Continuous Monitoring of Posttraumatic Cerebral Blood Flow Using Laser-Doppler Flowmetry

Abstract

Traumatic brain injury causes alterations in cerebral blood flow that are thought to influence secondary pathophysiology and neurologic outcome in humans. Since it is difficult to study early changes in blood flow in head-injured patients, animal models of brain injury must be employed. However, techniques to monitor brain blood flow in animals are labor intensive and generally provide discontinuous flow measurements. The present study examines the application of laser-Doppler flowmetry for measurement of cerebral blood flow following experimental brain injury. This method allows continuous monitoring of local cerebral blood flow before, during, and after injury. Rats (n = 9) were prepared for lateral fluid percussion injury under barbiturate anesthesia. Injury (2.10 +/- 0.02 atm) was induced over the right parietal cortex, and blood flow was monitored in the contralateral cortex. Seconds after the peak hypertension after injury, blood flow in the left parietal cortex increased 226% +/- 18% (means +/- SEM). This increase was transient, with blood flow falling below control values within minutes. Five minutes after injury, blood flow was 83% +/- 8% of control, and at 1 h, this value had fallen to 56% +/- 6%. Blood flow at 60 min was 93% +/- 5% of control in the sham-injured group (n = 10). The reduction in cerebral blood flow in our laser-Doppler study was of similar magnitude as previously reported in rats injured at a similar intensity when blood flow was examined with radiolabeled microspheres. Given these results, we believe laser-Doppler flowmetry can be used to continuously monitor posttraumatic blood flow following experimental brain injury.

Prolonged Cyclooxygenase-2 Induction in Neurons and Glia Following Traumatic Brain Injury in the Rat

“…In animal models of TBI, brain prostaglandin levels have been shown to rise rapidly postinjury (Ellis et al, 1989;Dewitt et al, 1988;Shohami et al, 1987). Prostaglandin changes in these studies seemed to be associated with brain injury itself; changes in cerebral blood flow following TBI rarely declined to levels associated with ischemia-induced prostaglandin increases (Obrist et al, 1984;Povlishock and Kontos, 1985;Kempski et al, 1987;Ellis et al, 1988;McIntosh, 1989, 1991;Bouma and Muizelaar, 1992;Muir et al, 1992;Kochanek et al, 1995;von Stück et al, 1996).…”

Superoxide and Nitric Oxide Mechanisms in Traumatic Brain Injury and Hemorrhagic Hypotension

“…In cats, CBF does not change significantly in the first hour after injury (DeWitt et al, 1986; Mclntosh et al, 1987) but then decreases significantly by 2 h after TBI (Mclntosh et al, 1987). In contrast, CBF decreases significantly within 15 min after TBI but returns to baseline within a few hours after TBI in rats and pigs Mclntosh, 1989, 1991;Yuan et al, 1989;Muir et al, 1992;. Both central and lateral FP TBI produce widespread decreases in CBF in rats.…”

“…Although electrode placement was uniform between animals in this study, the inability to know the distance between the source of Superoxide and the electrode with precision, among other things, makes it impossible to determine actual Superoxide anion production levels with the electrode other than on a relative basis. It is nevertheless valid to correlate Superoxide anion concentration changes with CBF as measured by LDF, even though the probes are in slightly different locations,'since CBF reductions after TBI tend to be widespread (Yuan et al, 1988;Muir et al, 1992). Central and lateral fluid percussion TBI produces widespread decreases in CBF in rats.…”

MRI Characterization of Progressive Brain Alterations After Experimental Traumatic Brain Injury: Region Specific Tissue Damage, Hemodynamic Changes and Axonal Injury

“…Hemodynamic disturbances found in experimental models of TBI include local CBF decrease from 15 minutes to 4 hours post-injury close to the LFP site (Ginsberg et al, 1997;Muir et al 1992;Ozawa et al, 1991) and transient hypoperfusion also in the contralateral hemisphere (Pasco et al, 2007). Perfusion deficits after traumatic impact can lead to a local ischemic state of the tissue where the oxygen and glucose delivery is so severely impaired that it causes disturbances in energy metabolism and mitochondrial function.…”