Global cerebral ischemia: effects of pentastarch after reperfusion.

There has been considerable interest in the use of synthetic hydroxyethyl starch macromolecules (e.g., pentastarch, a colloid used for intravascular fluid replacement) to reduce microvascular permeability and reperfusion injury after cerebral ischemia. A recent report found that hemodilution with pentastarch reduced brain injury and cerebral edema after temporary focal ischemia. We compared the effects of pentastarch versus 0.9% saline on brain edema after reperfusion in a model of temporary global ischemia in halothane-anesthetized rabbits. To ensure the validity of our model, we studied an additional group of animals in which we deliberately raised plasma osmolality with hypertonic saline (1.5%) in the expectation of finding a decreased brain water content at the conclusion of the experiment. Animals were hemodiluted to a hematocrit of 20% with normal saline (control group) (n = 9), pentastarch (n = 7), or hypertonic saline (n = 5). After hemodilution, the animals underwent a 25-min period of global cerebral ischemia, followed by 180 min of reperfusion. The animals were then killed and brain water content was assessed by microgravimetry and by the wet-dry weight method. As anticipated, colloid osmotic pressure was maintained in the pentastarch group, and plasma osmolality became significantly increased in the hypertonic saline group. There were no intergroup differences at any time for central venous pressure, mean arterial pressure, intracranial pressure, or PaCO2. Brain water content was significantly decreased in the hypertonic saline group. No difference in brain water content was detected between the control group and the pentastarch group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of THAM and sodium bicarbonate on intracranial pressure and mean arterial pressure in an animal model of focal cerebral injury.

Episodes of arterial hypotension are associated with an increased mortality in head injury patients. Rapid infusion of sodium bicarbonate in such patients may cause hypotension and elevate intracranial pressure. Therefore, we examined the effects of tromethamine (THAM) versus bicarbonate on intracranial pressure and blood pressure in a model of focal cerebral injury. THAM is a buffer that in previous studies has been shown to lower intracranial pressure. After creation of a cryogenic lesion in 13 New Zealand white rabbits, equivalent infusions (15 s duration) of sodium bicarbonate and THAM (2 mEq/kg) were administered sequentially to each animal in random order. Rapid infusion was chosen to simulate the administration of these drugs during a resuscitation. THAM infusion was associated with a significantly lower intracranial pressure and blood pressure than bicarbonate. The fall in blood pressure was great enough that cerebral perfusion pressure after THAM infusion was significantly lower than after bicarbonate infusion. In this model of cerebral injury, rapid infusion of THAM offered no therapeutic advantage over bicarbonate.

Specific binding of Staphylococcus aureus to cultured porcine cardiac valvular endothelial cells.

Infective endocarditis usually occurs in patients who have had previous cardiac damage or who have congenitally abnormal hearts. However, this infection may afflict otherwise normal individuals, and it is often caused by Staphylococcus aureus. In these individuals, interactions between circulating microorganisms and resident cardiac endothelial cells may initiate the infection. In the present studies we established an assay to measure in vitro binding of S. aureus to porcine cardiac valve endothelial cells. We found that this interaction was specific and saturable with respect to time. In contrast, there was no specific binding of Escherichia coli, an organism that rarely causes endocarditis. Exogenous fibronectin had no effect on specific binding of S. aureus, and heat-killed organisms adhered equally well as viable bacteria. Fixation of the endothelial cells with formalin abolished all specific binding. Soluble components from bacterial extracts inhibited S. aureus binding in dose-dependent fashion. These observations suggest that circulating S. aureus may interact with specific sites on cardiac endothelial cells, thereby potentially initiating infective endocarditis.