1 The binding of bupivacaine (400 ng/ml) to isolated al-acid glycoprotein was studied at two protein concentrations. At 20 mg/10O ml the extent of bupivacaine binding was 31.0 ± 1.8% (mean + s.d., n = 4), and at a protein concentration of 60 mg/100 ml binding of bupivacaine was 85.8 + 1.5% (n = 4).2 Bupivacaine and a,-acid glycoprotein concentrations were measured in plasma samples collected from a maternal peripheral vein and the umbilical vein at delivery (n = 23). The ratio of the foetal:maternal bupivacaine concentrations ranged from 0.17 to 0.52, while the foetal:matemal ratio for al-acid glycoprotein concentrations ranged from 0.20 to 0.96. A positive relationship emerged between the two ratios (P < 0.01).3 The al-acid glycoprotein concentration gradient across the placenta, and interindividual variability in the gradient appear to contribute to the low and variable transplacental bupivacaine concentration ratio observed.
The relative sajety oj carotid endarterectomy depends upon surgical expertise combined with appropriate monitoring oj cerebral perjusion and the ability to intervene either surgically or pharmacologically to match cerebral perjusion to cerebral oxygen requirement. Methods oj monitoring adequacy oj cerebral perjusion are reviewed and include regional cerebral blood jlow measurements, electroencepha/ographic monitoring, carotid stump pressure measurements, jugular venous oxygen partial pressure, neurological assessment and plethysmographic techniques. When cerebral perjusion is inadequate, such procedures as insertion oj a temporary bypass shunt and maintenance oj normocarbia may improve cerebral perjusion. Anticoagulants along with pharmacologic intervention to either increase cerebral perjusion pressure or reduce cerebral oxygen requirement may be used to preserve cerebral junction.
A case report illustrating possible cerebral protection from ischemia by barbiturate administration during carotid artery surgery where bypass shunting was indicated from the EEG recording but technically impossible to achieve. CASE REPORT A 77 year old 69 Kg man presented in June, 1978, with a history of transient ischaemic attacks. His symptoms during these attacks consisted of weakness and spasm of his right hand. These episodes usually lasted about one hour. He also complained of deteriorating vision over the previous six months but denied any involvement of speech or gait. He was a non-smoker with no known drug allergies, he was asymptomatic to other systems review. He had been treated for tuberculosis 20 years previously and, in 1976, he underwent emergency surgery for a ruptured abdominal aortic aneurysm. This was complicated by acute renal failure which subsequently resolved leaving some residual impairment. Examination revealed hypertension, 220/100 mmHg on admission. His medications included amiloride hydrochloride and bendrofluazide, along with allopurinol each morning and digoxin 0.25 mg second daily. Bilateral carotid bruits were audible, right greater than left. The pulse was irregular, there being ECG evidence of atrial fibrillation. No other evidence of cardiovascular or respiratory disease was apparent. Apart from diminished ability to coordinate with his right hand, he was neurologically intact. Investigations included four vessel angio
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