Responses of posttraumatic pericontusional cerebral blood flow and blood volume to an increase in cerebral perfusion pressure.

In and around traumatic contusions, cerebral blood flow (CBF) is often near or below the threshold for ischemia. Increasing cerebral perfusion pressure (CPP) in patients with head injuries may improve CBF in these regions. However, the pericontusional response to this intervention has not been studied. Using positron emission tomography (PET), we have quantified the response to an increase in CPP in and around contusions in 18 contusions in 18 patients. Regional CBF and cerebral blood volume (CBV) were measured with PET at CPPs of 70 and 90 mmHg using norepinephrine to control CPP. Based upon computed tomography, regions of interest (ROIs) were placed as two concentric ellipsoids, each of 1-cm width, around the core of the contusions. Measurements were compared with a control ROI in tissue with normal anatomic appearance. Baseline CBF and CBV increased significantly with increasing distance from the core of the lesion. The increase in CPP led to small increases in CBF in all ROIs except the core. The largest absolute CBF increase was found in the control ROI. Relative CBF increases did not differ between ROIs so that ischemic areas remained ischemic. Pericontusional oedema on computed tomography was associated with lower absolute values of CBF and CBV but did not differ from nonoedematous tissue in the relative response to CPP elevation.     

Validation of 133Xe clearance as a cerebral blood flow measurement technique during cardiopulmonary bypass.

133Xe clearance to measure cerebral blood flow (CBF) was examined in 10 dogs during cardiopulmonary bypass. As a reference method, a continuous Kety-Schmidt technique (CBFKS) with 133Xe as indicator was used. Extracranial tissue was removed to directly place the 133Xe detectors on the skull, and the head was covered with a 3 mm lead shield to minimize contamination of the 133Xe clearance curve with extracranial radiation. 133Xe detectors for the Kety-Schmidt technique were embedded in a shielded brass block to minimize interference with radiation from the animal's body. 133Xe clearance data were analyzed using stochastic (CBF10, CBF15, and CBFINF) and initial slope methods (CBFIS), and the results were compared with CBFKS using linear regression. CBF15 and CBFINF yielded similar CBF values as CBFKS (CBFKS = 0.97.CBF15-2.08, r = 0.92, p less than 0.01; CBFKS = 1.13.CBFINF-1.21, r = 0.92, p less than 0.01). CBF10 slightly overestimated CBFKS but still showed a close correlation to CBFKS (CBFKS = 0.89.CBF10-2.58, r = 0.92, p less than 0.01) and CBFIS considerably overestimated CBFKS (CBFKS = 0.60.CBFIS-1.27, r = 0.87, p less than 0.01). With extracranial contamination of the 133Xe clearance curve minimized, all 133Xe clearance techniques used to measure CBF were consistently related to CBFKS in a constant, significant manner. 133Xe clearance therefore is a valid method to assess CBF during cardiopulmonary bypass.     

Dynamic changes in cerebral blood flow, O2 tension, and calculated cerebral metabolic rate of O2 during functional activation using oxygen phosphorescence quenching.

Changes in cerebral blood flow (CBF) using laser-Doppler and microvascular O2 oxygen tension using oxygen-dependent phosphorescence quenching in the rat somatosensory cortex were obtained during electrical forepaw stimulation. The signal-averaged CBF response resulting from electrical forepaw stimulation consisted of an initial peak (t = 3.1 +/- 0.8 seconds after onset of stimulation), followed by a plateau phase that was maintained throughout the length of the stimulus. In contrast, microvascular O2 tension changes were delayed, reached a plateau level (t = 23.5 +/- 1.7 seconds after the onset of stimulation) that remained for the length of the stimulus and for several seconds after stimulus termination, and then returned to baseline. Using Fick's equation and these dynamic measurements, changes in the calculated cerebral metabolic rate of oxygen (CMRO2) during functional stimulation were determined. The calculated CMRO2 response initially was comparable with the CBF, but with protracted stimulation, CMRO2 changes were approximately one-third that of CBF changes. These results suggest that a complex relation exists, with comparable changes in CBF and CMRO2 initially occurring after stimulation but excessive changes in CBF compared with CMRO2 arising with protracted stimulation.     

Effects of clonidine on cerebral blood flow and the response to arterial CO2

CBF, as measured by the clearance of 133Xe or 85Kr in the pentobarbital-anesthetized cat, displays a monotonic increase as the PaCO2 is elevated over a range of 20-60 mm Hg (slope Xe, 1.65 +/- 0.14 ml/100g/min/mm Hg; slope Kr, 1.40 +/- 0.11 ml/100 g/min/mm Hg). Clonidine (20 micrograms/kg i.v.), a centrally acting, alpha 2-preferring agonist, reduced the slope of the PaCO2-CBF response functions for Xe and Kr by 70 and 64%, respectively. Clonidine reduced normocarbic CBF-Xe by 36%, but had no effect on normocarbic CBF-Kr. ST-91, a polar structural analog of clonidine that does not cross the blood-brain barrier, did not reproduce the effects of clonidine when administered at an equivalent dose. This indicates that the effects of clonidine observed were secondary to its action on central rather than peripheral sites. In addition to the effects on the clearance of CBF markers, clonidine reduced the increased MABP otherwise evoked by elevated PaCO2. Reduction in the MABP response to PaCO2 did not account for the lowering of CBF during hypercarbia. In separate experiments where MABP was elevated to correspond with the PaCO2-MABP response observed in the absence of clonidine, a comparable reduction in the slope of the PaCO2 response was also observed. In addition, the pressure autoregulatory response was unaltered after clonidine treatment. These observations suggest that the central action of alpha 2-receptors on the CBF-CO2 response cannot be attributed to an altered perfusion pressure.     

精神分裂症的阴性症状与脑血灌流量的相关研究

目的探讨精神分裂症患者脑血灌流量与阴性症状的关系。方法应用单光子发射计算机断层技术研究阴性症状为主和非阴性症状为主的精神分裂症患者各２５例的脑血灌流量，并与２１例正常对照组比较。结果发现两个研究组均存在额叶、颞叶及基底节脑血灌流量降低，但两组检测结果无差异；相关研究显示患者脑血灌流量与身高呈正相关性。结论精神分裂症的阴性症状与脑血灌流量降低无相关性。     

Relation between cerebral blood flow and the changes in perfusion pressure in patients with brain compression processes

In 20 patients with expanding intracranial lesions the cerebral blood flow was determined by the method of Kety-Schmidt in an own modification with an original device--N2O-meter, with simultaneous continuous measurement of the intraventricular pressure and arterial blood pressure. This made possible determination of the cerebral perfusion pressure and of the effect of its fluctuations on the cerebral blood flow. Lowering of the cerebral blood flow below the normal value occurred when the perfusion pressure fell below 60 mm Hg, but its further fall, even to 20 mm Hg, caused no proportional decrease of the cerebral blood flow.     

Responses of cerebral arteries to the changes in cerebral perfusion pressure

The responsiveness of cerebral pial arteries and arterioles to changes in systemic arterial blood pressure (SAP) was investigated. Using 9 cats anesthetized with chloralose and urethane, direct, simultaneous measurements of pial arterial pressure (PAP) and cerebral blood flow (CBF) were made during changes in SAP. SAP was varied between 25 and 140 mmHg by the hemorrhage and blood infusion methods. After a partial craniotomy. PAP was measured with a micropipette connected to a servo-controlled micropressure recording system. Punctured pial arteries were grouped into three types according to their diameters, 1A (291 +/- 33 microns), 2A (16 +/- 26 microns), and 3A (70 +/- 10 microns). CBF on the exposed cortex was measured with hydrogen clearance method. The PAPs measured were a linear function of SAP; PAP (1A) = 0.73/SAP-6.6 (r = 0.96), PAP (2A) = 0.62 X SAP-6.6 (r = 0.90), PAP (3A) = 0.61 X SAP-6.4 (r = 0.93). The result indicates that PAPs are entirely dependent on SAP and that SAP induced changes in PAPs are less in the smaller pial arteries. Regional CBF remained constant (55 +/- 4 ml/100 g/min) between 60 and 140 mmHg of SAP. A significant decrease in CBF was observed below 60 mmHg of SAP. Cerebrovascular resistances were calculated segmentally using the following formulas; large vessel resistances (LVR) = (SAP-PAP(1A]/CBF, middle vessel resistance = (PAP (1A)-PAP (3A]/CBF, and small vessel resistance = PAP (3A)/CBF. The changes in LVR, MVR, and SVR were almost identical between 70 and 140 mmHg of SAP. Below 70 mmHg of SAP, SVR showed the greatest decrease in resistance.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of intravenous dipyridamole on cerebral blood flow in humans. A PET study.

BACKGROUND AND PURPOSE: Dipyridamole increases the concentration of circulating adenosine, which is a potent vasodilator, by inhibition of uptake of adenosine into the erythrocytes, and hence produces coronary vasodilation. However, the effects of dipyridamole on cerebral circulation is not pronounced. This study investigates the effects of intravenous dipyridamole on cerebral blood flow (CBF) in humans with use of positron emission tomography (PET). METHODS: In each of 13 healthy subjects, CBF was measured using (15)O-labeled water and PET at rest and during hypercapnia, hypocapnia, and dipyridamole stress; corresponding CBF values were then compared. RESULTS: CBF values during dipyridamole stress were significantly lower than those measured at rest. The dipyridamole stress PaCO(2) was also significantly lower than the resting PaCO(2). The change in CBF during dipyridamole stress relative to PaCO(2) closely followed the relationship between CBF and PaCO(2) during hypocapnia. CONCLUSIONS: These results indicate that the observed decrease in CBF during dipyridamole stress was caused by a decrease in PaCO(2) rather than by any direct action of dipyridamole on CBF. The decrease in PaCO(2) during dipyridamole stress was most likely due to hyperventilation, which was a side effect of adenosine. These results support the hypothesis that circulating adenosine is largely prevented from binding to adenosine receptors of cerebral vessels by the blood-brain barrier.     

体外循环心内直视手术时脑血流速度改变的研究

目的研究体外循环心内直视手术期间脑血流速度的变化和影响因素。方法在１７例患者心内直视手术时应用双通道经颅多普勒于术中动态监测大脑中动脉血流速度的变化。结果在体外循环转流期间，脑血流速度降低并随平均动脉压的改变有一定波动，血流频谱呈锯齿状。结论ＴＣＤ动态监测脑血流速度在体外循环心脏手术过程中对了解脑灌注的改变有一定价值     

Carbon dioxide induced changes in cerebral blood flow and flow velocity: role of cerebrovascular resistance and effective cerebral perfusion pressure

In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO₂-induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO₂ levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure–flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean V_MCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39% despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak (r=0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP.     

Cerebral blood flow response to increases in arterial CO2 tension during alfentanil anesthesia in the rabbit.

The stability of cerebral function and blood flow (CBF), and the CBF response to changes in arterial carbon dioxide tension (CBF reactivity) during alfentanil anesthesia were examined in rabbits. This model was first shown to provide stable anesthesia, cortical function, and CBF for 4 h. CBF increased significantly to 159% [of baseline] in the left hemisphere and to 167% in the right within 5 min of an exposure to 5% CO2 (p = 0.009 on the left and p = 0.003 on the right), but then decreased to 123% on the left and to 137% on the right (not significantly different from baseline, p = 0.11 on the left and p = 0.07 on the right) while PaCO2 was still rising. Steady state reactivity levels (0.8 ml 100 g-1/min-1/mm Hg-1 CO2 on the left and 0.65 ml 100 g-1/min-1/mm Hg-1 CO2 on the right) were consistent with previous work and were reached at 20 min. These results suggest that mechanisms other than perivascular hydrogen ion concentration mediate the CBF response to changes in arterial CO2 tension during alfentanil anesthesia.     

Effects of extra-intracranial arterial bypass on cerebral blood flow and oxygen metabolism in humans

Twelve patients, eleven with a carotid obstruction and one with an occlusion of the middle cerebral artery, were studied before and after a successful unilateral extra-intracranial arterial by-pass, (EIAB) using PET and the 15-0 steady-state technique to measure regional cerebral blood flow (CBF), oxygen extraction fraction and oxygen metabolic rate (CMRO2). In the whole group of patients, both CBF and CMRO2 increased significantly on both cerebral hemispheres after EIAB, returning toward control levels defined in age-matched subjects. Mean oxygen extraction fraction, on the other hand, was not affected. Individually, three different effects of EIAB emerged: 1) Alleviation of a state of long standing unilateral "misery-perfusion", as reported earlier; 2) parallel increase of CBF and CMRO2 bilaterally, which appeared due to improvement of a hemodynamic depression of metabolism, the precise mechanism of which remains obscure; 3) Complex, unexpected changes in the CBF-CMRO2 couple again resulting in increases in CMRO2. This metabolic improvement afforded by EIAB in our patients has not been reported before; it suggests that long-standing hemodynamic failure may induce a metabolic depression that is still potentially reversible by surgical revascularization.     

Local cerebral blood flow response to locally infused 2-chloroadenosine during hypotension in piglets

Brain interstitial adenosine increases during hypotension in piglets. If adenosine is to participate in the regulation of neonatal cerebral blood flow (CBF) during hypotension, it must retain its vasodilatory action under that condition. To examine this issue, we studied the effects of locally infused 2-chloroadenosine (2-CADO), a stable adenosine analog, on local CBF in the piglet frontal cortex during normotension and graded hemorrhagic hypotension. We used the modified brain microdialysis/hydrogen clearance technique to simultaneously infuse 2-CADO into the frontal cortex and measure local CBF from the same area. When 2-CADO from 10(-8) M to 10(-3) M was infused under control conditions (n = 7), CBF increased 61% at 10(-5) M, 167% at 10(-4) M, and 210% at 10(-3) M. In hypotension experiments, local infusion of 10(-5) M 2-CADO (n = 8) caused significant increases in CBF (P less than 0.05) under control conditions (MABP = 65 mmHg) and at hypotensive blood pressures of 55 mmHg and 44 mmHg, respectively. At a blood pressure of 33 mmHg, however, infusion of the analog failed to increase CBF. Local infusion of 10(-3) M 2-CADO also produced a similar change in CBF during graded hypotension. These results indicate that 2-CADO dilates intracerebral vessels during normotension, and mild and moderate hypotension, and support the hypothesis that endogenous adenosine mediates autoregulatory adjustments of CBF during hypotension in newborn piglets.