Effects of angiotensin and atrial natriuretic peptide on the cerebral circulation.

The purpose of the present study was to determine effects of angiotensin (ANG) II on the cerebral circulation. We measured the pial artery pressure (PAP) and CBF in anesthetized rabbits. ANG II (5 micrograms/min) was infused into each carotid artery, and systemic arterial pressure was maintained constant. During infusion of ANG II, there was a significant increase in CBF and fall of PAP, with no change in the large artery resistance (LAR) and a significant decrease in the small vessel resistance (SVR). To investigate whether prostaglandin modulated the ANG II-induced increase in CBF, indomethacin was administered (10 mg/kg i.v.) in another group of animals. Indomethacin itself reduced PAP and increased LAR significantly without changing CBF or SVR. Indomethacin did not attenuate the effects of ANG II on the cerebral circulation. The CMRO2 was assessed during ANG II intracarotid infusion in another group of rabbits. CMRO2 did not change during infusion of ANG II. We also investigated effects of alpha-atrial natriuretic peptide (ANP) on the cerebral circulation. Infusion of ANP (1 microgram/min) decreased LAR by 28% (p less than 0.05) without altering SVR. Administration of ANG II after ANP tended to reduce LAR (p greater than 0.05), with a significant decrease in SVR. The results of the present study suggest that high doses of ANG II can produce cerebral vasodilatation, particularly of small vessels. Blood-borne ANP dilated the large arteries of the cerebral circulation selectively and neither interfered with nor reversed the ANG II-induced increase in CBF.     

Effect of perfluorochemicals on experimental cerebral ischemia

It has been noted that perfluorochemicals (PFC) which were developed as artificial blood substitutes, protect against ischemic brain injury by their ability to serve as oxygen carriers. It is also known that normovolemic hemodilution (HD) improves cerebral blood flow (CBF) and neurological symptoms in cerebral infarction. However, there are few reports concerning the effect of PFC on the collateral circulation via pial anastomoses in cases of middle cerebral artery (MCA) occlusion. The ability to record the pial arterial blood pressure (PAP) without interfering blood flow now makes it possible to measure the segmental resistance of cerebral vessels. By using this method, one can measure collateral vessel resistance through pial anastomoses following MCA occlusion. In this paper, we studied the protective effects of PFC combined with HD on ischemic brain injury with the focus on the collateral circulation via pial anastomoses following occlusion of the MCA. Twenty adult cats were studied: control, 8; HD, 5; Fluosol (Fluosol-DA), 7. The systemic arterial pressure (SAP) and PeCO2 were continuously monitored. Subsequently the MCA was occluded via the transorbital approach. CBF in the ectosylvian gyrus (central area of the ischemic lesion) was measured by the hydrogen clearance method. A small pial artery about 100 microns in diameter on the exposed ectosylvian gyrus was punctured nonocclusively with a micropipette filled with 2 M sodium chloride which was connected to a servo-null micropressure system (Model 900, W-P Instruments, Inc. U.S.A.). The electroencephalogram (EEG) was recorded from the ectosylvian gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Autoregulatory response of pial vessels in the cat

Pial vessel responses to mean arterial pressures (MAP) between 40 and 160 mmHg, induced by withdrawal and reinfusion of blood, were studied in twelve cats under barbiturate- and N2O-anaesthesia, using the cranial window technique and videoangiometry. Very minor changes of pial arterial calibres were noted between MAP 80 and 120 mmHg. During further reduction of MAP, small arteries dilated more than large arteries and measured 43 +/- 4.6% and 30 +/- 1.9% at MAP 40 mmHg, respectively. When MAP was elevated to 140 mmHg, large arteries constricted more than small ones; at MAP 160 mmHg, however, they started to redilate, while small arteries continued to constrict to -13 +/- 2.3%. Within the autoregulatory range, pial veins remained unchanged; at MAPs of 40 and 160 mmHg, venous calibre variations remained below 10%.     

Effect of 2-chloroadenosine on cerebrovascular reactivity to hypercapnia in newborn pig.

The effect of local administration of vasodilative concentrations of the adenosine receptor agonist 2-chloroadenosine (2-CADO) on the hyperemic responses of the pial and parenchymal microcirculations to graded hypercapnia was determined. The cranial window and brain microdialysis-hydrogen clearance techniques were utilized in two groups of isoflurane-anesthetized newborn pigs to measure changes in pial diameters and local CBF, respectively, in response to graded hypercapnia in the absence and presence of 2-CADO. Progressive size-dependent dilations of pial arterioles [small = 41 +/- 7 microns (mean +/- SD), intermediate = 78 +/- 13 microns, and large = 176 +/- 57 microns in diameter] occurred in response to graded hypercapnia alone (PaCO2 = 58 and 98 mm Hg) and to superfusions of 2-CADO (10(-5) M) during normocapnia; the magnitude of the dilative response to each of these stimuli was inversely proportional to vessel size. When hypercapnia was induced concomitantly with 2-CADO superfusion, the dilative effects of each stimulus were directly additive. Similarly, local microdialysis infusion of 10(-5) M 2-CADO, which doubled CBF during normocapnia, did not affect the hyperemic response of the parenchymal circulation to graded hypercapnia (PaCO2 = 69 and 101 mm Hg). Our findings are consistent with the participation of adenosine in the mediation of cerebral hypercapnic hyperemia. If, however, adenosine is not involved in this dilative response, our results indicate that concomitant vascular and neuromodulatory actions induced by adenosine receptor stimulation do not affect the mechanism responsible for the hypercapnic hyperemic response.     

Autoregulatory response of pial vessels in the cat

Pial vessel responses to mean arterial pressures (MAP) between 40 and 160 mmHg induced by withdrawal and reinfusion of blood, were studied in twelve cats under barbiturate- and N₂O anaesthesia, using the cranial window technique and videoangiometry. minor changes of pial arterial calibres were noted between MAP 80 and 120 mmHg. During further reduction MAP small arteries dilated more than large arteries and measured 43 ± 4.6% and at MAP 40 mmHg, respectively. When MAP was elevated to 140 mmHg, large arteries constricted more than small ones; at MAP 160 mmHg, however, they started to redilate, while small arteries continued to constrict to -13 ± 2.3%. Within the autoregulatory range, pial veins remained unchanged; at MAPs of 40 and 160 mmHg, venous calibre variations remained below 10%.     

Blood flow velocity in the pial arteries of cats, with particular reference to the vessel diameter

The blood flow velocity and diameter of feline pial arteries, ranging in diameter from 20 to 200 microns, were measured simultaneously using a newly developed video camera method under steady-state conditions for all other parameters. There was a linear relationship between blood flow velocity and pial artery diameter (y = 0.340x + 0.309), the correlation coefficient being 0.785 (p less than 0.001). The average values for blood flow velocity in pial arteries less than 50 microns, greater than or equal to 50 but less than 100 microns, greater than or equal to 100 but less than 150 microns, and greater than or equal to 150 microns in diameter were 12.9 +/- 1.3, 24.6 +/- 3.4, 42.1 +/- 4.7, and 59.9 +/- 5.3 mm/s, respectively. Blood flow rate was calculated as a product of the cross-sectional area and the flow velocity. The blood flow rate increased exponentially as the pial artery diameter increased (y = 2.71 X 10(-4) x2.98). The average values for blood flow rate in pial arteries less than 50 microns, greater than or equal to 50 but less than 100 microns, greater than or equal to 100 but less than 150 microns and greater than or equal to 150 microns in diameter were 12.8 +/- 1.5, 122.1 +/- 24.8, 510.2 +/- 74.8, and 1524.2 +/- 174.4 10(-3) mm3/s, respectively. Hemorheological parameters such as the wall shear rate and Reynolds' number were also calculated. The data obtained provide a useful basis for further investigations in the field of cerebral circulation.     

Pial arteriolar constriction following cortical spreading depression is mediated by prostanoids.

The mechanism of pial arteriolar constriction during post-cortical spreading depression (CSD) was examined in anesthetized adult rabbits. Using a closed cranial window and intravital microscopy, the diameter of a pial arteriole was determined. A single CSD was induced by KCl micro-injection and its propagation was monitored by recording slow potential changes accompanying CSD. Prostanoid levels in cortical cerebrospinal fluid (CSF) were determined by radioimmunoassay. Pial arteriolar diameter increased significantly from 76 +/- 6 to a maximum of 119 +/- 5 microns (57%, n = 8) for 1.6 +/- 0.1 min when CSD (velocity, 2.8 +/- 0.1 mm/min) reached the cortex just beneath the vessel irrespective of its location. Shortly after CSD expiration from the cortex, pial arteriolar diameter decreased from the pre-CSD level to a minimum of 67 +/- 5 microns (12%, n = 8) for 19.5 +/- 2.1 min. CSD was elicited again in the same animal while the cortical surface under the window was continuously superfused with artificial CSF at a flow rate of 3.2-4.5 ml/min. Pial arteriolar dilation (from 75 +/- 6 to 115 +/- 3 microns, 53 +/- 9%, for 1.6 +/- 0.1 min, n = 8) was observed again during CSD (velocity, 2.7 +/- 0.2 mm/min), however, no constriction of the vessel was seen after CSD expiration. Indomethacin pretreatment (n = 11) to inhibit prostanoid production enhanced the magnitude of CSD-induced vasodilation from the pretreatment levels of 59 +/- 9% (from 82 +/- 5 to 130 +/- 8 microns for 1.7 min) to the post-treatment levels of 82 +/- 13% (from 78 +/- 5 to 142 +/- 12 microns for 1.8 min).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of (D-Met2,Pro5)-enkephalinamide and naloxone on pial vessels in cats

To elucidate the fundamental actions of endogenous opioids and naloxone on the cerebral circulation, the effects of (D-Met2,Pro5)-enkephalinamide and naloxone on pial vessels were investigated in cats. Pial arteries (165.7 +/- 24.9 microns) were found to dilate after the intravenous administration of 1 mg/kg of (D-Met2,Pro5)-enkephalinamide, and a definite dilatation of 7.1-7.6% persisted for 15 min. Pial veins (100.6 +/- 20.2 microns) also dilated but to a lesser degree. The MABP (118.7 +/- 10.5 mm Hg) decreased by 20 mm Hg immediately after the injection, but gradually returned to the initial value 15 min later. The observed cerebral vasodilatation may be attributable to sympathetic inhibition mediated either by the presynaptic opiate receptors of the cerebral vessels or by the opiate receptors in the brainstem. After the intravenous administration of 1 mg/kg of naloxone, pial arteries (122.0 +/- 17.2 microns) showed a slight but significant dilatation of 2.3-5.3%. There were no significant changes in pial veins (87.0 +/- 12.4 microns). MABP (130.4 +/- 12.3 mm Hg) was slightly increased after the injection. Although the mechanism involved was unclear, the cerebral vasodilatation occurring after the administration of naloxone may contribute to its ameliorating effect on the neurological symptoms following cerebral ischemia.     

A study of pial vessel behavior on superior sagittal sinus and cortical venous occlusion

In cerebral circulation, it is suspected that neurogenic or myogenic mechanism protect blood vessel and blood-brain barrier during sudden increase in arterial pressure. To discriminate metabolic mechanism from neurogenic and myogenic mechanism, complete cerebral venous occlusion model of cat was used to obtain high venous pressure. In twenty-one anesthetized cats, 0.3 ml of cyanoacrylate were injected into anterior part of SSS to occlude SSS and cortical vein. Diameter of pial vessels and ICP were measured through the cranial window. An average of ICP was 6.7 +/- 1.8 mmHg before occlusion. 5 minutes after occlusion ICP was elevated to an average of 10.4 +/- 4.8 mmHg. Finally, ICP increased over 20 mmHg in nine animals. All pial vein dilated immediately after injection of cyanoacrylate and the dilatation rate was 2-55%. Pial arteriole between 50 microns and 100 microns in diameter was observed. In early stages, 2-24% contraction of arteriole were observed in fifteen animals and 2-16% dilatation were observed in six animals. In later stages, 1-87% dilatation of arteriole were observed in ten cats. Ten of twelve ( 83%) cases with ICP under 20 mmHg showed contraction of pial arteriole. Eight of nine (89%) cases with ICP over 20 mmHg showed dilatation of pial arteriole. In addition, the elevation of ICP and the dilatation of pial arteriole were observed simultaneously. Correlation between ICP and arterial diameter is obvious. The dominant mechanism of cerebral blood flow control is metabolic, not neurogenic and myogenic. Increase of ICP, dilatation of vein and dilatation of artery with increasing ICP are consistent with the theory.(ABSTRACT TRUNCATED AT 250 WORDS)     

Quantitative measurement of blood flow velocity in feline pial arteries during hemorrhagic hypotension and hypercapnia

Due to methodologic difficulties, few investigations have been made on the blood flow velocity in the cerebral microcirculation. Using a newly developed video camera method, we simultaneously measured the blood flow velocity and diameter of pial arteries during hemorrhagic hypotension, after blood pressure recovery, and during CO2 inhalation in cats. When the mean arterial blood pressure was lowered from 129.7 +/- 6.6 to 71.5 +/- 4.1 mm Hg, the blood flow velocity inevitably decreased from 36.6 +/- 5.3 to 27.0 +/- 3.9 mm/sec (p less than 0.001). The calculated blood flow rate [pi X (diameter/2)2 X flow velocity] was preserved in cases with concomitant vasodilation. Conversely, the blood flow velocity increased from 25.3 +/- 5.1 to 31.0 +/- 5.4 mm/sec (p less than 0.001) after mean arterial blood pressure recovery from 67.1 +/- 3.7 to 129.8 +/- 5.8 mm Hg. The blood flow rate was again preserved in vessels with a vasoconstrictive response. Each pial artery apparently dilated or constricted in proportion to the decrease or increase in flow velocity during blood pressure changes, maintaining a constant cerebral blood flow. This indicated the importance of the pial arteries in the mechanisms of cerebral blood flow autoregulation. During 5% CO2 inhalation, the blood flow velocity increased markedly from 25.4 +/- 4.6 to 37.2 +/- 10.0 mm/sec (p less than 0.05), while the pial artery diameter (85.0 +/- 13.7 microns) increased by 9.6 +/- 1.5% (p less than 0.01). The increased flow velocity might be attributable to preferential dilatation of small arterioles or intraparenchymal vessels during hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pial artery pressure after one hour of global ischemia

Pial artery pressure was measured in anesthetized control cats and in animals subjected to 1 h of global ischemia and 6 h of recirculation. Cerebral blood flow (CBF) was measured with the intraarterial 133Xe technique before and after ischemia, and lumped segmental resistances upstream and downstream to the pial artery were calculated. In the control brain, upstream resistance was 1.30 +/- 0.28 and downstream resistance 0.94 +/- 0.1 mm Hg ml-1 100 g min. During the postischemic hypoperfusion period, both resistances significantly increased, indicating that hypoperfusion constitutes a dysregulation of both large extracerebral and small intracerebral vessels. Hypercapnia induced an increase of CBF in the control brain and was accompanied by a fall in downstream resistance, demonstrating intracortical vasodilation. By contrast, hypercapnia did not provoke changes in either CBF or segmental resistances in the hypoperfusion period. In conclusion, during the postischemic hypoperfusion period, both extra- and intracortical resistances are increased and vascular reactivity to CO2 is abolished.     

Volume reduction in cerebral blood flow in patients with Alzheimer's disease: a sonographic study

Neuroimaging techniques such as PET and SPECT demonstrated a consistent reduction of cerebral blood flow (CBF) in Alzheimer's disease (AD). The aim of the study was to assess the potential role of ultrasonography for CBF measurement in AD patients and whether the CBF volume correlates positively with disease severity. Fifty patients who met the diagnostic criteria of probable AD (NINDS-ADRDA) were compared to 50 age-matched healthy elderly volunteers. The extracranial internal carotid arteries (ICAs) and the vertebral arteries (VAs) of the patients and controls were examined. Angle-corrected time-averaged flow velocity (TAV) and the diameter of the vessel were measured. Intravascular flow volumes were calculated as the product of TAV and the cross-sectional area of the circular vessel. CBF volume was calculated as the sum of flow volumes in the ICAs and VAs of both sides. All subjects underwent the MMSE. The mean global CBF (474.87 +/- 94.085 vs. 744.26 +/- 94.082 ml/min; p < 0.0001) was lower in AD patients than in healthy volunteers. A significant decline in global flow volumes (r = 0.48; p < 0.0007) with the degree of cognitive impairment was also present. The ability of ultrasonography to characterize flow decreases makes such a technique an attractive tool for the study of AD, for the evaluation of pharmacological therapies and, possibly, for early diagnosis.     

Pial vascular behavior during bilateral and contralateral cervical sympathetic stimulation

The present study in cats investigates the effect of cervical sympathetic stimulation on changes of diameter of pial arteries and veins, CBF, and intracranial pressure (ICP) using the cranial window and hydrogen clearance techniques. During 20 min of bilateral stimulation, pial arteries maximally constricted by 12%, veins by 13-15%. While the constriction of the large arteries remained stable during the whole 20-min period of bilateral stimulation, small arteries escaped after some 2 min. A similar though weaker trend was noted for the veins. CBF was reduced at 2 min by 31%, and was not different from resting at 18 min. Contralateral stimulation for 20 min induced early constriction only in small arteries, while all other vessels remained more or less unreactive. This phenomenon is explained by interhemispheric arterial collaterals that bring sympathetic fibers mainly to small arteries contralaterally. ICP was lowered initially by 47 +/- 12% during bilateral and by 23 +/- 5% during contralateral stimulation. ICP escaped after 2 and 5 min during bilateral and contralateral stimulation, respectively, and even started to rise after some 10 min. From these data, it is concluded that the sympathoadrenergic system exerts a short-lasting protective effect upon cerebral vascular volume. Small arteries escape from constriction as a consequence of primarily myogenic counteraction of pial and intraparenchymal vessels, and probably additional metabolic dilatation of intraparenchymal vessels.     

Color duplex measurement of cerebral blood flow volume in healthy adults

BACKGROUND AND PURPOSE: Global cerebral blood flow (CBF) is an important yet largely unknown quantity in the treatment of neurological intensive care patients. Color duplex sonography of the extracranial cerebral arteries can be used to measure global CBF volume directly at the bedside. To establish reference data on global CBF volume and to test the influence of sex and age on this parameter, a prospective study was performed in a group of 78 healthy adults aged 20 to 85 years (39 women, 39 men; mean age, 52+/-19 years in either sex). METHODS: The common, external, and internal carotid arteries and the vertebral arteries were examined with the use of a 7.0-MHz transducer of a computed sonography system. Angle-corrected time-averaged flow velocity and the diameter of the vessel were measured. Intravascular flow volumes were calculated as the product of angle-corrected time-averaged flow velocity and the cross-sectional area of the circular vessel. CBF volume was determined as the sum of flow volumes in the internal carotid and vertebral arteries of both sides. RESULTS: From 20 to 85 years of age, CBF volume decreased significantly (P相似文献   

Dysfunction of mouse cerebral arteries during early aging

Aging leads to a gradual decline in the fidelity of cerebral blood flow (CBF) responses to neuronal activation, resulting in an increased risk for stroke and dementia. However, it is currently unknown when age-related cerebrovascular dysfunction starts or which vascular components and functions are first affected. The aim of this study was to examine the function of microcirculation throughout aging in mice. Microcirculation was challenged by inhalation of 5% and 10% CO₂ or by forepaw stimulation in 6-week, 8-month, and 12-month-old FVB/N mice. The resulting dilation of pial vessels and increase in CBF was measured by intravital fluorescence microscopy and laser Doppler fluxmetry, respectively. Neurovascular coupling and astrocytic endfoot Ca²⁺ were measured in acute brain slices from 18-month-old mice. We did not reveal any changes in CBF after CO₂ reactivity up to an age of 12 months. However, direct visualization of pial vessels by in vivo microscopy showed a significant, age-dependent loss of CO₂ reactivity starting at 8 months of age. At the same age neurovascular coupling was also significantly affected. These results suggest that aging does not affect cerebral vessel function simultaneously, but starts in pial microvessels months before global changes in CBF are detectable.     

Physiological mechanisms controlling cerebral blood flow

The major conceptions of cerebral blood flow (CBF) control developed in the 19th and 20th centuries are listed. The systems of CBF regulation are considered from the viewpoint of automatic control. In the classification of CBF regulation mechanisms, 4 types are identified. The effectors of CBF regulation, i.e. the specific arterial segments through which each type of regulation is accomplished, were found to be mainly the major arteries of the brain and the small pial arteries rather than the intracerebral arterioles. Review of controlling influences on these effectors of regulation, (myogenic, humoral and neurogenic), show that priority should be given to neurogenic mechanisms. Several criteria governing efficiency of CBF regulation are proposed. Review of interactions of different types of CBF regulation shows that there may be both synergistic and antagonistic relationships. Information about the processes is important for medical practice.     

Locus coeruleus stimulation exerts different influences on the dynamic changes of cerebral pial and intraparenchymal vessels.

The present experimental study was undertaken to investigate the effects of locus coeruleus stimulation on the dynamic changes of intraparenchymal vessels and pial vessels. Twelve cats were anaesthetized with alpha-chloralose and urethane. For stimulation of the locus coeruleus, a concentric stainless-steel needle electrode was inserted stereotaxically. During the stimulation, volumetric changes of the intraparenchymal vessels were monitored by a photoelectric method for estimating the cerebral blood volume (CBV) (6 cats), and the diameters of pial arteries were measured continuously using a video camera system (6 cats). The CBV followed a decreasing course during the stimulation of the locus coeruleus. The decrease in CBV from the control value (6.3 vol%) was 0.14 +/- 0.04 vol% at 80 s (p less than 0.05), 0.15 +/- 0.05 vol% at 100 s (p less than 0.05), and 0.15 +/- 0.03 vol% at 120 s (p less than 0.01). After cessation of the stimulation, CBV showed a gradual recovery. On the other hand, the diameters of the pial arteries did not change during or after the stimulation of the locus coeruleus. The above results suggest that the locus coeruleus has a vasoconstrictive effect on the intraparenchymal vessels, although it exerts no apparent influence on the pial arteries.     

Cerebrovascular nerve fibers immunoreactive for tryptophan-5-hydroxylase in the rat: distribution, putative origin and comparison with sympathetic noradrenergic nerves

The distribution of serotonergic nerves in major basal and isolated small pial arteries (diameter > or = 50 microns) was investigated immunohistochemically using an antibody directed against tryptophan-5-hydroxylase (TPOH), the rate-limiting enzyme in the synthesis of 5-hydroxytryptamine (5-HT or serotonin), and compared to that of the noradrenergic system labeled for the selective noradrenaline (NA) synthesizing enzyme, dopamine-beta-hydroxylase (DBH). In addition, the possible peripheral and/or central origins of the cerebrovascular serotonergic (TPOH-positive) nerve fibers were examined. Strongly labeled TPOH-immunoreactive (TPOH-I) fiber bundles were observed in major basal arteries and gave rise to small varicose fibers organized in a meshwork pattern. The highest density of TPOH-I fibers was found in the middle cerebral artery followed by the anterior cerebral and the anterior communicating arteries, with a moderate to low density in the internal carotid and the vertebro-basilar trunk. Of the isolated pial arteries, only the larger ones (diameter > 75 microns) were significantly endowed with TPOH-I varicose fibers. However, free floating TPOH-I nerves were observed coursing through the pia-arachnoid membranes and reaching small pial vessels. In contrast, DBH-I nerve fibers were fine and were visualized primarily as numerous varicosities distributed in a circumferential manner around the vessel wall. A very high density of DBH-I varicosities was seen in the rostral part of the circle of Willis, with the internal carotid being the most richly supplied followed by the anterior cerebral and the anterior communicating arteries; comparatively, the middle cerebral artery was moderately innervated. The differences in distribution pattern and density between TPOH-I and DBH-I cerebrovascular fibers clearly suggest that these two innervation systems are not exactly superimposable. Superior cervical ganglionectomy caused an almost complete disappearance of TPOH-I nerves in all vascular segments, with some residual fibers in selected vessels. Lesion of the central serotonergic component with the neurotoxin 5,7-dihydroxytryptamine had virtually no effect on the TPOH-I fibers in the major basal and isolated pial arteries. These results strongly suggest that the serotonergic innervation of major cerebral as well as pial arteries has a prominent peripheral origin closely related to the sympathetic system. Processing of superior cervical ganglion slices for TPOH immunocytochemistry, however, failed to unequivocally detect TPOH-I neurons.     

Does vasospasm occur in small pial arteries and arterioles of rabbits?

BACKGROUND: Vasospasm is a serious complication associated with subarachnoid hemorrhage. Successful management of vasospasm will ultimately depend on a clear understanding of the scope of this phenomenon, including whether arterial elements of different calibers are equally affected. We therefore examined the responses to subarachnoid hemorrhage in rabbit basilar arteries, small pial arteries, and arterioles. SUMMARY OF REPORT: We compared the brain stem pial arteries of 10 perfusion-fixed male New Zealand White rabbits after experimental subarachnoid hemorrhage to those of five control rabbits using morphological analysis of cross-sections of plastic-embedded vessels. After subarachnoid hemorrhage, the internal elastic lamina was highly corrugated in all basilar arteries (mean diameter 319 +/- 51 microns). These arteries were severely constricted in comparison with the control group, in which the mean diameter was 691 +/- 17 microns, and corrugation of the internal elastic lamina was not present. In contrast, small pial arteries and arterioles very rarely demonstrated a vasoconstrictive configuration after subarachnoid hemorrhage. The contractility of the smaller vessels was confirmed by injecting 2 mg/kg BaCl2 intracisternally. Following BaCl2 injection, corrugation of the internal elastic lamina was detected in the small arteries and arterioles as well as the basilar arteries. CONCLUSIONS: We conclude that experimental chronic vasospasm after subarachnoid hemorrhage in rabbits tends to occur in large conducting arteries rather than in smaller pial arteries and arterioles.     

Intraoperative laser flowmetry reflects levels of cerebral blood flow during neurosurgical procedures

Abstract

Changes in cerebral blood flow (CBF) during craniotomies (mean 62.2 years, n = 31) were studied using a laser flowmeter (LFM) to evaluate the utility in CBF monitoring. A small flat probe was applied to the brain surface near the surgical field. The output voltage from LFM was recorded as CBF changes. The percent change in CBF was calculated using the formula [intrasurgical-CBF-control-CBF]/control-CBF x 100. Postoperative neurologic status was evaluated. Control-CBF values were similar among the groups representing different pathologies. The mean CBF decrease ranged from -7.3% following phenytoin injection (n = 9) to -32.7% during induced intrathoracic pressure (n= 10). The mean CBF increase was 41.4% following vascular anastomosis. A decrease > 50%) for more than 15 min was associated with a severe permanent neurologic deficit. The CBF monitoring using an LFM during craniotomy may be useful in detecting critical CBF levels for reducing post-operative neurological deficits. [Neurol Res 1996; 18: 457-461]