Sagittal Sinus Pressure Research Articles

Effect of Sevoflurane on Intracranial Pressure, Sagittal Sinus Pressure, and the Intracranial Volume-Pressure Relation in Cats

The effect of sevoflurane on intracranial pressure (ICP), sagittal sinus pressure (SSP), and the intracranial volume-pressure (V-P) relation was examined in cats. In experiment 1, on nine cats, changes in ICP and SSP were studied for 180 min during anesthesia with 1 MAC sevoflurane (2.6%, inspired) and 50% nitrous oxide (N2O) in oxygen (O2). ICP significantly (p <0.01) increased from 8.4 +/- 3.8 cm H2O (mean +/- SD), the control level to 10.6 +/- 5.1 cm H2O immediately after the administration of sevoflurane. ICP was unchanged for the subsequent 120 min but then increased significantly (p <0.05) 140 min after administration, being 15.5 +/- 9.0 cm H2O at 180 min. There were no changes in SSP or blood gases. In experiment 2, the rapid injection technique of mock cerebrospinal fluid was used to determine the intracranial V-P relation in ten cats. Measures of V-P relationships included (a) ICP before volume injection (Po), (b) peak ICP caused by volume injection (Pp), (c) intracranial compliance (C) calculated as the ratio of change of intracranial volume Delta V) to change of ICP (Delta P), and (d) the pressure volume index (PVI) calculated as the ratio of Delta V to log Pp/Po. The subjects were divided into two groups, one administered 2.6% sevoflurane and 50% N2O in O2 (n = 6) and the other 50% N2O in O2 (n = 4). Each cat in both groups was given two bolus injections into the lateral ventricle at 180 min after the start of anesthesia. Then, C and PVI were calculated. C and PVI in the group treated with sevoflurane were significantly (p <0.05) lower than in the other group. These findings suggest that prolonged use of sevoflurane increases the intracranial elastance.

Elevated cortical venous pressure in hydrocephalus

To gain a better understanding of cerebrospinal fluid (CSF) hydrodynamics and their relationship to the cerebrovascular system, normal and naturally hydrocephalic dogs were studied to determine transmantle [lateral ventricle (LV) to subarachnoid space] and transparenchymal [LV to cortical vein (CV)] pressures. Pressure was also measured in the sagittal sinus, cisterna magna, and femoral artery. CV pressure has not previously been measured in hydrocephalus. Ventricular volume was determined by computed tomography. Four groups of animals were studied. In Group 1 (n = 5) transmantle pressure was measured; in Group 2 (n = 5), transparenchymal pressure in normal animals was measured. In Group 3 (n = 5) was measured all the pressures in spontaneously normal animals, and in Group 4 (n = 6) was measured the pressures in hydrocephalic animals. The pressure-volume index and CSF outflow resistance were also measured. LV volume in the normal dogs was 1.3 +/- 0.7 ml and in the hydrocephalic dogs was 5.1 +/- 2.7 ml (P less than 0.005). Although LV, subarachnoid space, and sagittal sinus pressures were elevated in the hydrocephalic dogs (15.1 versus 10.2, 16.4 versus 10.5, and 8.4 versus 5.2 mm Hg, respectively), the transmantle pressure and subarachnoid space to sagittal sinus gradients were not significantly altered. CV pressure was markedly elevated in the hydrocephalic animals (21.5 versus 11.7 mm Hg, P less than 0.005). The pressure-volume index and outflow resistance were not significantly different. These results suggest that an elevated CV pressure plays a role in the development and/or maintenance of hydrocephalus, and that the pathway for CSF absorption includes transcapillary or transvenular absorption of CSF from the interstitial space.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular response to changes of cerebral venous pressure and cerebrospinal fluid pressure

Using parietal cranial windows and multichannel videoangiometry, pial vessel responses were studied in cats during stepwise elevation of superior sagittal sinus pressure (Psss) to a level of 50 mmHg or reduction of CSF-pressure (PCSF). PCSF was monitored via a needle in the great cistern, known from previous studies to be identical to supratentorial CSF-pressure. During elevation of PSSS, large and small pial veins dilated by 14 +/- 6.1% from resting diameter. Small arteries remained unresponsive until they were dilated by 9 +/- 2.1% at the level of PSSS 50 mmHg. Large arteries dilated by 18 +/- 5.5% at the level of PSSS 50 mmHg. PSSS was always approximately twice as high as PCSF during increase of PSSS. During reduction of PCSF to -5 mmHg, pial veins also dilated, by 7.4 +/- 1% on the average. This observation suggests that normal PCSF is a result of mainly venous vascular pressure, and that the level of normal venous pressure is not dictated by PCSF but by the function and architecture of the cerebral vasculature. Since the rapid reduction of cerebral perfusion pressure CPP by elevation of venous pressure does not induce autoregulatory adjustment according to the level of CPP, but to the level of arterial transmural pressure, it is concluded, that the basic mechanism underlying autoregulation of CBF is myogenic.

Pressure Ventilation Increases Brain Vascular Prostacyclin Production in Newborn Pigs

Using awake, chronically catheterized newborn pigs, we measured cerebral blood flow (CBF), net cerebral vascular 6-keto-prostaglandin F1 alpha production, and cerebral metabolic rate of oxygen (CMRO2) during hypercapnia and during hypercapnia at increased mean airway pressure (Paw), both before and after treatment with indomethacin. CBF nearly doubled during hypercapnia. The hypercapnia-induced cerebral hyperemia was maintained when Paw was increased from 3 +/- 2 to 16 +/- 4 cm H2O during hypercapnia. Sagittal sinus pressure increased in proportion to the increase in Paw, and cardiac output was unchanged. Net cerebral production of 6-keto-prostaglandin F1 alpha increased from 9 +/- 1 to 15 +/- 1 ng/min/100 g tissue during hypercapnia and increased dramatically to 57 +/- 1 ng/min/100 g when hypercapnia was coupled with an increase in Paw. CMRO2 was not changed by either hypercapnia or increased Paw. After indomethacin, CBF decreased and cerebral vasodilation to hypercapnia did not occur. After indomethacin, adding increased Paw during hypercapnia dropped CBF below baseline, adversely affecting CMRO2. These results suggest that cerebral hypercapnia hyperemia requires brain prostanoid production and that when Paw is increased during hypercapnia, the contribution of prostanoids to maintaining CBF is increased. Increasing ventilation pressure during hypercapnia in piglets pretreated with indomethacin compromises CBF sufficiently to reduce CMRO2.

Blood-brain barrier integrity during cardiopulmonary resuscitation in dogs.

Blood-brain barrier integrity during cardiopulmonary resuscitation may be important because of the potential effects of adrenergic agonists administered during arrest on cerebral metabolism and the cerebral vasculature. As an index of blood-brain barrier permeability to small molecules, we measured the brain uptake of [14C]alpha-aminoisobutyric acid during a 10-minute period in 25 anesthetized dogs. To correct for the amount of carbon-14 label in the plasma space, we administered [3H] inulin 2 minutes before death. The mean transfer coefficient in 14 brain regions of five control dogs ranged from 0.002 to 0.007 ml/g/min. After 8 (n = 15) or 15 (n = 5) minutes of cardiac arrest, external chest compression was instituted to maintain aortic blood pressure above 60 mm Hg. The transfer coefficient was not elevated during chest compression (n = 10), immediately following defibrillation (n = 5), or 4 hours after resuscitation (n = 5); in some brain regions the transfer coefficient decreased. However, the decrease in the transfer coefficient was proportional to the decrease in the cerebral plasma volume as measured by the ratio of the [3H]inulin concentration in the tissue to that in the plasma. Thus, it is unlikely that a decrease in capillary surface area masked an increase in blood-brain barrier permeability. Therefore, we found no evidence of blood-brain barrier disruption during or after cardiopulmonary resuscitation in dogs. Despite the large phasic increases in sagittal sinus pressure associated with external chest compression, concurrent increases in cerebrospinal fluid pressure apparently protect the microcirculation from increased transmural pressure.

Intracranial hypertension associated with unruptured cerebral arteriovenous malformations

Only 6 patients with intracranial hypertension associated with unruptured cerebral arteriovenous malformations have been reported. We report 6 additional patients seen at the Cleveland Clinic during the past 10 years. The average age was 28 years (range, 19-44 years); 4 were women. Symptoms and signs included papilledema (6 patients), headache (6), transient nonepileptic focal symptoms (4), visual obscurations (3), ipsilateral carotid or ocular bruits (3), abnormal visual fields (3), focal seizures (2), and progressive visual loss (1). Enhanced computed tomography (CT) or magnetic resonance imaging (MRI) demonstrated the malformations in all 6 patients. The malformations were large, supplied by the branches of the middle and anterior cerebral arteries, with the posterior cerebral artery contributing in 3 patients, and all drained into the superior sagittal sinus. Associated venous obstruction was seen in 2 patients. Four patients underwent excision of the arteriovenous malformation, with resolution of papilledema in all 4. Measurements of cortical arterial and venous pressures during surgery in 3 patients showed decreased feeding artery pressures and elevated draining vein pressures, which normalized after removal of the malformation. Treatment in the 2 remaining patients consisted of medical therapy (acetazolamide, furosemide, steroids) alone in 1 patient, and in conjunction with proton beam radiation in the other. Papilledema resolved in the former patient, but the patient receiving proton beam radiation still had papilledema 2 years later. Intracranial hypertension associated with unruptured cerebral arteriovenous malformations occurs in young patients with high flow malformations that drain into the superior sagittal sinus, and is likely the result of increased cortical venous and superior sagittal sinus pressure. Excision of the malformation effectively reduces the intracranial pressure.

Age-related effects of compression rate and duration in cardiopulmonary resuscitation

The effects of various compression rate and duration combinations on chest geometry and cerebral perfusion pressure during cardiopulmonary resuscitation (CPR) were studied in immature swine. Pentobarbital-anesthetized 2- and 8-wk-old piglets received CPR after ventricular fibrillation. At compression rates of 40, 60, 80, 100, 120, and 150/min, duty cycle (compression duration/total cycle time) was increased from 10 to 80% by 10% increments. Mean aortic and sagittal sinus pressures, pulsatile displacement, and deformity of the anterior chest wall were measured. Increasing duty cycle increased cerebral perfusion pressure until chest relaxation time was compromised. Inadequate chest recoil, development of static chest deformation, and limitation of pulsatile chest wall movement occurred in both age groups when relaxation time was very short (150-200 ms in 2-wk-old piglets, 250-300 ms in 8-wk-old piglets). These changes in chest geometry correlated with deterioration of cerebral perfusion pressure only in 8-wk-old piglets. In the younger group, perfusion pressures plateaued but did not deteriorate. These data emphasize the importance of duty cycle in generating cerebral perfusion pressure and indicate that younger animals can tolerate high compression rates except at extremely long duty cycles.

Cerebrovascular Responsiveness to Carbon Dioxide in Dogs with 1.4% and 2.8% Isoflurane

Cerebral blood flow (CBF) responsiveness to alterations in arterial CO2 tensions (PaCO2) during 1.4% and 2.8% isoflurane anesthesia was assessed. Dogs were initially anesthetized with thiopental (12 mg/kg, iv bolus), their tracheae intubated, after which anesthesia was maintained with 1.4% isoflurane. In eight animals three levels of PaCO2 (25, 40, and 60 mmHg) were studied during 1.4% and 2.8% isoflurane. Mean arterial blood pressure, sagittal sinus pressure, and cerebrospinal fluid pressure were measured and CBF was determined using radiolabeled microspheres. Cerebral perfusion pressure (CPP) was maintained constant at approximately 80 mmHg by inflation of a balloon in the midthoracic aorta. CBF during normocapnia was 70 +/- 14 and 118 +/- 18 ml.min-1.100 g-1 with 1.4% and 2.8% isoflurane, respectively. As PaCO2 was decreased and increased, CBF decreased and increased to 42 +/- 7% and 185 +/- 16% of control, respectively, during 1.4% isoflurane. During 2.8% isoflurane, hypocapnia decreased CBF to 39 +/- 6% of control, but CBF did not increase with hypercapnia. In a second group of animals (n = 8), the effects of changes in CPP during hypercapnia with 1.4% and 2.8% isoflurane were assessed. Increasing CPP approximately 25 mmHg with both 1.4% and 2.8% isoflurane increased CBF but did not change CVR from control. With 1.4% isoflurane, the cerebral vasculature constricts with hypocapnia and dilates with hypercapnia, whereas with 2.8% isoflurane, vasoconstriction to hypocapnia is retained but vasodilation to hypercapnia is absent.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of isoflurane on cerebral autoregulation in dogs.

The effect of decreased cerebral perfusion pressure (CPP) on regional cerebral blood flow (CBF) with radiolabeled microspheres in dogs receiving either 1.4% or 2.8% isoflurane following anesthesia induction with thiopental (12 mg/kg, iv bolus) was studied. Mean arterial blood pressure (MABP), cerebrospinal fluid pressure (Pcsf), and sagittal sinus pressure (Pss) were measured. CPP of 83, 63, 53, 43, 33, and 23 mmHg were studied in three groups of animals. In group 1 (n = 6, isoflurane 1.4%) CPP was decreased by hemorrhage, in group 2 (n = 6, isoflurane 1.4%) CPP was decreased by increasing Pcsf while MABP was maintained constant, and in group 3 (n = 6; isoflurane 2.8%) CPP was decreased by hemorrhage. Control total CBF in groups 1, 2, and 3 was 69 +/- 8, 72 +/- 7, and 150 +/- 25 ml.min-1.100 g-1, respectively, at CPP of 84 +/- 1 mmHg. Flow to both cerebral hemispheres and brain stem in animals receiving 2.8% isoflurane was approximately twice that found with 1.4% isoflurane while CMRO2 was similar (about 3.5 ml.min-1.100 g-1). In groups 1 and 2 flow in all brain areas was maintained as CPP decreased to 43 mmHg and then flow decreased as CPP decreased further (P less than 0.05). In group 3 flow to all brain areas decreased progressively as CPP decreased from 83 to 23 mmHg. At CPP of 43 mmHg and below, flow to cerebrum was similar in the three groups; however, flow to brain stem in group 3 animals remained elevated above groups 1 and 2 until CPP was decreased to 23 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between intracranial and sagittal sinus pressure in normal and hydrocephalic dogs.

The relationship between intracranial and sagittal sinus pressure in normal and kaolin-induced hydrocephalic greyhounds was examined. In normal dogs there was an average 14 mm Hg pressure difference between the ventricles and the sagittal sinus. Elevations of intraventricular pressure were accompanied by small but consistent elevations in sagittal sinus pressure. In hydrocephalic dogs the average pressure differential was only 2 mm Hg. Also elevations of intraventricular pressure were accompanied by greater elevations in sagittal sinus pressures than those seen in normal dogs. The volume-buffering capacity of the sagittal sinus was decreased, and sinography revealed filling of unusual venous collaterals in hydrocephalic dogs--both suggesting an increased resistance to outflow in the sagittal sinus.

Effect of PEEP and jugular venous compression on canine cerebral blood flow and oxygen consumption in the head elevated position.

Cerebral blood flow (CBF) (radiolabelled microspheres) and oxygen consumption (CMRO2) were studied in nine dogs during 30 min of either neck vein compression or application of positive end-expiratory pressure (PEEP) ventilation. With the animal in the prone position, elevation of the head from horizontal to 30 cm above the heart markedly decreased cisterna magna (PCSF) and dorsal sagittal sinus pressure (PCV). With the head elevated, compression of neck veins using neck tourniquet (pressure 40 mmHg) increased PCSF and PCV from 3.6 +/- 2.2 to 6.8 +/- 4.8 and -2.5 +/- 2.7 to 2.3 +/- 2.3 mmHg (mean +/- SE, P less than 0.05), respectively, while total or regional CBF and CMRO2 remained unchanged. Application of PEEP (15 cm H2O) increased right atrial pressure (-4.7 +/- 1.7 to -0.1 +/- 3.4 mmHg, P less than 0.05), but did not affect PCSF or PCV (3.4 +/- 3.3 to 3.3 +/- 3.7 and -3.5 +/- 2.6 to -4.1 +/- 2.4 mmHg, respectively, P greater than 0.05). Total or regional CBF and CMRO2 were also unaffected. These data demonstrate that, although neither maneuver affects CBF or CMRO2, neck vein compression elevates PCV above atmospheric pressure, but PEEP does not. In patients at risk for cerebral venous embolism, intermittent neck vein compression should be used as a prophylactic measure to prevent air embolism.

Relationship between mean airway pressure, cardiac output, and organ blood flow with normal and decreased respiratory compliance

We investigated the relation between blood flow and mean airway pressure in two groups of anesthetized newborn piglets. The first group had normal respiratory compliance; the second group had pulmonary surfactant depleted by repeated saline lavage, which decreased static respiratory compliance by 42%. In the normal group, cardiac output decreased linearly from 292 +/- 43 mL/min/kg at 5 cm H2O airway pressure to 134 +/- 37 ml/min/kg at 20 cm H2O airway pressure, a drop of 43% (r2 = 0.79). Blood flow to the heart, kidney, and intestines had a similar decline, but brain, hepatic artery, and adrenal flow were constant. Mean arterial blood pressure did not decrease significantly until the highest airway pressure was reached, whereas sagittal sinus pressure increased as mean airway pressure increased. In contrast, the surfactant-depleted group maintained cardiac output up to a mean airway pressure of 15 cm H2O. At 20 cm H2O, cardiac output fell to 40% of the original value. Blood flow to the heart and kidneys fell at a mean airway pressure of 20 cm H2O; intestinal blood flow decreased beginning at 10 cm H2O. As in the normal piglets, brain, hepatic arterial, and adrenal blood flow were not affected by increasing ventilation pressure. Our data show that positive pressure ventilation in the neonate has important cardiovascular effects that are blunted when respiratory compliance is decreased. More important, because cardiac output decreased prior to a significant decline in arterial blood pressure, these data suggest that in a clinical setting considerable cardiovascular alterations can occur before a decline in arterial blood pressure is detected.

Changes in superior sagittal sinus pressure in children with head elevation, jugular venous compression, and PEEP.

Air embolism is a potential hazard during craniotomy whenever intracranial venous pressure is subatmospheric. In order to better understand both the risk of air embolism and its treatment in neurosurgical patients, the authors have investigated the relationship of superior sagittal sinus pressure (SSP) to head position in 15 children and examined the effects of both jugular venous compression and positive end-expiratory airway pressure (PEEP) on SSP. Progressive head elevation significantly decreased mean SSP and, in five patients, SSP was less than 0 mm Hg at 90 degrees torso elevation. A PEEP of 10 cm H2O was ineffective in significantly increasing SSP at any degree of head elevation, whereas bilateral internal jugular compression always caused a significant increase in SSP. The authors conclude that children are at risk for venous air embolism when undergoing suboccipital craniectomy in the sitting position because intracranial venous pressure is often subatmospheric when the head is elevated. Furthermore, maintaining PEEP does not appear to be a reliable treatment for increasing SSP, whereas bilateral internal jugular compression is effective.

What is Comprehensible from the Infusion Test?

The purpose of this report is to clarify the origin of the pressure-response (p-r) curve after a bolus normal saline injection into the subarachnoid space. Eighteen adult mongrel dogs weighing 9-13 kg were intubated and ventilated artificially. A bolus normal saline injection (0.8 ml-sec) was performed and the changes in intracranial pressure, superior sagittal sinus pressure, and systemic arterial pressure were monitored and recorded continuously for 30 minutes. The following results were elicited: 1) The shape of the p-r curve was determined by three resistances: resistance to the cerebrospinal fluid (CSF) absorption (r), blood inflow resistance into the sinus (Ri), and blood outflow resistance from the sinus to the extracranial venous system (Ro). A new intracranial volume-pressure model was proposed for detailed analysis of the volume-pressure relationship. 2) Changes in the CSF pressure after a bolus injection were characterized by two components. The steep decay of the p-r curve was thought to occur because of the CSF absorption, and the gentle decay should be the result of sinus outflow resistance which might be equivalent to the CSF absorption resistance, since the CSF absorption resistance should be rapidly changeable and pressure dependent. Patterns of the p-r curve were divided into three groups, namely “normal, ” “borderline, ” and “delayed” patterns. The last one could result either from high r state or from high Ro conditions. The borderline group contained dogs in which the intracranial cavity was tight. The CSF absorption resistance could be obtained by careful analysis of the p-r curve, but it might be modified by the spatial compensation of the venous system. It is thought to be important for the reasonable analysis of the p-r curve that the shape consideration, the baseline-peak pressure gradient (pressure increment), and the recovery time to the baseline pressure should all be included in a single analytical theory.

The CSF pulse wave in hydrocephalus.

Twenty-one dogs were rendered hydrocephalic by the intracisternal injection of kaolin. After various intervals between 1 and 44 days the animals were anesthetized for the measurement of arterial (lingual), ventricular, and sagittal sinus pressures. Following the recordings the animals were sacrificed by formalin infusion, the brains sectioned serially, and ventricular size measured. In general, the longer the period of incubation the larger the ventricles. There was no correlation between the degree of hydrocephalus and mean or pulsatile ventricular pressure. All animals with a pressure of less than 9 torr demonstrated non-linear transmission of the arterial wave into the CSF (which is the same as the pulse in the venous bed). All animals with a pressure greater than 12 torr had linear transmission of the wave. These findings in the hydrocephalic animals are the same as those found in nonhydrocephalic animals with similar pressures. It is concluded that the CSF pulse wave seen in hydrocephalic dogs is a result of how the cerebrovascular bed processes the cardiac pulse wave and is independent of the hydrocephalic process. There is no evidence that the pulse wave produces hydrocephalus.

1457 AUTOREGULATION OF CEREBRAL BLOOD FLOW (CBF) IN THE EARLY AND LATE POST-ASPHYXIC PERIOD IN NEWBORN DOGS

Autoregulation (AR) of CBF in newborns is thought to be easily impaired. We tested AR at 20 minutes (early) after an asphyxic insult in paralyzed ventilated newborn dogs age l-5d. CBF was measured with microspheres; cerebral perfusion pressure (CPP) was calculated as mean arterial pressure minus sagittal sinus pressure. Baseline (I) measurements in experimental (EXP n=12) and control (CON n=12) groups were followed by a series of 3 × 3 1/2 minute asphyxic insults produced by interrupting ventilation; a 5 minute recovery period separated successive insults. In EXP, AR was then tested at 20 minutes post-asphyxia during hypovolemic hypotension (II) followed by volume repletion (III); CON served as time controls. PaO2 >80 torr and PaCO2=30-45 torr for all flow studies. All results mean ± SE. Conclusion: Thus, in the early post-asphyxic period, CBF is independent of CPP. Preliminary results at 60 minutes post-asphyxia (late) shows similar results (EXP n=3, CON n=4). Overall, AR appears to be functional in the post-asphyxic period in newborn dogs.

INFLUENCE OF VENOUS PRESSURE (VP) ON CEREBRAL BLOOD FLOW NEWBORN DOGS

Marked increases in VP occur frequently in premature newborns with RDS. Since VP affects cerebral perfusion pressure (CPP) (CPP=Mean arterial pressure (MAP)-VP) it may alter CBF or its autoregulation. To examine this we studied CBF under conditions of normal and elevated VP in 7 anesthetized, paralyzed, ventilated newborn dogs, 4-12d. MAP and sagittal sinus pressure (an estimate of cerebral VP) were measured continuously. CBF, cerebellar-brainstem blood flow (CBrBF) and cardiac output (CO) were measured using microspheres; cerebral vascular resistance was calculated. VP was elevated by a snare-ligature placed about the intrathoracic SVC after ligation of the azygos vein. In each animal, 2 measurements were made with VP normal, and 2 with VP elevated and their order was randomized. PaO2 was > 100 torr. Results as mean ± SEM; * p < 0.01, t-test.Thus with moderate elevation of VP, CBF and CBrBF remain independent of CPP, demonstrating autoregulation.

Effect of cranioplasty on cerebrospinal fluid hydrodynamics in patients with the syndrome of the trephined.

Forty patients with cranial bone defects after craniectomy underwent extensive cerebrospinal fluid (CSF) hydrodynamic investigations by means of a CSF infusion test before and after cranioplasty. The results of these investigations were related to the clinical signs of the patients before and after cranioplasty and to the size and location of the skull bone defect. Twenty-two patients were considered to have "the syndrome of the trephined" (ST). The remaining patients were either free of symptoms or had symptoms not related to ST. CSF hydrodynamic variables that were changed before and normalized after cranioplasty include the following: Resting pressure, sagittal sinus pressure, buffer volume, elastance at resting pressure and pulse variations at resting pressure. The changes were statistically significant mainly in ST patients who were also relieved of their symptoms after cranioplasty.

Hydraulic model of myogenic autoregulation and the cerebrovascular bed: the effects of altering systemic arterial pressure.

Systemic arterial (Ps), cerebrospinal fluid (Pcsf), and sagittal sinus (Pss) pressures were measured in 39 dogs divided into eight groups in which Ps was altered pharmacologically or by bleeding. The pharmaceuticals used were norepinephrine (N-EP), dopamine (DOP), sodium nitroprusside (SNP), and nitroglycerin (NTG). SNP and NTG were examined with and without methohexital (MHX) anesthesia and during chronic infusion and bolus injection. The various pressures were subjected to systems analysis in accordance with a previously published model of myogenic autoregulation. Myogenic autoregulation seemed to be impaired only during infusions of N-EP, DOP, and SNP without MHX and during hypovolemic hypotension. The various observed changes in Pcsf are explained by using a hydraulic model of the cerebrovascular bed in which Pcsf represents the pressure drop across the outflow resistance of the bridging veins and lateral lacunae and myogenic autoregulation at the arteries and arterioles represents the major inflow resistance. Impaired myogenic autoregulation is associated with a rise in Pcsf. In addition, variation in pulse pressure is demonstrated to be related to the arterial pulse pressure and the degree of arterial and arteriolar vasodilation.

Late cerebral arterial spasm: The cerebrovascular response to hypercapnia, induced hypertension and the effect of Nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates

1. 1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14–33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO 2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. 2. One week after the blood injections were started there was about 10–20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of P aCO 2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.