Intracranial Pressure In Rabbits Research Articles

The Effect of Body Position on Intraocular and Intracranial Pressure in Rabbits.

The correlation between cerebrospinal fluid (CSF) and intraocular pressure (IOP) is still unclear. We compared CSF and IOP measured by the same invasive technique using a new experimental model in rabbits during changes of body position. Pressure changes were recorded in the lateral ventricle (LV), the cortical subarachnoid space (CSS), and the anterior ocular chamber of anesthetized rabbits (n = 12). Animals and measuring instruments were both fixed on a board at an adequate hydrostatic level. In a horizontal position, control IOP (15.1 ± 1.6 cmH2O) and CSF pressure in the LV (12.4 ± 0.6 cmH2O) and CSS (12.2 ± 0.9 cmH2O) were similar during the 60-min period. When changing the body position from horizontal to vertical (upright), CSF pressures decreased drastically (LV = -5.5 ± 2.6 cmH2O and CSS = -7.7 ± 2.3 cmH2O), while the IOP decreased moderately (IOP = 13.3 ± 0.5 cmH2O). Change in body position from horizontal to vertical causes drastic changes in CSF pressure and moderate changes in IOP. Thus, IOP is not reflected by the CSF pressure. In an upright position, the values of CSF pressure were equal to the hydrostatic distance between measuring points and the foramen magnum, which suggests that CSF pressure inside the cranium depends on its anatomical and biophysical features, and not on CSF secretion and absorption.

Outer skull landmark-based coordinates for measurement of cerebral blood flow and intracranial pressure in rabbits

Despite the increased use of intracranial neuromonitoring during experimental subarachnoid hemorrhage (SAH), coordinates for probe placement in rabbits are lacking. This study evaluates the safety and reliability of using outer skull landmarks to identify locations for placement of cerebral blood flow (CBF) and intraparenchymal intracranial pressure (ICP) probes. Experimental SAH was performed in 17 rabbits using an extracranial–intracranial shunt model. ICP probes were placed in the frontal lobe and compared to measurements recorded from the olfactory bulb. CBF probes were placed in various locations in the frontal cortex anterior to the coronary suture. Insertion depth, relation to the ventricular system, and ideal placement location were determined by post-mortem examination. ICP recordings at the time of SAH from the frontal lobe did not differ significantly from those obtained from the right olfactory bulb. Ideal coordinates for intraparenchymal CBF probes in the left and right frontal lobe were found to be located 4.6 ± 0.9 and 4.5 ± 1.2 anterior to the bregma, 4.7 ± 0.7 mm and 4.7 ± 0.5 mm parasagittal, and at depths of 4 ± 0.5 mm and 3.9 ± 0.5 mm, respectively. The results demonstrate that the presented coordinates based on skull landmarks allow reliable placement of intraparenchymal ICP and CBF probes in rabbit brains without the use of a stereotactic frame.

Craniosacral Therapy: The Effects of Cranial Manipulation on Intracranial Pressure and Cranial Bone Movement

Quasi-experimental design. To determine if physical manipulation of the cranial vault sutures will result in changes of the intracranial pressure (ICP) along with movement at the coronal suture. Craniosacral therapy is used to treat conditions ranging from headache pain to developmental disabilities. However, the biological premise for this technique has been theorized but not substantiated in the literature. Thirteen adult New Zealand white rabbits (oryctolagus cuniculus) were anesthetized and microplates were attached on either side of the coronal suture. Epidural ICP measurements were made using a NeuroMonitor transducer. Distractive loads of 5, 10, 15, and 20 g (simulating a craniosacral frontal lift technique) were applied sequentially across the coronal suture. Baseline and distraction radiographs and ICP were obtained. One animal underwent additional distractive loads between 100 and 10,000 g. Plate separation was measured using a digital caliper from the radiographs. Two-way analysis of variance was used to assess significant differences in ICP and suture movement. No significant differences were noted between baseline and distraction suture separation (F = 0.045; P>.05) and between baseline and distraction ICP (F = 0.279; P>.05) at any load. In the single animal that underwent additional distractive forces, movement across the coronal suture was not seen until the 500-g force, which produced 0.30 mm of separation but no corresponding ICP changes. Low loads of force, similar to those used clinically when performing a craniosacral frontal lift technique, resulted in no significant changes in coronal suture movement or ICP in rabbits. These results suggest that a different biological basis for craniosacral therapy should be explored.

Dispersion of cerebral temperature, cerebral perfusion and intracranial pressure in rabbits placed with epidural balloons

This study examines the intracranial pressure and temperature dispersion in a rabbit model after epidural balloon compression. Right and left supratentorial, intraventricular and infratentorial pressures and temperatures of the rabbits have been measured before epidural balloon was placed. Afterwards, the epidural balloon was placed in right parietal epidural area. The intracranial pressure and temperature dispersion values were recorded after inflation with 0.3 and 0.6 ml, respectively. The control values of intracranial pressure measurements of four different brain regions were found to be similar. When the balloon was inflated to 0.3 ml, the intracranial pressure distribution was found to be equal in all the fields. After the balloon was inflated up to 0.6 ml, right and left supratentorial intracranial pressure values were found to be equal. However, infratentorial pressure values were lower and intraventricular pressure values were higher when compared with the right hemisphere. Before the inflation and at two different inflation volumes, perfusion pressure and temperature dispersion were found to be similar between right hemisphere and other compartments. We conclude that, the effective mechanism in cerebral temperature regulation may be related to preserved cerebral perfusion pressure and cerebral blood flow.

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.

Effect of intravenous prostaglandin E1 on pial vessel diameters and intracranial pressure in rabbits.

The main advantages of prostaglandin E1 (PGE1) for induced hypotension during neurosurgery include a rapid onset of action, a quick recovery from hypotension, lack of toxicity, maintenance of adequate perfusion to vital organs, and maintenance of cerebral blood flow reactivity to carbon dioxide during hypotension. However, there is no report that shows the effect of PGE1 on cerebral microvessel diameter and only a few data are available that show the effect of PGE1 on intracranial pressure. The aim of this study was to measure cerebral arteriole and venule diameters and intracranial pressure (ICP) during PGE1-induced hypotension to evaluate whether PGE1 is suitable for neuroanesthesia. We measured the effects of 0.1, 0.3, 1.0, 3.0, and 10.0 microg x kg(-1) x min(-1) of intravenous PGE1 on mean arterial pressure (MAP), cerebral arteriole and venule diameters and ICP in anesthetized rabbits. MAP decreased statistically significantly from baseline at the infusion rates of 1.0, 3.0, and 10.0 microg x kg(-1) x ml(-1). Arteriole diameter increased significantly from the baseline at the infusion rate of 10.0 microg x kg(-1) x ml(-1) (18% from control). Venule diameter did not change from baseline value at any infusion rate. ICP did not change from baseline value at any infusion rate. We conclude that PGE1 might be a suitable drug for induced hypotension in neurosurgery from the viewpoint of its small effect on the cerebral microvessels and ICP.

The effects of 30% and 60% xenon inhalation on pial vessel diameter and intracranial pressure in rabbits.

Xenon may increase cerebral blood flow and intracranial pressure (ICP). To evaluate the effects of xenon on brain circulation, we measured pial vessel diameter changes, CO(2) reactivity, and ICP during xenon inhalation in rabbits. Minimum alveolar anesthetic concentration (MAC) for xenon was established in rabbits (n = 6). By using a cranial window model, pial vessel diameters were measured at 30% and 60% xenon inhalation and in time control groups (n = 15). ICP, mean arterial blood pressure, and heart rate were recorded during 30% and 60% xenon inhalation (n = 5). Pial vessel diameters were measured during hypocapnia and hypercapnia conditions in 60% Xenon and Control groups (n = 14). MAC for xenon was 85%. Xenon (0.35 and 0.7 MAC) dilated the arterioles (10% and 18%, respectively) and venules (2% and 4%, respectively) (P < 0.05). Dilation of arterioles was more prominent than that of venules. ICP, mean arterial blood pressure, and heart rate did not change during xenon inhalation. No difference in CO(2) reactivity was observed between Xenon and Control groups (P = 0.79). Sixty percent xenon (0.7 MAC) dilated brain vessels, but venule changes were small. Xenon did not increase ICP and preserved CO(2) reactivity of the brain vessels. Xenon might increase cerebral blood flow; however, 0.7 minimum alveolar anesthetic concentration xenon preserved both low intracranial pressure and CO(2) reactivity of the cerebral vessels in the normal rabbit.

Room E, 10/17/2000 2: 00 PM - 4: 00 PM (PS) The Effects of Xenon on the Cerebral Blood Flow and Intracranial Pressure in Rabbits

<b>Room E, 10/17/2000 2: 00 PM - 4: 00 PM (PS) The Effects of Xenon on the Cerebral Blood Flow and Intracranial Pressure in Rabbits</b>

Age-Related Changes in Intracranial Pressure in Rabbits with Uncorrected Familial Coronal Suture Synostosis

Abstract Objective: Chronic, elevated intracranial pressure (ICP) in craniosynostotic infants may result in ocular and neurocapsular problems; however, not all infants exhibit elevated ICP. Clinical ICP studies are further confounded by small and heterogeneic samples, multiple-suture involvement, and varying surgical management protocols. The present study was designed to describe longitudinal changes in ICP in a large, homogenous sample of rabbits with uncorrected familial, nonsyndromic coronal suture synostosis. Methods: Ninety-one rabbits were divided into four groups: (1) normal rabbits (n = 28), (2) rabbits with delayed-onset coronal suture synostosis (DOCS; n = 25), (3) rabbits with unilateral coronal suture synostosis (UCS; n = 12), and (4) rabbits with bilateral coronal suture synostosis (BCS; n = 26). ICP was measured at 24 and 42 days of age using a Codman epidural microtransducer. Results: Rabbits with BCS had a significantly (p < .05) higher mean ICP at 25 days of age than rabbits in the other...

Increased intracranial pressure after coronal suturectomy in craniosynostotic rabbits.

It has been suggested that the complications associated with intracranial hypertension in craniosynostotic infants may be managed with surgical release of the synostosed sutures. However, both postoperative increases and decreases in intracranial pressure (ICP) have been reported in heterogeneous samples of infants with syndromic and nonsyndromic craniosynostoses. The present study was designed to describe longitudinal changes in ICP in a homogeneous sample of rabbits with uncorrected and corrected familial coronal suture synostosis and compare them with age-matched normal control rabbits. Fifty-three rabbits were divided into three groups: normal rabbits (n = 28), rabbits with uncorrected bilateral coronal suture synostosis (n = 9), and rabbits with bilateral coronal suture synostosis with coronal suturectomy at 25 days of age (n = 16). ICP was measured at 25 and 42 days of age using a Codman epidural microtransducer. Results revealed that rabbits with uncorrected craniosynostosis had significantly (P < 0.05) higher ICP at 25 days of age than normal control rabbits by approximately 86%. However, by 42 days of age, ICP in normal rabbits increased by 75%, whereas ICP in rabbits with uncorrected craniosynostosis decreased by 69% over the same time. Synostotic rabbits with coronal suturectomy showed a 50% decrease in ICP immediately after surgical release and then followed the normal, age-related ICP pattern, which significantly increased by 75% at 42 days of age. Results suggest that, in the rabbit model, the postsuturectomy rise in ICP may simply be normal, age-related changes, although a longer follow-up will be needed to determine the recurrence of pathological ICP. Possible multifactorial explanations for intracranial decompression and compensation in the craniosynostotic rabbit model are also discussed.

Acute brain death alters left ventricular myocardial gene expression

Objectives: The depressed myocardial function observed in brain dead organ donors has been attributed to massive sympathetic discharge and catecholamine cardiotoxicity. Because elevated catecholamines are associated with altered myocardial gene expression, we investigated whether acute brain death from increased intracranial pressure alters the expression of myocardial gene products important in contractility. Methods: A balloon expansion model was used to increase intracranial pressure in rabbits (n = 22). At timed intervals after brain death, mean arterial pressure, heart rate, electrocardiograms, histologic myocardial injury, and systemic catecholamines were assessed. Messenger RNA levels encoding myofilaments, adrenergic receptors, sarcoplasmic reticulum proteins, transcription factors, and stress-induced programs were measured with blot hybridization of total left ventricular RNA. Results: Increased intracranial pressure induced an immediate pressor response that temporally coincided with diffuse electrocardiographic ST segment changes. Systemic epinephrine and norepinephrine levels concurrently increased (5- to 8-fold within 1 minute), then fell below baseline within 2 hours, and remained depressed at 4 hours. By 1 hour, histologic injury was evident. Four hours after the induction of increased intracranial pressure, levels of messenger RNA–encoding skeletal and cardiac α-actins, egr-1, and heat shock protein 70 were significantly increased. Sham-operated animals did not exhibit these changes. Conclusions: Select changes in myocardial gene expression occur in response to increased intracranial pressure and implicate ventricular remodeling in the myocardial dysfunction associated with acute brain death. (J Thorac Cardiovasc Surg 1999;117:365-74)

The Effect of Phenylephrine on Raised Intracranial Pressure in Rabbits

The Effect of Phenylephrine on Raised Intracranial Pressure in Rabbits

Propofol and hyperventilation for the treatment of increased intracranial pressure in rabbits.

Using a rabbit model of intracranial hypertension, we studied (a) the additive effect of propofol and hyperventilation (HV) on increased intracranial pressure (ICP), (b) the ICP-lowering effect of additive therapy (i.e., propofol plus HV versus HV plus propofol), and (c) whether combined therapy induced cerebral ischemia. Twenty-three New Zealand White rabbits were studied, of which seven were control animals. The animals were anesthetized with midazolam and fentanyl. An extradural balloon was used to increase ICP to 26+/-2 mm Hg. Elevation of ICP resulted in a >50% reduction in ipsilateral somatosensory evoked potential (SEP) amplitude. The rabbits were then randomized to be treated with propofol followed by HV (Group 1, n = 8) or HV then propofol (Group 2, n = 8). With HV, PaCO2 was reduced from 41+/-2 mm Hg to 27+/-3 mm Hg. In Group 1 rabbits, the ICP decreased with treatment (from 26+/-2 to 12+/-2 mm Hg). The reduction in ICP was significantly greater (P = 0.008) than that in Group 2 rabbits (from 26+/-2 to 16+/-5 mm Hg). In both groups, propofol and HV had an additive effect in reducing ICP. Further, when propofol was used as the initial treatment, there was a significant increase in SEP amplitude that was not apparent in Group 2 rabbits. In conclusion, we found propofol and HV to be additive in the treatment of increased ICP. In animals treated with propofol followed by HV, there was a greater decrease in ICP than in rabbits treated initially with HV and then propofol. We have demonstrated that propofol has a greater effect on increased intracranial pressure than hyperventilation when used as the initial treatment and that the two treatments are additive. Should control of intracranial pressure be required after the administration of propofol, then hyperventilation may be added to the treatment.

Propofol and Hyperventilation for the Treatment of Increased Intracranial Pressure in Rabbits

Using a rabbit model of intracranial hypertension, we studied (a) the additive effect of propofol and hyperventilation (HV) on increased intracranial pressure (ICP), (b) the ICP-lowering effect of additive therapy (i.e., propofol plus HV versus HV plus propofol), and (c) whether combined therapy induced cerebral ischemia. Twenty-three New Zealand White rabbits were studied, of which seven were control animals. The animals were anesthetized with midazolam and fentanyl. An extradural balloon was used to increase ICP to 26 +/- 2 mm Hg. Elevation of ICP resulted in a >50% reduction in ipsilateral somatosensory evoked potential (SEP) amplitude. The rabbits were then randomized to be treated with propofol followed by HV (Group 1, n = 8) or HV then propofol (Group 2, n = 8). With HV, PaCO2 was reduced from 41 +/- 2 mm Hg to 27 +/- 3 mm Hg. In Group 1 rabbits, the ICP decreased with treatment (from 26 +/- 2 to 12 +/- 2 mm Hg). The reduction in ICP was significantly greater (P = 0.008) than that in Group 2 rabbits (from 26 +/- 2 to 16 +/- 5 mm Hg). In both groups, propofol and HV had an additive effect in reducing ICP. Further, when propofol was used as the initial treatment, there was a significant increase in SEP amplitude that was not apparent in Group 2 rabbits. In conclusion, we found propofol and HV to be additive in the treatment of increased ICP. In animals treated with propofol followed by HV, there was a greater decrease in ICP than in rabbits treated initially with HV and then propofol. Implications: We have demonstrated that propofol has a greater effect on increased intracranial pressure than hyperventilation when used as the initial treatment and that the two treatments are additive. Should control of intracranial pressure be required after the administration of propofol, then hyperventilation may be added to the treatment. (Anesth Analg 1998;87:564-8)

Mechanisms of increased intracranial pressure in rabbits exposed to head-down tilt.

Changes in intracranial pressure (ICP) resulting from head-down tilt (HDT) were studied in rabbits, and a possible role of edema formation in the change of ICP was examined. Animals were anesthetized with pentobarbital sodium and artificially ventilated. ICP was continuously monitored through a catheter inserted into the subarachnoid space. It increased depending on the tilt angle and decreased when the tilt angle was reduced. ICP elevated from 4.6 +/- 0.7 mmHg (mean +/- standard error of the mean) at horizontal prone position to 13.7 +/- 1.0 mmHg immediately after the onset of 45 degrees HDT and gradually reduced toward the pre-HDT baseline in the next 8 h. ICP decreased below the pre-HDT baseline value immediately after returning to the horizontal prone position, and gradually increased toward the baseline during the 2 h of recovery period. Histological examination (HE stain) demonstrated that exposure to 8 h of HDT did not cause remarkable edema in either the gray matter or the white matter in rabbits. Water content and specific gravity of brain tissues both were increased in the HDT group in comparison with the control group. These results suggest that edema formation plays little role in the elevation of ICP during the acute phase of HDT in rabbits.

Effects of Fentanyl-induced Rigidity on the Intracranial Pressure in Rabbits

Effects of Fentanyl-induced Rigidity on the Intracranial Pressure in Rabbits

Brain edema in rabbits with galactosamine-induced fulminant hepatitis

Abstract Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% ± 0.49% with significant elevations to 81.96% ± 0.47% and 82.95% ± 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2–9 mmHe and the ranee or peak values in galactosamine-treated rabbits was 18–55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.

Brain edema in rabbits with galactosamine-induced fulminant hepatitis: Regional differences and effects on intracranial pressure

Brain edema and intracranial hypertension are major complications of fulminant hepatic failure. We investigated the development of brain edema and monitored intracranial pressure in rabbits with toxic hepatitis induced by galactosamine. Using a gravimetric technique to assay small tissue samples, we found that brain water was increased in cortical grey matter, but not in subcortical, mesencephalic, and pontine white matter, or in the cerebellum. The proportion of water in cerebral grey matter in control animals was 80.96% ± 0.49% with significant elevations to 81.96% ± 0.47% and 82.95% ± 1.49% in mild and severe encephalopathy, respectively. This corresponds to mean increases in tissue volume of 5.5% and 11.7%. The hippocampal grey matter also accumulated water in severe encephalopathy with a 30% increase in mean tissue volume. The regional increase in brain water was confirmed by the wet-dry weight method. Neither hypotension, hypoxia, nor severe hypoglycemia were present to account for the edema. Intracranial pressure was monitored continuously in unanesthetized rabbits via an intraventricular cannula as encephalopathy developed. The pressure was normal in the mild stage, but was intermittently elevated in animals with severe encephalopathy. The normal range of intracranial pressure was 2–9 mmHe and the ranee or peak values in galactosamine-treated rabbits was 18–55 mmHg. The regional differences in brain water accumulation suggest that cellular swelling and abnormalities in the movement of water across the blood-brain barrier may account for the brain edema in this model.

An investigation of the role of lactic acid production in the causation of metabolic acidosis resulting from raised intracranial pressure in rabbits.

Intracranial pressure (ICP) was acutely raised in anaesthetized rabbits by the injection of saline into the cisterna magna. The raised ICP was maintained at 200 mm Hg for 3 min after which it was allowed to return to baseline values. The profound metabolic acidosis produced (mean base deficit reaching 17.99 +/- SD 4.06 mmol/1 30 min after raised ICP) was found to be in part related to an increase in arterial blood lactate (from mean 7.04 +/- SD 3.26 mmol/l before raised ICP to mean 13.57 +/- SD 5.28 mmol/l 30 min after raised ICP). It would appear that systemic sympathetic nervous system discharge consequent upon raising ICP results in intense vasoconstriction and thus an increase in anaerobic metabolism and inorganic acid production.

Effect of chain length of short-chain fatty acids on their effect on intracranial pressure in rabbits.

The short-chain fatty acids propionic, butyric, valeric, isovaleric and octanoic produced elevations in intracranial pressure during intravenous infusion in rabbits. Serum concentrations of these compounds are elevated in patients with Reye's syndrome, and may contribute to the intracranial pressure elevations found in these patients.