The (in)effectiveness of anticipatory vibrotactile cues in mitigating motion sickness.

The introduction of (fully) automated vehicles has generated a re-interest in motion sickness, given that passengers suffer much more from motion sickness compared to car drivers. A suggested solution is to improve the anticipation of passive self-motion via cues that alert passengers of changes in the upcoming motion trajectory. We already know that auditory or visual cues can mitigate motion sickness. In this study, we used anticipatory vibrotactile cues that do not interfere with the (audio)visual tasks passengers may want to perform. We wanted to investigate (1) whether anticipatory vibrotactile cues mitigate motion sickness, and (2) whether the timing of the cue is of influence. We therefore exposed participants to four sessions on a linear sled with displacements unpredictable in motion onset. In three sessions, an anticipatory cue was presented 0.33, 1, or 3 s prior to the onset of forward motion. Using a new pre-registered measure, we quantified the reduction in motion sickness across multiple sickness scores in these sessions relative to a control session. Under the chosen experimental conditions, our results did not show a significant mitigation of motion sickness by the anticipatory vibrotactile cues, irrespective of their timing. Participants yet indicated that the cues were helpful. Considering that motion sickness is influenced by the unpredictability of displacements, vibrotactile cues may mitigate sickness when motions have more (unpredictable) variability than those studied here.

[The role of the superoxide dismutase for predicting long-term adverse events in patients with acute coronary syndrome.]

To study the relationship between the blood concentration of superoxide dismutase in at the end of the hospital period of acute coronary syndrome without ST-segment elevation (nonST-ACS) and the development of adverse events in the long-term follow-up period. 415 patients with nonST-ACS are included in the local register study. The follow-up period was 60 months. The blood concentration of superoxide dismutase (SOD) determined in 200 patients on the 10-13th day of hospitalization in addition to clinical procedures. Within five years after discharge in 178 (47 %) patients reported the development of adverse events. Patients with poor outcome were older, had a history of myocardial infarction (PICS), stenoses of extracranial arteries more than 30% and decreased left ventricular ejection fraction (LVEF). There were significant differences in the concentration of SOD10-13 day, which was lower in the patients with development of adverse cardiovascular events (p = 0.0003). Multivariate analysis identified the factors that are most strongly associated with the development of the adverse events during a 5-year follow-up period in patients with nonST-ACS: SOD blood concentration ≤ 175,4 ng / ml (OR-3,85; р=0,0008), myocardial infarction in anamnesis (OR-3,26; р=0,006), LVEF ≤ 52% (OR-2,8; р=0,035). The incidence of adverse cardiovascular events during five years follow-up in patients with nonST-ACS was 47 % of cases. Adverse factors associated with the development of an unfavorable outcome in the long-term period follow are: SOD blood concentration ≤ 175,4 ng / ml, myocardial infarction in anamnesis, LVEF ≤ 52%.

ICP Monitoring and Phase-Contrast MRI to Investigate Intracranial Compliance.

OBJECTIVE: The amplitude of intracranial pressure (ICP) can be measured by ICP monitoring. Phase-contrast magnetic resonance imaging (PCMRI) can quantify blood and cerebrospinal fluid (CSF) flows. The aim of this work was to investigate intracranial compliance at rest by combining baseline ICP monitoring and PCMRI in hydrocephalus patients. MATERIALS AND METHODS: ICP monitoring was performed before infusion testing to quantify ΔICP_rest at the basal condition in 33 suspected hydrocephalus patients (74 years). The day before, patients had had a PCMRI to assess total cerebral blood flow (tCBF), intracranial blood volume change (stroke volume SVblood), and cervical CSF volume change (the stroke volume CSV). Global (blood and CSF) intracranial volume change (ΔIVC) during each cardiac cycle (CC) was calculated. Finally, Compliance: C_rest = ΔIVC/ΔICP_rest was calculated. The data set was postprocessed by two operators according to blind analysis. RESULTS: Bland-Altman plots showed that measurements presented no significant difference between the two operators. ΔICP_rest = 2.41 ± 1.21 mmHg, tCBF = 469.89 ± 127.54 mL/min, SVblood = 0.82 ± 0.32 mL/cc, CSV = 0.50 ± 0.22 mL/cc, ΔIVC = 0.44 ± 0.22 mL, and C_rest = 0.23 ± 0.15 mL/mmHg. There are significant relations between SVblood and CSV and also SVblood and tCBF. CONCLUSIONS: During "basal" condition, the compliance amplitude of the intracranial compartment is heterogeneous in suspected hydrocephalus patients, and its value is lower than expected! This new parameter could represent new information, complementary to conventional infusion tests. We hope that this information can be applied to improve the selection of patients for shunt surgery.

CSF Lumbar Drainage: A Safe Surgical Option in Refractory Intracranial Hypertension Associated with Acute Posttraumatic External Hydrocephalus.

INTRODUCTION: External lumbar drainage (ELD) of cerebrospinal fluid (CSF) in posttraumatic refractory intracranial hypertension (ICHT) is controversial. We report our experience of ELD in ICHT associated with acute disturbance of CSF flow within subarachnoid spaces (SASs). MATERIALS AND METHODS: Four adult patients admitted to the neurointensive care unit for severe TBI who presented with secondary ICHT are retrospectively reported. When refractory to second-tier therapy, if external ventricular drainage were not possible or failed, and in the absence of an indication for craniotomy to treat a mass lesion or decompressive craniectomy, we assessed the evolution of CSF volume within cranial SAS and checked the presence of basal cisterns and the absence of tonsillar herniation to evaluate interest in and the safety of ELD. RESULTS: As second-tier therapy failed to lower intracranial pressure (ICP; mean ICP 37 ± 5 mmHg), and computed tomography (CT) showed abnormally enlarged cranial SAS following traumatic subarachnoid hemorrhage, patients received ELD. ICP decreased, with immediate and long-term effect (mean ICP 5 mmHg ± 2 mmHg). There were no complications to report. DISCUSSION: Acute traumatic external hydrocephalus may explain some of the specific situations of secondary increased ICP, with a "normal" CT scan, that is refractory to medical treatment. In these situations, lumbar drainage should be considered to be a safe, minimally invasive, and effective surgical option.

Intracranial Hypertension Is Painless!

INTRODUCTION: Headache is usually considered a key symptom of intracranial hypertension (ICHT). However, there are no published experimental data to support the concept that increased intracranial pressure (ICP) is painful in humans. MATERIALS AND METHODS: This prospective study was performed in 16 patients with suspected normal-pressure hydrocephalus, necessitating a lumbar infusion test with measurement of cerebrospinal fluid (CSF) hydrodynamics. During the test, ICP was increased from baseline to a plateau. Headache was scored on a visual analog scale (VAS) (0 = no pain, 10 = very severe pain) at baseline ICP and when ICP plateaued. RESULTS: At baseline, mean ICP was 11 ± 3.6 mmHg and VAS was 0. At plateau, mean ICP was 28 ± 9.5 mmHg and VAS was 0. There was a significant increase in ICP (p <0.001), but no increase in headache intensity (VAS). An acute (20-min) moderate increase in ICP was not accompanied by a headache. DISCUSSION: We demonstrate that an acute, isolated increase in CSF pressure does not produce a headache. To occur, a headache needs activation of the pain-sensitive structures (dura and venous sinuses) or central activation of the cerebral nociceptive structures. This peripheral or central activation does not occur with an isolated increase in CSF pressure.

Pulse amplitude of intracranial pressure waveform in hydrocephalus.

BACKGROUND: There is increasing interest in evaluation of the pulse amplitude of intracranial pressure (AMP) in explaining dynamic aspects of hydrocephalus. We reviewed a large number of ICP recordings in a group of hydrocephalic patients to assess utility of AMP. MATERIALS AND METHODS: From a database including approximately 2,100 cases of infusion studies (either lumbar or intraventricular) and overnight ICP monitoring in patients suffering from hydrocephalus of various types (both communicating and non-communicating), etiology and stage of management (non-shunted or shunted) pressure recordings were evaluated. For subgroup analysis we selected 60 patients with idiopathic NPH with full follow-up after shunting. In 29 patients we compared pulse amplitude during an infusion study performed before and after shunting with a properly functioning shunt. Amplitude was calculated from ICP waveforms using spectral analysis methodology. FINDINGS: A large amplitude was associated with good outcome after shunting (positive predictive value of clinical improvement for AMP above 2.5 mmHg was 95%). However, low amplitude did not predict poor outcome (for AMP below 2.5 mmHg 52% of patients improved). Correlations of AMP with ICP and Rcsf were positive and statistically significant (N = 131 with idiopathic NPH; R = 0.21 for correlation with mean ICP and 0.22 with Rcsf; p< 0.01). Correlation with the brain elastance coefficient (or PVI) was not significant. There was also no significant correlation between pulse amplitude and width of the ventricles. The pulse amplitude decreased (p < 0.005) after shunting. CONCLUSIONS: Interpretation of the ICP pulse waveform may be clinically useful in patients suffering from hydrocephalus. Elevated amplitude seems to be a positive predictor for clinical improvement after shunting. A properly functioning shunt reduces the pulse amplitude.

Asymmetry of critical closing pressure following head injury.

OBJECTIVE: Critical closing pressure (CCP) is the arterial pressure below which the vessels collapse. Hypothetically it is the sum of intracranial pressure (ICP) and vessel wall tension in the cerebral circulation. This study investigated transhemispherical asymmetry of CCP by studying its correlation with radiological findings on computed tomography (CT) scans in head injury patients. METHOD: ICP, arterial blood pressure, and middle cerebral artery blood flow velocity were recorded daily in 119 ventilated patients. Waveforms were processed to calculate CCP. CT scans were analysed according to a system based on the Marshall classification. RESULTS: Left-right differences in CCP correlated with midline shift on the CT scan (r = 0.48; p<0.02). Asymmetry of CCP also corresponded with the side of the head lesion (p<0.007) and the side of the craniotomy where it was performed (p<0.006). Absolute CCP weakly correlated with brain swelling (r = -0.23; p<0.03) and arterial pressure (r = 0.21; p<0.02) but did not correlate with ICP. Cerebral perfusion pressure calculated as the difference between mean arterial pressure and CCP did not correlate with outcome, but "traditional" cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) did. CONCLUSIONS: Critical closing pressure is disturbed by localised brain lesions. Its asymmetry corresponds to asymmetrical findings on CT scans. CCP seems to describe vascular resistance better than ICP.

Association between outcome, cerebral pressure reactivity and slow ICP waves following head injury.

OBJECTIVE: To investigate the relationships between slow vasogenic waves ('B waves') of intracranial pressure (ICP), pressure-reactivity and outcome after traumatic brain injury. MATERIAL AND METHOD: 193 head-injured patients (age 34 +/- 16.7 years; median GCS 6) were monitored from 1997 to 2002. ICP, arterial blood pressure (ABP) were continuously monitored. Pressure-reactivity index (PRx) and magnitude of ICP slow waves were evaluated using the bed-side computers. RESULTS: Distribution of PRx in different outcome groups indicated that pressure-reactivity was significantly worse in patients with fatal outcome. A magnitude of spontaneous slow waves of ICP was gradually decreasing in poorer outcome grades. Mortality indicated threshold rise from 20% to 70% when averaged PRx increased above 0.3 (p < 0.01). There was no threshold for mortality observed along distribution of magnitude of ICP slow waves. Mortality gradually increased when the magnitude of slow waves decreased (R = -0.26; p < 0.0001). CONCLUSION: Inadequate pressure-reactivity and low magnitude of slow vasogenic waves of ICP are associated with fatal outcome after head injury. Based on brain monitoring data, differentiation between favourable outcome and severe disability is more problematic than differentiation between survivors and non-survivors.

Clinical testing of CSF circulation in hydrocephalus.

INTRODUCTION: Recent 'NPH Dutch trial' has re-emphasised the importance of the resistance to cerebrospinal fluid (CSF) outflow (Rcsf) in the diagnosis of hydrocephalus. We re-evaluated the clinical utility of the physiological measurements revealing CSF dynamics. The results were summarized from our previous publications. The Computerised Infusion Test was designed to perform quick and low-invasive assessment of CSF dynamics described by parameters as Rcsf, brain compliance, elasticity coefficient, estimated sagittal sinus pressure, CSF formation rate and other variables. Overnight ICP monitoring with quantitative analysis of CSF dynamics was used in those cases where infusion study was unreliable or producing results close to the borderline. We found that the threshold of normal and increased Rcsf should be age-matched because in patients older than 55 Rcsf increases 0.2 mm Hg/(ml/min) per year (p < 0.04: N = 56). Rcsf was positively correlated with cerebral autoregulation (R = 0.41; p < 0.03; N = 36) indicating that in patients with symptoms of NPH but normal Rcsf underlying cerebrovascular disease is more frequent. Computerized infusion tests and overnight ICP monitoring are useful diagnostic technique alone or in conjunction with other forms of physiological measurement.

Intracranial baroreflex yielding an early cushing response in human.

The Cushing response is a pre-terminal sympatho-adrenal systemic response to very high ICP. Animal studies have demonstrated that a moderate rise of ICP yields a reversible pressure-mediated systemic response. Infusion studies are routine procedures to investigate, by infusing CSF space with saline, the cerebrospinal fluid (CSF) biophysics in patients suspected of hydrocephalus. Our study aims at assessing systemic and cerebral haemodynamic changes during moderate rise of ICP in human. Infusion studies were performed in 34 patients. This is a routine test perform in patients presenting with symptoms of NPH during their pre-shunting assessment. Arterial blood pressure (ABP) and cerebral blood flow velocity (FV) were non-invasively monitored with photoplethysmography and transcranial Doppler. The rise in ICP (8.2 +/- 5.1 mmHg to 25 +/- 8.3 mmHg) was followed by a significant rise in ABP (106.6 +/- 29.7 mmHg to 115.2 +/- 30.1 mmHg), drop in CPP (98.3 +/- 29 mmHg to 90.2 +/- 30.7 mmHg) and decrease in FV (55.6 +/- 17 cm/s to 51.1 +/- 16.3 cm/s). Increasing ICP did not alter heart rate (70.4 +/- 10.4/min to 70.3 +/- 9.1/min) but augmented the heart rate variance (0.046 +/- 0.058 to 0.067 +/- 0.075/min). In a population suspected of hydrocephalus, our study demonstrated that a moderate rise of ICP yields a reversible pressure-mediated systemic response, demonstrating an early Cushing response in human and a putative intracranial baroreflex.

Predictive value of Glasgow Coma Scale after brain trauma: change in trend over the past ten years.

BACKGROUND: Age and the Glasgow Coma Scale (GCS) score on admission are considered important predictors of outcome after traumatic brain injury. We investigated the predictive value of the GCS in a large group of patients whose computerised multimodal bedside monitoring data had been collected over the previous 10 years. METHODS: Data from 358 subjects with head injury, collected between 1992 and 2001, were analysed retrospectively. Patients were grouped according to year of admission. Glasgow Outcome Scores (GOS) were determined at six months. Spearman's correlation coefficients between GCS and GOS scores were calculated for each year. RESULTS: On average 34 (SD: 7) patients were monitored every year. We found a significant correlation between the GCS and GOS for the first five years (overall 1992-1996: r = 0.41; p<0.00001; n = 183) and consistent lack of correlations from 1997 onwards (overall 1997-2001: r = 0.091; p = 0.226; n = 175). In contrast, correlations between age and GOS were in both time periods significant and similar (r = -0.24 v r = -0.24; p<0.002). CONCLUSIONS: The admission GCS lost its predictive value for outcome in this group of patients from 1997 onwards. The predictive value of the GCS should be carefully reconsidered when building prognostic models incorporating multimodality monitoring after head injury.

Pressure-autoregulation, CO2 reactivity and asymmetry of haemodynamic parameters in patients with carotid artery stenotic disease. A clinical appraisal.

OBJECTIVES: Patients with carotid artery stenotic disease and poor cerebral haemodynamic reserve are in increased risk of stroke. Haemodynamic reserve can be estimated by measuring cerebrovascular reactivity induced by breathing CO2 and pressure-autoregulation by analyzing spontaneous slow fluctuation in arterial pressure and MCA blood flow velocity. We evaluated the relationship between clinical status, CO2 reactivity, pressure-autoregulation and other haemodynamic variables derived from Transcranial Doppler ultrasonography in patients with carotid artery disease. METHODS: 38 patients were investigated. Arterial pressure and blood flow velocity were monitored during CO2 reactivity tests. Arterial pressure-corrected and non-corrected indices of CO2 reactivity were calculated to compare an influence of rise in arterial pressure during the test. The pressure-autoregulation index was calculated as correlation coefficient between slow waves in blood flow velocity and arterial pressure. RESULTS: The increase in CO2 produced a consistent rise in arterial pressure and blood flow velocity and weakened the pressure autoregulation. The value of pressure-corrected CO2 reactivity was lower (p<0.0001) than the non-corrected one, indicating that the rise in arterial pressure during the test tends to over-estimate CO2 reactivity. The pressure-corrected reactivity was correlated with pressure autoregulation (r=-0.46; p<0.005). Both CO2 reactivity and pressure-autoregulation index correlated with a degree of carotid artery stenosis. Side-to-side difference of TCD pulsatility index demonstrated a close relationship with the asymmetry of stenosis (r=-0.61; p<0.0002) and symptoms (r=-0.49; p<0.003). CONCLUSIONS: When calculating CO2 reactivity in patients with carotid artery disease, changes in arterial pressure should be considered. Both CO2 reactivity and pressure-autoregulation describe the magnitude of haemodynamic deficit caused by stenosis, pulsatility index expresses the asymmetry of stenosis.

Asymmetry of cerebral autoregulation following head injury.

OBJECTIVES: To investigate asymmetry of cerebra autoregulation in head-injured patients with lateral brain contusions. METHODS: Sixty five patients were admitted to Addenbrooke's Hospital suffering from head injuries with mean Glasgow Coma Score 6 (range 3 to 10). The patients were paralyzed, sedated and ventilated to achieve mild hypocapnia. Intracranial pressure (ICP), arterial pressure (ABP) were monitored directly. The left and right Middle Cerebral Arteries were insonated daily and flow velocity (FV) was recorded. Correlation coefficients between slow waves in cerebral perfusion pressure (CPP) and FV were calculated for every 3 minute period. Positive value of Mx denotes a positive association between waves in FV and CPP, therefore deranged autoregulation. Zero or slightly negative value of Mx denotes a good autoregulatory capacity. In each patient all CT scans were reviewed to assess a dominant side of brain contusion and a level of brain compression. RESULTS: The side-to-side difference in FV, pulsatility indices or critical closing pressures, did not correlate with the side of contusion or midline shift. In contrary, the side-to-side difference in Mx indices were significantly (p < 0.05) worse at a side of contusion and at the side of brain expansion in patients presenting with a midline shift (p < 0.05). Of those patients who died in hospital, significantly more presented within meaningful (ABS(Mx) > 0.2) asymmetry in cerebral autoregulation (40% versus 12%; p < 0.05). CONCLUSIONS: Side-to-side difference in cerebral hemodynamic reserve of injured brain is a predictor of fatal outcome following head injury and correlates with the side of contusion or brain expansion.

Preliminary experience of the estimation of cerebral perfusion pressure using transcranial Doppler ultrasonography.

OBJECTIVE: The direct calculation of cerebral perfusion pressure (CPP) as the difference between mean arterial pressure and intracranial pressure (ICP) produces a number which does not always adequately describe conditions for brain perfusion. A non-invasive method of CPP measurement has previously been reported based on waveform analysis of blood flow velocity measured in the middle cerebral artery (MCA) by transcranial Doppler. This study describes the results of clinical tests of the prototype bilateral transcranial Doppler based apparatus for non-invasive CPP measurement (nCPP). METHODS: Twenty five consecutive, paralysed, sedated, and ventilated patients with head injury were studied. Intracranial pressure (ICP) and arterial blood pressure (ABP) were monitored continuously. The left and right MCAs were insonated daily (108 measurements) using a purpose built transcranial Doppler monitor (Neuro Q(TM), Deltex Ltd, Chichester, UK) with software capable of the non-invasive estimation of CPP. Time averaged values of mean and diastolic flow velocities (FVm, FVd) and ABP were calculated. nCPP was then computed as: ABPxFVd/FVm+14. RESULTS: The absolute difference between real CPP and nCPP (daily averages) was less than 10 mm Hg in 89% of measurements and less than 13 mm Hg in 92% of measurements. The 95% confidence range for predictors was no wider than +/-12 mm Hg (n=25) for the CPP, varying from 70 to 95 mm Hg. The absolute value of side to side differences in nCPP was significantly greater (p<0.05) when CT based evidence of brain swelling was present and was also positively correlated (p<0.05) with mean ICP. CONCLUSION: The device is of potential benefit for intermittent or continuous monitoring of brain perfusion pressure in situations where the direct measurement is not available or its reliability is in question.

Non-invasive cerebral perfusion pressure (nCPP): evaluation of the monitoring methodology in head injured patients.

The method of direct calculation of cerebral perfusion pressure (CPP) as the difference between mean arterial pressure and intracranial pressure (ICP) produces a number, which not always adequately expresses brain perfusion. We investigated an alternative non-invasive method, based on waveform analysis of Transcranial Doppler blood flow velocity in Middle Cerebral Arteries (MCA). 25 consecutive head injured patients, paralysed, sedated and ventilated were studied. Intracranial pressure (ICP) arterial blood pressure (ABP) were monitored continuously. The left and right MCAs were insonated daily (116 measurements) using a purpose-built transcranial Doppler monitor (Deltex Ltd, Chichester, U.K.) with software capable of the non-invasive estimation of CPP. Time averaged values of ABP, mean and diastolic flow velocities (FVm, FVd) were calculated and CPPe was computed as: ABP*FVd/FVm + 14. An absolute difference between real CPP and CPPe was less than 10 mm Hg in 82% of measurements and less than 13 mm Hg in 90% of measurements. The method demonstrated a high potential to detect both short-term and long-term changes in CPP. The method is of potential benefit for the intermittent measurement and continuous monitoring of changes in brain perfusion pressure in situations where the direct measurement of CPP is not available or its reliability is in question.

Continuous assessment of cerebral autoregulation--clinical verification of the method in head injured patients.

Previously, using transcranial Doppler ultrasonography, we investigated whether the hemodynamic response to spontaneous variations in cerebral perfusion pressure (CPP) provides reliable information about cerebral autoregulatory reserve. In the present study we have verified this method in 166 patients after head trauma. Waveforms of intracranial pressure (ICP), arterial pressure and transcranial Doppler flow velocity (FV) were captured daily over 0.5-2.0 hour periods. Time-averaged mean flow velocity (FV) and CPP were resolved. The correlation coefficient indices between FV and CPP (Mx) were calculated over 3 minutes epochs, and averaged for each investigation. An index of CBF (flow velocity diastolic to mean ratio) was calculated independently for each investigation. Mx depended on CPP (p < 0.0001) increasing to positive values when CPP decreased below 60 mm Hg. This threshold coincided with an averaged breakpoint for autoregulation, expressed by the index of CBF. Mx depended on outcome following head injury stronger than the Glasgow Coma Score on admission (ANOVA, F values 18 and 15 respectively; N = 166). In patients who died, cerebral autoregulation was disturbed during the first two days following injury. These results indicate an important role for the continuous monitoring of autoregulation following head trauma.

Hemodynamic characterization of intracranial pressure plateau waves in head-injury patients.

OBJECT: Plateau waves of intracranial pressure (ICP) are often recorded during intensive care monitoring of severely head injured patients. They are traditionally interpreted as meaningful secondary brain insults because of the dramatic decrease in cerebral perfusion pressure (CPP). The aim of this study was to investigate both the hemodynamic profile and the clinical consequences of plateau waves. METHODS: One hundred sixty head-injured patients were studied using continuous monitoring of ICP; almost 20% of these patients exhibited plateau waves. In 96 patients arterial pressure, ICP, and transcranial Doppler (TCD) blood flow velocity were studied daily for 20 minutes to 3 hours. Sixteen episodes of plateau waves in eight patients were recorded and analyzed. The dramatic increase in ICP was followed by a profound fall in CPP (by 45%). In contrast, flow velocity fell by only 20%. Autoregulation was documented to be intact both before and after plateau but was disturbed during the wave (p < 0.05). Pressure-volume compensatory reserve was always depleted before the wave. Cerebrovascular resistance decreased during the wave by 60% (p < 0.05) and TCD pulsatility increased (p < 0.05). Plateau waves did not increase the probability of an unfavorable outcome following injury. CONCLUSIONS: The authors have confirmed that the plateau waves are a hemodynamic phenomenon associated with cerebrovascular vasodilation. They are observed in patients with preserved cerebral autoregulation but reduced pressure-volume compensatory reserve.

Reserpine-induced increases in neuropeptide Y mRNA of guinea pig sympathetic ganglia using in situ hybridization.

BACKGROUND: Neuropeptide Y (NPY) is synthesized in sympathetic ganglia by specific mRNA, to which rat probes are currently available. In the rat model, reserpine treatment increases NPY mRNA through a mechanism involving enhanced preganglionic activity. Probes for NPY mRNA have been used exclusively in rat models. In this study, we assessed whether a rat NPY cRNA probe could be used to index reserpine-induced changes in NPY mRNA levels of sympathetic ganglia in the guinea pig. METHODS: Guinea pigs were given vehicle or reserpine pretreatment. In situ hybridization for NPY mRNA was done on the superior cervical and stellate ganglia of four control and four reserpine-treated rats. Autoradiographic density was digitized using an automated image analysis system. RESULTS: Following in situ hybridization of tissue sections, autoradiographic density of specific NPY mRNA binding was evident in nerve cell bodies in the superior cervical and stellate ganglia. Reserpine pretreatment was associated with an increase in NPY mRNA levels in both types of ganglia. CONCLUSION: These results indicate that reserpine treatment in the guinea pig produces increased neuronal NPY mRNA levels. The study also showed that rat NPY cRNA probe can be used to quantify alterations in NPY mRNA levels in the guinea pig.

[Simulation in the teaching of the cardiorespiratory system: a report of innovative experience]. / Simulação no ensino do sistema cardiorrespiratório: relato de uma experiência inovadora.

The nurse teachers in charge of the Auxiliary Nursing Course at the Heart Institute (InCor-FMUSP) propose simulation as an innovative teaching strategy and describe its application to the Cardiorespiratory System. By doing this, they make their students participate actively in their classes, thus improving the teaching-learning process.