Intracranial pressure response to induced hypertension: role of dynamic pressure autoregulation.

OBJECTIVE: Induced hypertension is commonly used to improve cerebral perfusion, but this treatment may have the deleterious side effect of raising intracranial pressure (ICP). We tested the hypothesis that dynamic pressure autoregulation testing could identify patients who might develop increased ICP during induced hypertension. METHODS: Twenty-two studies were performed in 21 patients. Baseline dynamic testing of autoregulation by cuff deflation and carotid compression techniques was performed. After phenylephrine was infused to increase mean arterial pressure by 20 to 30 mm Hg, cuff deflation tests were repeated. RESULTS: The average increase in mean arterial pressure was 32.2 +/- 16.1 mm Hg. This increase was accompanied by increased flow velocity (P < 0.001), brain tissue PO2 (P = 0.011), and regional cerebral blood flow (P = 0.008). Also, dynamic pressure autoregulation consistently improved (P = 0.015). Induced hypertension caused increased ICP (iICP) in 12 patients and a decrease in ICP (dICP) in 9. Baseline jugular venous oxygen saturation in the iICP group was 82 +/- 10% compared with 70 +/- 10% in dICP patients (P = 0.02). Baseline dynamic autoregulatory index for the cuff deflation tests (1.8 +/- 1.4) and baseline transient hyperemic response ratio for the carotid compression tests (1.11 +/- 0.07) were significantly lower in iICP patients (dICP group: autoregulatory index 3.2 +/- 1.7, P = 0.06; transient hyperemic response ratio 1.26 +/- 0.11, P = 0.009). Flow velocity increased more with the increase in blood pressure in the iICP group than in the dICP group: 19.0 +/- 6.8 cm/s versus 10.2 +/- 6.3 cm/s (P = 0.007). CONCLUSION: The patients who had an increase in ICP with induced hypertension had a greater degree of impairment of autoregulation and induced hypertension resulted in a greater increase in flow velocity.

Laser Doppler flow and brain tissue PO2 after cortical impact injury complicated by secondary ischemia in rats treated with arginine.

BACKGROUND: Traumatic brain injury (TBI) makes the brain susceptible to secondary insults such as ischemia. This study tested the hypothesis that L-arginine would increase regional CBF (rCBF) and brain tissue PO2 (PbtO2) at the injury site. METHODS: A secondary insult model was employed in rodents. rCBF was measured with laser doppler flowmetry (LDF) and PbtO2 with a PO2 catheter at the impact site. Animals were randomized to receive L-arginine, D-arginine or saline intravenously, 5 minutes after impact. RESULTS: In animals who received L-arginine, the percentage rCBF from baseline (%CBF) was higher at the impact site after impact (p < 0.001), during bilateral carotid occulation (BCO) (p = 0.001) and during reperfusion (p = 0.032). In contrast, PbtO2 was not significantly increased throughout the experiment for the L-arginine group. CONCLUSIONS: Administration of L-arginine increased rCBF in the injured brain tissue, and resulted in better preservation of CBF during BCO than D-arginine and saline.