Effect of increased intracranial pressure on gastric acid secretion

The effects of intracranial pressure on gastric acid secretion were studied in 30 rabbits. Intracranial pressure was increased in a graded and controlled fashion using a barostat connected to a cannula in the lateral cerebral ventricle. Eighteen rabbits were studied under urethane anesthesia with a background subthreshold intravenous infusion of bethanechol. Twelve rabbits were studied in the conscious state. Increases in intracranial pressure led to immediate and significant increases in gastric acid output in a dose-related manner in both conscious and anesthetized animals. Serum gastrin levels did not increase in either group of animals. Vagotomy only partially abolished the increase in acid outputs seen with increased intracranial pressure, whereas atropine completely blocked the response. We conclude that increased intracranial pressure causes stimulation of acid secretion by a gastrin-independent cholinergic mechanism that is only partially mediated by the vagus.     

The effect of increased intracranial pressure (ICP) on gastric motility

This study evaluates the effect of increased intracranial pressure (ICP) on gastric motility. Nine male cats (weight, 4.84 +/- 1.16 kg) were anesthetized with ketamine and underwent laparotomy for placement of bipolar (silver-silver chloride) electrodes on the serosal surface of the gastroesophageal junction (GEJ), antrum, and prepyloric areas of the stomach. At 1 week frontoparietal burr holes were performed with placement of an epidural Fogarty catheter. Migrating myoelectric complexes (MMCs) were evaluated at the GEJ, antrum, and prepyloric areas at varying levels of ICP (baseline and 20, 40, and 60 mm Hg) using balloon inflation. MMCs at the GEJ were triphasic with a period of 4 sec (+/- 1 sec) at baseline levels. At ICP levels above baseline, periodicity and waveforms at the GEJ became irregular. Waveforms became multiphasic with 1- to 2-sec periods and variable amplitudes. In the antral and prepyloric areas, duration and amplitude of the triphasic MMCs was unchanged from baseline. At 60 mm Hg ICP periodicity was significantly altered at both 1 and 2 weeks. MMCs returned to baseline levels with balloon deflation. The data indicate that elevated ICP (to 60 mm Hg) results in consistent and reproducible alterations of MMC periodicity, suggesting that such alterations may influence gastric motility.     

Elevated intracranial pressure from cerebral venous obstruction by Masson's vegetant intravascular hemangioendothelioma. Case report

The case is described of a 15-year-old girl with papilledema and visual obscurations caused by a rare lesion, Masson's vegetant intravascular hemangioendothelioma, within the venous sinus at the torcular herophili. This lesion impeded cranial venous outflow, leading to intracranial hypertension.     

Multiparametric monitoring of brain under elevated intracranial pressure in a rat model

Intracranial hypertension may develop in most patients exposed to traumatic head injury. In many cases, patients enduring elevated intracranial pressure (ICP) will incur morbidity or mortality. Several methods are used in animal models to investigate the influence of ICP elevation on physiological parameters. In this study, we developed a cisterna magna model by adding a mechanism for warming the mock cerebrospinal fluid (CSF) entering the cisterna space to a temperature of 37 degrees C and combined this method for ICP elevation with the multiparametric monitoring system (Multiprobe Assembly [MPA]). Using the MPA, we monitored, for the first time, mitochondrial NADH redox state as well as ionic homeostasis under elevated ICP in a rat model. In addition, we monitored cerebral blood flow (CBF) by laser Doppler flowmetry, ECoG (bipolar electrodes), and surface temperature. Blood pressure was measured in the cannulated femoral artery. The ICP (monitored by Camino probe) was elevated to 50-60 mm Hg for 13-15 min, followed by 2 h of recovery. The results show that CBF was decreased by 90%, while NADH was elevated by 80% as compared to the normoxic levels. Complete depolarization occurred as evidence by the decrease in extracellular Ca2+ and a significant increase in K+. All parameters recovered 10 min after reopening the cannula to the cisterna magna to air pressure. We conclude that ICP elevation through the cisterna magna infusion method, used simultaneously with multiparametric monitoring, supplies reliable information on the brain tissue metabolic state with intracranial hypertension in a rat model.     

Raised intracranial pressure

Opinion statement Raised intracranial pressure is a relatively common problem facing the clinician treating neurocritically ill patients. It is a leading cause of death in patients with intracranial pathology. There is a lack of controlled clinical trials evaluating most of the therapies currently available for raised intracranial pressure. The basic pathophysiologic and clinical principles of raised intracranial pressure are discussed and the major treatment options are presented. Patients with raised intracranial pressure should be evaluated immediately with particular attention to airway and hemodynamic status. Controlled hyperventilation and hyperosmolality (using mannitol or hypertonic saline solutions) frequently are administered simultaneously. In patients with refractory elevation of intracranial pressure other therapies such as barbiturate coma and surgical interventions are available.     

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.     

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)     

The intracranial volume pressure response in increased intracranial pressure patients: Part 1. Calculation of the volume pressure indicator

Background

The intracranial pressure (ICP) is usually continuously monitored in the management of patients with increased ICP. The aim of this study was to discover a mathematic equation to express the intracranial pressure–volume (P–V) curve and a single indicator to reflect the status of the curve.

Methods

Patients with severe brain damage who had bilateral external ventricular drainage (EVD) from December 2008 to February 2010 were included in this study. The EVD was used as drainage of CSF and ICP monitor. The successive volume pressure response [6] values were obtained by successive drainage of CSF from ICP 20–25 to 10?mmHg. Parabolic, exponential, and linear regression models were designed to have a single parameter as the indicator to determine the P–V curves.

Results

The mean of parameter “a” in the exponential equation is 1.473?±?0.054; in the parabolic equation, it is 0.332?±?0.061; and in the linear equation, it is 1.717?±?0.209. All regression equations of P–V curves had statistical significance (p?<?0.005). Parabolic and exponential equations are closer to the original ICP curve than linear equation (p?<?0.005). There is no statistically significant difference between parabolic and exponential regressions.

Conclusions

The P–V curve can be expressed with linear, parabolic, and exponential regression models in increased ICP patients. The parabolic and exponential equations are more accurate methods to represent the P–V curve. The single parameter in the three regression equations can be compared in different conditions of one patient in clinical practice.     

Elevated hydrostatic pressure stimulates ATP release which mediates activation of the NLRP3 inflammasome via P2X<Subscript>4</Subscript> in rat urothelial cells

Partial bladder outlet obstruction (pBOO) is a prevalent urological condition commonly accompanied by increased intravesical pressure, inflammation, and fibrosis. Studies have demonstrated that pBOO results in increased NLRP3 inflammasome and caspase-1 activation and that ATP is released from urothelial cells in response to elevated pressure. In the present study, we investigated the role of elevated pressure in triggering caspase-1 activation via purinergic receptors activation in urothelial cells. Rat urothelial cell line, MYP3 cells, was subjected to hydrostatic pressures of 15 cmH₂O for 60 min, or 40 cmH₂O for 1 min to simulate elevated storage and voiding pressure conditions, respectively. ATP concentration in the supernatant media and intracellular caspase-1 activity in cell lysates were measured. Pressure experiments were repeated in the presence of antagonists for purinergic receptors to determine the mechanism for pressure-induced caspase-1 activation. Exposure of MYP3 cells to both pressure conditions resulted in an increase in extracellular ATP levels and intracellular caspase-1 activity. Treatment with P2X₇ antagonist led to a decrease in pressure-induced ATP release by MYP3 cells, while P2X₄ antagonist had no effect but both antagonists inhibited pressure-induced caspase-1 activation. Moreover, when MYP3 cells were treated with extracellular ATP (500 µM), P2X₄ antagonist inhibited ATP-induced caspase-1 activation, but not P2X₇ antagonist. We concluded that pressure-induced extracellular ATP in urothelial cells is amplified by P2X₇ receptor activation and ATP-induced-ATP release. The amplified ATP signal then activates P2X₄ receptors, which mediate activation of the caspase-1 inflammatory response.     

The role of the pulsatile pressure variations in intracranial pressure monitoring

Summary The magnitude of the pulsatile intracranial pressure variations (CSF pulse pressure) is determined by the elastance of the craniospinal system and by the magnitude of the pulsatile variations in cerebral blood volume (CBV). The pulsatile change in CBV is, among other factors, determined by the compliance of the cerebral vascular bed which, in its turn, is dependent on the cerebral vasomotor tone. This concept has led the authors to devise a method for the assessment of both the elastance and the state of the cerebral vasomotor tone based on the relationship between CSF pulse pressure and intracranial pressure. This relationship was found to be of a linear nature both in clinical patients and in experimental animals. A significant, positive correlation was found between the slope of this relationship and the value of the craniospinal volume-pressure relationship: the elastance coefficient. During elevation of the intracranial pressure a breakpoint was observed in the relationship between CSF pulse pressure and the intracranial pressure above which the pulse pressure increased more rapidly. The elastance remained constant above this breakpoint. The same phenomenon was observed during plateau waves in clinical patients. Induced changes in systemic arterial pressure produced opposite effects on CSF pulse pressure and elastance coefficient. In these cases the discrepancy between pulse pressure and elastance was attributed to the pulsatile changes in CBV and this could be verified by means of electromagnetic flowmetry. The advantage of this method is that all the information is contained within the intracranial pressure signal itself, from which it can be extracted by simple means without the use of invasive tests.     

A simple and reliable technique to monitor intracranial pressure in the rat: technical note.

A technique for intracranial pressure (ICP) monitoring in the rat that uses a permanent cisterna magna cannula is described. The cannula is placed into the subarachnoid space through the atlanto-occipital membrane with the operating microscope and is secured with cement. The distal end is connected to a pressure transducer and a polygraph recorder. To study the consistency of this technique, 12 anesthetized adult rats were subjected to baseline ICP measurements 2 days after placement of the cannula. Baseline pressures ranged between 1.0 and 10.0 cm H2O, with a mean of 5.6 cm H2O. Respiratory variations were detected in all tracings, and manual abdominal compressions (Valsalva maneuver) correlated with immediate transient rises in ICP in all rats. While CSF pressure was being continuously monitored, rats were subjected to subarachnoid hemorrhage induced by transclival basilar artery puncture. Of the 12 rats, 10 showed a moderate transient rise in cerebrospinal fluid pressure, which peaked approximately 2 minutes after subarachnoid hemorrhage (mean peak change, 10.5 cm H2O; range, 0-32.5 cm H2O). Reliable pressure tracings were obtained in three of five animals examined 3 days after subarachnoid hemorrhage (ICP range, 4.0-4.5 cm H2O; mean, 4.2 cm H2O). We conclude that this cannula is easy and inexpensive to construct and that it provides reliable ICP tracings during experimental procedures in the rat.     

Relationship between intracranial pressure and intracranial volume in craniosynostosis.

Premature fusion of cranial sutures in craniosynostosis has been thought to lead to craniostenosis, which in turn may lead to increased intracranial pressures. In 41 consecutive patients with craniosynostosis, intracranial pressure and intracranial volume were measured. Of the 41 patients, 38 (92.6%) had raised intracranial pressure but only 4 (9.7%) had a decreased skull volume. In the present study, there is no correlation between intracranial volume and intracranial pressure. This study confirms that the measurement of intracranial volume, a non invasive procedure, cannot be used to assess intracranial pressure and to avoid an invasive procedure.