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Endotoxemia has been reported as a mechanism for the fatal sequela after heatstroke. Subsequent disseminated fungal infection in a heatstroke patient has been also described. Beta-D-glucan, a constituent of the fungal cell wall, is an early diagnostic measure for fungal infection. In a heatstroke case, we examined for the first time levels of serum beta-d-glucan and endotoxin. A 34-year-old man with a body temperature of 43.5 degrees C was admitted in a state of shock. Prior to the development of disseminated intravascular coagulopathy (DIC), a remarkable elevation of serum beta-D-glucan level to 116 pg/mL (normal level6.0 pg/mL) was revealed on the first day of admission. However, serum endotoxin was not detected when using a method that excluded beta-D-glucan contamination from endotoxin measurement (normal level1.0 pg/mL). This change of beta-D-glucan level was accompanied by a depressed neutrophil function, especially in phagocytosis of 34% (normal range 70-90%) but not in bacterocidal function (81% versus a normal range of 70-100%). After intensive care including continuous hemodiafiltration, the patient regained consciousness but remained ataxic due to cerebellar infarction, which might have resulted from DIC, and subsequent bilateral fungal oculitis were revealed 45 days after admission. This case report demonstrates the elevation of serum beta-D-glucan but normal endotoxin levels after heatstroke, which may prompt further study to re-examine the serum levels of endotoxin in such catastrophic insults.

The following parameters were monitored simultaneously in 15 dogs, in order to evaluate the efficacy of conventional CPR (C-CPR), new CPR (N-CPR), and open-chest CPR (O-CPR) on cerebral perfusion: arterial blood pressure (BP), central venous pressure (CVP), intrathoracic airway pressure, blood flow in carotid artery, intracranial pressure (ICP), sagittal sinus blood flow (sinus BF) and pressure (sinus P), and blood flow in cerebral cortex (cortical BF). The sinus blood flow was measured by the direct-method and with a cannulating electromagnetic flowmeter. The cortical blood flow was measured with a termocouple tissue flowmeter. Intracranial pressure was obtained by measuring subarachmoid cerebrospinal fluid pressure. Ventricular fibrillation was induced electrically. Chest compression and ventilation were always done manually in all cardiopulmonary resuscitation. The mean blood pressures during C-CPR, N-CPR and O-CPR were 52, 68 and 95 mmHg, respectively, and mean carotid blood flows per stroke were 36, 71 and 131% of the control values, respectively. The intracranial pressures were 30, 42 and 36 mmHg, respectively, giving the calculated cerebral perfusion pressures (BP-ICP) of 22, 27 and 60 mmHg, respectively. This should have been reflected in cerebral blood flow. Sinus blood flows/min were 18, 18 and 42%, and sinus blood flows per stroke were 55, 45 and 127% of control values, respectively; the differences between C-CPR and N-CPR were not significant. This was also true for cortical blood flow. From this we conclude that, firstly, N-CPR is not significantly better than C-CPR in cerebral perfusion because of its accompanying high intracranial pressure, secondly, O-CPR is far superior to the other two methods in respect of cerebral perfusion.

We have developed a new method producing total cerebral ischemia (TCI) in dogs; clamping ascending aorta with aorto-atrial bypass formation. Clamping ascending aorta provides TCI, the duration of which can be controlled up to the periods of 10 min. Beyond this interval, it is difficult to maintain TCI because of heart failure from high afterload. Blood outflow from left ventricle is completely obstructed except for coronary circulation which is small relative to the blood volume expelled from left ventricle, even if venous return to the heart is reduced. Aorto-atrial bypass formation during aortic clamping provides two distinctive advantages. First, adjusting aortic pressure in an appropriate level low enough not to overload myocardium but still high enough to maintain sufficient coronary blood flow is possible by regulating the blood flow through the bypass tubing, and secondly drug administration and blood volume control is possible through the tubing. These result in better preservation of myocardium, enabling longer TCI and longer survivals after TCI. We were successful in having up to 18 min of TCI with this method. Seventy-five percent of dogs of 12 min TCI and 40% of 15 min TCI survived 7 days, limit of experiment, after TCI, but no dogs of 18 min TCI survived for more than 3 days.