Catecholamine response to a gradual increase of intracranial pressure

1993 ◽  
Vol 79 (5) ◽  
pp. 705-709 ◽  
Author(s):  
Johan van Loon ◽  
Bharati Shivalkar ◽  
Chris Plets ◽  
Jan Goffin ◽  
T. Budya Tjandra-Maga ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Gradual Increase ◽  
Hemodynamic Changes ◽  
Content Type ◽  
Catecholamine Response ◽  
Cushing Response ◽  
The Mean ◽  
The Brain

✓ To determine the catecholamine response to progressive intracranial hypertension, intracranial pressure (ICP) was raised gradually by continuous expansion of an epidural balloon in seven dogs. Hemodynamic parameters, ICP, and cerebral perfusion pressure (CPP) were monitored continuously and serum catecholamine levels began to rise when CPP was in the low-positive range (20 to 30 mm Hg), reaching a peak just after brain death (CPP ≤ 0 mm Hg). There was no correlation between ICP and the catecholamine peak. Compared to control values, the mean increase was 286-fold for epinephrine and 78-fold for norepinephrine. Temporally, the catecholamine peak corresponded well with the observed hemodynamic changes. These results suggest that ischemia in certain parts of the brain stem is responsible for the hemodynamic changes observed in intracranial hypertension (such as the Cushing response), and they show that catecholamines play an important role in these hemodynamic changes.

Barbiturate-augmented hypothermia for reduction of persistent intracranial hypertension

1974 ◽  
Vol 40 (1) ◽  
pp. 90-100 ◽  
Author(s):  
Harvey M. Shapiro ◽  
Stephen R. Wyte ◽  
John Loeser
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Combined Therapy ◽  
Pressure Reduction ◽  
Content Type ◽  
Cardiovascular Instability ◽  
Previously Treated ◽  
The Brain

✓ Thiopental and pentobarbital caused further reductions in intracranial pressure (ICP) in five patients with persistent intracranial hypertension who had been previously treated with diuretics, steroids, and hyperventilation therapy. The ICP reduction obtained with these patients at normothermia was rapid. Abrupt increases in ICP could be quickly checked by barbiturate treatment. Frequently, the ICP reduction was accompanied by an improvement in the cerebral perfusion pressure. Reduction of ICP by thiopental was brief while that due to pentobarbital was more prolonged. Sustained intracranial pressure reduction could be maintained for up to 5 days by combining pentobarbital (serum concentration 3 mg%) and hypothermia (30°C) without cardiovascular instability or other untoward side-effects. The cerebral metabolic depression due to this combined therapy may be additive and therefore offer a greater protection to the brain during periods of elevated ICP.

Intracranial pressure changes induced by sodium nitroprusside in patients with intracranial mass lesions

1978 ◽  
Vol 48 (3) ◽  
pp. 329-331 ◽  
Author(s):  
James E. Cottrell ◽  
Katie Patel ◽  
Herman Turndorf ◽  
Joseph Ransohoff
Keyword(s):  
Intracranial Pressure ◽  
Sodium Nitroprusside ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Intracranial Tumors ◽  
Cerebral Blood Vessels ◽  
Content Type ◽  
The Mean ◽  
Pressure Changes ◽  
Mass Lesions

✓ Because of the ability of sodium nitroprusside (SNP) to dilate cerebral blood vessels, intracranial pressure (ICP) should increase with its use. In patients with vascular intracranial tumors following SNP (0.01%) infusion, ICP increased from 14.58 ± 1.85 to 27.61 ± 3.33 torr (p > 0.0005) and cerebral perfusion pressure decreased from 89.32 ± 3.5 to 43.23 ± 4.60 torr (p < 0.0005) when the mean arterial pressure had reduced by 33%. These results suggest that SNP not be used in patients with raised ICP unless previous measures have been taken to improve intracranial compliance.

Acute intracranial hypertension and brain-stem blood flow

1984 ◽  
Vol 60 (3) ◽  
pp. 566-571 ◽  
Author(s):  
Seigo Nagao ◽  
Norio Sunami ◽  
Takumi Tsutsui ◽  
Yutaka Honma ◽  
Fumiyuki Momma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Brain Stem ◽  
Inferior Colliculus ◽  
Medulla Oblongata ◽  
Systemic Arterial Pressure ◽  
Content Type ◽  
Cushing Response ◽  
The Mean ◽  
Mass Lesions

✓ This study has been carried out to evaluate the effect of supratentorial mass lesions on the local cerebral blood flow (CBF) of the brain stem. Local CBF of the thalamus, inferior colliculus, and medulla oblongata, and supra- and infratentorial pressure were serially measured in 52 cats with intracranial hypertension produced by supratentorial balloon expansion. The mean control local CBF's in the thalamus, inferior colliculus, and medulla oblongata were 37.5, 42.1, and 30.7 ml/100 gm/min, respectively. At 20 to 30 mm Hg of supratentorial pressure, the local CBF of the thalamus started to decrease, and at 20 mm Hg of infratentorial pressure, the local CBF of the inferior colliculus began to decrease. Finally, at 40 to 60 mm Hg of infratentorial pressure, the local CBF of the medulla oblongata was affected. At the beginning of uncal herniation, indicated by anisocoria, the mean local CBF of the inferior colliculus abruptly decreased from 33.7 to 19.6 ml/100 gm/min in 16 cats. The Cushing response was evoked at a mean supratentorial pressure of 93.4 mm Hg and infratentorial pressure of 49.9 mm Hg in 16 cats. When the systemic arterial pressure was increased to the highest level in 13 cats, the mean local CBF of the medulla oblongata did not show significant change (a decrease from 22.8 to 20.9 ml/100 gm/min). The results suggest that at the beginning of uncal herniation, the local CBF of the upper brain stem markedly decreased. During the Cushing response, the local CBF of the medulla oblongata did not change significantly.

Experimental neurogenic pulmonary edema

1981 ◽  
Vol 54 (5) ◽  
pp. 627-631 ◽  
Author(s):  
Julian T. Hoff ◽  
Merry Nishimura ◽  
Jose Garcia-Uria ◽  
Sandra Miranda
Keyword(s):  
Pulmonary Edema ◽  
Intracranial Hypertension ◽  
Perfusion Pressure ◽  
Systemic Arterial Pressure ◽  
Neurogenic Pulmonary Edema ◽  
Content Type ◽  
Systemic Arterial Hypertension ◽  
Cushing Response ◽  
Intraventricular Infusion ◽  
Sympathetic Discharge

✓ Neurogenic pulmonary edema (NPE) was produced consistently in normal cats by increasing intracranial pressure with an intraventricular infusion of mock cerebrospinal fluid. The usual elevation of systemic arterial pressure (SAP) that follows severe intracranial hypertension (the “Cushing response”) was controlled by blood withdrawal at variable rates to achieve and maintain constant cerebral perfusion pressure (CPP) in three groups of cats of 50, 20, and 0 mm Hg, respectively, for 30 minutes. In this model, NPE occurs in the absence of increased SAP and in the presence of decreasing CPP. These results indicate that systemic arterial hypertension is not an essential stimulus for the development of NPE, and suggest that the lungs are directly affected by the intense sympathetic discharge evoked by severe intracranial hypertension.

Effects of nifedipine on intracranial pressure in neurosurgical patients with arterial hypertension

1988 ◽  
Vol 69 (2) ◽  
pp. 213-215 ◽  
Author(s):  
Akio Tateishi ◽  
Takanobu Sano ◽  
Hiroshi Takeshita ◽  
Toshihisa Suzuki ◽  
Hisao Tokuno
Keyword(s):  
Intracranial Pressure ◽  
Arterial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Neurological Signs ◽  
Arterial Blood ◽  
Neurosurgical Patients ◽  
The Mean ◽  
Made In

✓ The effects of nifedipine, 20 mg administered via a nasogastric tube, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were examined. Nifedipine was administered to treat arterial hypertension (> 180 mm Hg, systolic). Ten measurements were made in eight patients with cerebrovascular disease or head trauma. The mean arterial blood pressure (MABP) and ICP were measured before and for 30 minutes after the administration of nifedipine. The MABP gradually decreased and reached its lowest value at approximately 10 minutes after initiation of nifedipine administration, and thereafter remained unchanged. The MABP decreased significantly from 128 ± 8 (mean ± standard deviation) to 109 ± 7 mm Hg, and the CPP decreased from 105 ± 11 to 84 ± 10 mm Hg. The ICP increased by 1 to 10 mm Hg in eight of 10 measurements, and the mean change of ICP from 19 ± 7 to 22 ± 6 mm Hg was statistically significant. These changes were not accompanied by alterations in neurological signs. The results suggest that enteral nifedipine produces a small but statistically significant increase in ICP. Accordingly, neurological signs must be closely observed to detect deterioration, which can be caused by an increase in ICP and/or a decrease in CPP.

Vascular pathology of the brain stem due to experimentally increased intracranial pressure: changes noted in the micro- and macrocirculation

1973 ◽  
Vol 39 (5) ◽  
pp. 601-609 ◽  
Author(s):  
Stanley J. Goodman ◽  
Donald P. Becker
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Brain Stem ◽  
Neurological Status ◽  
Vascular Pathology ◽  
Vascular Lesions ◽  
Vascular Abnormality ◽  
Content Type ◽  
The Brain ◽  
Supratentorial Mass

✓ The neurological status and supra- and infratentorial intracranial pressures were studied in awake unsedated cats during expansion of a supratentorial mass. The pontomesencephalic portion of the brain stem was removed, serially sectioned, stained with sodium nitroprusside benzidine, and microscopically examined. Three types of vascular abnormality were seen: macrocirculation hemorrhages, microcirculation hemorrhages, and vascular stasis. As the supratentorial mass expanded and the intracranial pressure rose, there was a progression of vascular lesions from stasis to microcirculation hemorrhages, and finally to macrocirculation hemorrhages. The microcirculation hemorrhages occurred in stuporous animals, and the macrocirculation hemorrhages in comatose animals. Microcirculation hemorrhages were distributed primarily in the tectum, and macrocirculation hemorrhages were mainly in the tegmentum. Microcirculation hemorrhages first appeared in association with moderate to severe intracranial hypertension; macrocirculation hemorrhages were seen mainly with extreme intracranial hypertension. The clinical implications of these brain-stem vascular lesions are discussed.

Effects of positive end-expiratory pressure on intracranial pressure in dogs with intracranial hypertension

1981 ◽  
Vol 55 (5) ◽  
pp. 704-707 ◽  
Author(s):  
Jon S. Huseby ◽  
John M. Luce ◽  
Jeffrey M. Cary ◽  
Edward G. Pavlin ◽  
John Butler
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Clinical Situation ◽  
Positive End Expiratory Pressure ◽  
Content Type ◽  
Neurosurgical Patients

✓ Positive end-expiratory pressure (PEEP) is used to improve oxygenation in patients with the adult respiratory distress syndrome. Nevertheless, this treatment may increase intracranial pressure (ICP) and be detrimental to certain neurosurgical patients. This clinical situation was simulated by administering PEEP to dogs with normal and elevated ICP. Increases in PEEP increased ICP in all animals. However, the presence of intracranial hypertension diminished the increase in ICP seen at a given level of PEEP. Cerebral perfusion pressure also fell less in the presence of intracranial hypertension than it did in its absence, although in the former situation cerebral perfusion pressure was at the lower limits of the range of cerebral autoregulation. These findings suggest that PEEP is no more detrimental to patients with elevated ICP than it is to patients whose ICP is normal, assuming that their cerebral autoregulation is not impaired.

Continuous monitoring of cerebral oxygenation in acute brain injury: injection of mannitol during hyperventilation

1990 ◽  
Vol 73 (5) ◽  
pp. 725-730 ◽  
Author(s):  
Julio Cruz ◽  
Michael E. Miner ◽  
Steven J. Allen ◽  
Wayne M. Alves ◽  
Thomas A. Gennarelli
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebral Oxygenation ◽  
Jugular Bulb ◽  
Oxyhemoglobin Saturation ◽  
Content Type ◽  
Closed Head Trauma

✓ Global cerebral oxygenation, perfusion pressure, and expired pCO2 were continuously monitored in 10 adults with acute severe closed head trauma. Cerebral oxygenation was monitored by fiberoptic catheter oximetry, which allowed simultaneous measurements of arterial and jugular bulb oxyhemoglobin saturation. Intracranial pressure levels over 20 mm Hg were recorded several times in all patients, in spite of sedation, muscle paralysis, and profound hyperventilation. Intracranial hypertension was frequently associated with oligemic cerebral hypoxia, identified as abnormally low jugular oxygen saturation in the presence of normal arterial oxygenation. Intracranial hypertension was then managed with intravenous administration of mannitol boluses, which yielded simultaneous decreases in intracranial pressure and increases in cerebral oxygenation to highly statistically significant levels. Monitoring cerebral oxygenation was clinically useful because it allowed identification of impaired cerebral oxygenation even when cerebral perfusion pressure was normal. It is therefore proposed as a new monitoring technique, to supplement conventional monitoring of cerebral perfusion pressure.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 318-322 ◽  
Author(s):  
Lawrence F. Marshall ◽  
David I. Graham ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Raised Intracranial Pressure ◽  
Content Type ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ The authors studied the morphological sequelae of 15 minutes of cerebral oligemia (20 torr cerebral perfusion pressure) and complete cerebral ischemia produced by raised intracranial pressure in rabbits. Ischemic cell change was present in five of seven ischemic animals; it was most extensive in the striatum and hippocampus, with only a few ischemic nerve cells in the thalamus and neocortex. The brains of control and oligemic animals were normal. These results indicate the following: 1) ischemia is a more severe insult than oligemia; 2) compression ischemia results in a pattern of damage that differs from that produced by other types of ischemia; and 3) the method used to reduce cerebral perfusion pressure is an important factor in determining the pattern and extent of brain damage produced.

Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Circulatory Arrest ◽  
Transcranial Doppler Ultrasonography

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.

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