Effect of Intra-arterial Sodium Nitroprusside on Intracranial Pressure and Cerebral Autoregulation

Abstract

Sodium nitroprusside (SNP) is employed to reduce systemic blood pressure in cerebrovascular surgery. Its application has also been suggested to improve cerebral vasospasm when administered intravenously or intra-arterially in combination with a-adrenergic agents. The purpose of this study is to investigate the vascular response of normal and elevated intracranial pressure (ICP). Twelve adult cats were anesthetized and intubated. Each animal was paralysed and mechanically normoventilated. ICP was measured through a 22G needle into the left lateral ventricle and connected to a strain gauge transducer. Different levels of ICP were achieved using an artificial cerebro-spinal fluid, which exerted a variable hydrostatic pressure via a 21G cannula introduced into the cisterna magna. The effects of SNP were studied in each animal at three ICP levels: normal (control), 20 mmHg, and 40 mmHg. A catheter was inserted into the left internal carotid through the lingual artery, and SNP (40 μg/kg/min) was infused intra-arterially through this catheter. Administration of SNP always caused an increase of ICP. This increment degree of ICP caused by SNP (ΔICP=ICPSNP-ICPinitial) was more marked in the control group with normal ICP, amounting to 5.27±2.51 mmHg (P<0.01). In the groups with ICP levels of 20 and 40 mmHg, ΔICP were 2.21±0.66 and 0.21±0.40 mmHg, respectively (not significant). Comparison of the three groups revealed that the increase of ICP of the groups with mild or high ICP was significantly lower than that of the control group (t-test, P<0.01 for 20 mmHg and P<0.001 for 40 mmHg group). As the initial level of ICP was raised, ΔICPs decreased. The results confirmed the observations made by other investigators that SNP has an influence on ICP. Because cerebral autoregulation should be intact at the ICP levels as such induced in the present study (20 and 40 mmHg), the high-dosage (40 μg/kg/min) and the route of administration of SNP in this series (internal carotid) might exert a direct influence on the cerebral vessel walls. SNP seems to cause cerebral vasoparalysis and disturb pressure autoregulation.