-degree penetration angle, penetration force was lower in catheters with an obtuse-tapering design; the penetration force was significantly higher (120 g) in Surflo^® catheters with acute-tapering design. All six Surflo^® catheters had visible tip damage under the electron microscope. The seven other brands of catheters showed no tip damage regardless of inner needle grinding method.
Conclusion: In clinical practice, the insertion angle for peripheral venipuncture is 30 degrees or less. Our results show that catheters with an obtuse-tapering tip design were better than those with an acute-tapering tip design. If an intravenous catheter with an acute-tapering tip is inserted into a vein at an obtuse angle, the catheter tip will be damaged, resulting in insertion failures.

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Since oxidative stress is reported to be one of the mediators of synthesis of heat shock protein 70 (HSP70) induced by hyperthermia, we investigated the effects of N-2-mercaptopropionyl glycine (MPG), a diffusible antioxidant, in in vivo rabbit model of heat stress (HS) preconditioning. Three groups of rabbits were studied: Group I, control rabbits treated with anesthetic alone; Group II, rabbits subjected to HS by raising core temperature to 42°C for 15 min; Group III, given MPG (50mg/kg/hr i.v.), beginning 30 min prior to HS and continued up to 15 min post HS. Twenty-four hours later, all animals were treated with 30 min of the left anterior descending coronary artery occlusion followed by 180 min of reperfusion under ketamine/xylazine anesthesia. Risk area was delineated by Evans blue and infarct size determined by tetrazolium staining. The risk area ranged from 59.3±5.8 % to 66.3±3.4 % with no significant difference among all the groups. Infarct size/area risk was 53.6±5.9 % in control rabbits, and decreased significantly to 26.7±4.3 % in the HS hearts. Treatment with MPG of HS rabbits resulted in a significant increase in the infarct size (48.6±11.8 %). The results show that prior HS significantly reduced infarct size (P<0.05) which was inhibited by MPG (P<0.01). Western blot analysis revealed significant synthesis of HSP70 in HS rabbit hearts and that synthesis was blocked with MPG. We conclude that oxidative stress is one of critical mediators of HS induced myocardial protection in vivo and trigger expression of HSP70.

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Severe cerebral acidosis has been reported to worsen cerebral ischemic injury. Recent works have suggested that apoptosis as well as necrosis can be observed following cerebral ischemia. Acidosis was reported to activate some kind of endonuclease, which may lead cells to apoptosis. Accordingly, cerebral acidosis may worsen cerebral ischemic injury by increasing apoptotic cell death. In this study, we evaluated whether the ratio of apoptotic cell death increased in proportion as the degree of acidosis progressed after hypoxic insult in neuronal cells. We utilized PC 12 cells, which are derived from rat phenochromocytoma. The cells were incubated in N-[2-hydroxyethyl] piperazine-N’-[2-ethanesulfonic acid]-buffered mediu, the pH of which was adjusted at 7.4, 6.8, 6.2, 5.6 or 5.0. Hypoxic insult was induced by filling the chamber with N₂. Eight, 24, 48 or 72 hours after incubation, cells were stained with Hoechst 33342 and propidium iodide and analyzed under a nonconfocal fluorescence microscope to distinguish whether cells were apoptotic or necrotic. The percentage of apoptosis at pH 6.2 was 9.4±2.9 and 19.9±7.5 % at 8 and 24 hours, which was slightly but significantly higher compared to pH 7.4 (3.1±1.5 and 12.7±5.1 %, respectively). After that, apoptosis was not enhanced by any degrees of acidosis. Acidosis below pH 5.6 increased the percentage of necrosis to more than 80 % during the entire period. Contrary to our expectation, apoptosis was slightly enhanced by moderate acidosis only in the early phase of hypoxic insult, while severe acidosis increased necrotic cell death during the total period of hypoxic insult. Accordingly, we propose that the main cause of aggravation of hypoxic neuronal damage by acidosis is enhancement of necrosis, whereas apoptosis may play only a small role.

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The prognosis of ventricular arrhythmia after myocardial infarction is fatal. Veughan Williams Class I drugs are usually selected to treat it, but in some cases they are not effective. In addition, Class I drugs are difficult to use for patients with poor cardiac function because of their negative inotropic effects. Class III drugs Nifekalant was effective for drug-resistant ventricular tachycardia after myocardial infarction in 3 cases. The drug does not suppress cardiac function, and is useful for drug-resistant ventricular arrhythmia in patient with poor cardiac function.

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Echocardiographic examination is useful in diagnosis of infective endocarditis, with transesophageal echocardiography (TEE) being more accurate than transthoracic echocardiography. However there are few reports how vegetation changes successively in TEE observation. And central nervous system involvement in conjunction with infective endocarditis typically emerges from septic embolism. The case we described suggests that observation of vegetation with TEE informs us the beginning of cerebral infarction. A 77-year-old woman with a history of third degree burn and diabetes mellitus was admitted to ICU with persistent fever, shortness of breath, and pneumonia. Transthoracic echocardiography detected no vegetation. On the second ICU day, blood culture was positive for methicillin resistant Staphylococcus aureus (MRSA). And on the third ICU day, TEE revealed oscillating mass on the mitral valve, and infective endocarditis was defined according to the Duke’s criteria. Head CT scan showed cerebral infarction. On the sixth ICU, TEE showed significant changes in vegetation size before and after sudden pupil dilation. TEE could demonstrate the cause of pupil dilation in this endocarditis patient without CT observation.

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