The use of indomethacin in the treatment of plateau waves: effects on cerebral perfusion and oxygenation

2005 ◽  
Vol 102 (3) ◽  
pp. 455-459 ◽  
Author(s):  
Roberto Imberti ◽  
Marinella Fuardo ◽  
Guido Bellinzona ◽  
Michele Pagani ◽  
Martin Langer
Keyword(s):  
Blood Flow ◽  
Cerebral Perfusion ◽  
Arterial Blood Flow ◽  
Cerebral Tissue ◽  
Initial Value ◽  
Content Type ◽  
Arterial Blood ◽  
Plateau Waves ◽  
Fine Print ◽  
Flow Velocities

Object. Plateau waves are sudden and steep increases in intracranial pressure (ICP) that can develop in patients with cerebral injuries, reduced pressure—volume compensatory reserve, and preserved autoregulation. They are caused by cerebral vasodilation in response to a reduction in cerebral perfusion and are associated with increased cerebral blood volume and reduced cerebral blood flow. The authors evaluated the hypothesis that administration of indomethacin, a potent cerebral arteriolar vasoconstrictor, could interrupt the vicious cycle that occurs during plateau waves, extinguishing these waves and, ultimately, restoring cerebral perfusion and oxygenation. Methods. Plateau waves developed in nine patients, seven with severe traumatic brain injury and two with intraparenchymal hemorrhage. One to four episodes of plateau waves per patient were treated with indomethacin (15–20 mg), which was delivered by an intravenous bolus injection. Each patient's mean arterial blood flow (MABP), ICP, cerebral perfusion pressure (CPP), and cerebral tissue PO2 were continuously monitored and the data obtained were stored in a personal computer. Each patient's jugular venous O2 saturation (SjvO2) and venoarterial difference in PCO2 were evaluated by intermittent blood sampling. During five episodes of plateau waves, middle cerebral artery flow velocities were evaluated by transcranial Doppler ultrasonography. Indomethacin extinguished all plateau waves. On average, the ICP decreased from an initial value of 58.9 ± 11.6 mm Hg to 21.2 ± 8.6 and 25.8 ± 13.7 mm Hg after 5 and 10 minutes, respectively (p < 0.01). The MABP did not change significantly. As a consequence the CPP increased by 98 and 81% after 5 and 10 minutes, respectively (p < 0.01). Five and 10 minutes after indomethacin was administered, SjvO2 increased from an initial value of 50 ± 10.5% to 62 ± 7.6 and 59.9 ± 9.3%, respectively (p < 0.01); the cerebral tissue PO2 increased from an initial value of 13.4 ± 10.6 mm Hg to 23.6 ± 9.58 and 21.9 ± 9.2 mm Hg, respectively (p < 0.05); and the venous—arterial PCO2 decreased significantly. The mean and diastolic flow velocities increased significantly, whereas the pulsatility index decreased from 1.39 ± 0.56 to 1.09 ± 0.4 at 5 minutes and 1.06 ± 0.36 at 10 minutes (p < 0.05). Conclusions. The findings confirm that plateau waves are caused by vasodilation and show that indomethacin, by constricting the cerebral arteries, is effective in extinguishing plateau waves, ultimately restoring cerebral perfusion and oxygenation.

Cerebral arterial blood flow and aneurysm surgery

1977 ◽  
Vol 47 (6) ◽  
pp. 810-818 ◽  
Author(s):  
Helge Nornes ◽  
Per Wikeby
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Arterial Blood Flow ◽  
Anterior Portion ◽  
Flow Measurements ◽  
Content Type ◽  
Aneurysm Neck ◽  
Flow Monitoring ◽  
Arterial Blood ◽  
Fine Print

✓ Cerebral arterial blood flow was monitored in 22 patients undergoing surgery for intracranial saccular aneurysms. An electromagnetic flow probe was used to record the internal carotid artery (ICA) flow in the neck or intracranially in seven patients. The ICA flow ranged between 100 and 175 ml/min (average 144 ml/min). Intracranial flow measurements with specially designed probes were made in 17 patients. The middle cerebral artery (MCA) showed flow values between 75 and 120 ml/min (average 97 ml/min). Flow figures recorded from the proximal anterior cerebral artery (ACA) were lower (average 65 ml/min), and had a wider range from 30 to 110 ml/min. Test occlusion of the terminal ICA showed a retrograde flow in the proximal ACA to the MCA ranging from 15 to 125 ml/min (average 78 ml/min). This test was used to investigate the collateral potential of the anterior portion of the circle of Willis, which is essential to the decision of whether to undertake trap ligation procedures in this location. Flow monitoring in the parent vessel was also of use in some patients to assess flow conditions after the clipping of the aneurysm neck.

Effect of naloxone on cerebral perfusion and cardiac performance during experimental cerebral ischemia

1986 ◽  
Vol 64 (5) ◽  
pp. 780-786 ◽  
Author(s):  
Robert J. Hariri ◽  
Elizabeth L. Supra ◽  
John Paul Roberts ◽  
Michael H. Lavyne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Perfusion ◽  
Blood Gases ◽  
Experimental Stroke ◽  
Arterial Blood Gases ◽  
Content Type ◽  
Arterial Blood ◽  
Fine Print

✓ Transient global cerebral ischemia (TGI) was induced in awake rats using the “four-vessel” occlusion model of Pulsinelli and Brierley. Blood pressure, arterial blood gases, cerebral blood flow, and cardiac output were measured during the acute (up to 2 hours) and chronic (2 to 72 hours) postischemic time periods. Coincident with the onset of TGI, cardiac output and caudate blood flow were depressed. The former returned to baseline within 30 minutes after the conclusion of TGI, and the latter progressed to hyperemia at 12 hours (81.8 ± 4.9 vs 68.6 ± 3.9 ml/min/100 gm tissue (mean ± standard error of the mean)) and oligemia at 72 hours (45.5 ± 4.8 ml/min/100 gm tissue) post-TGI in the untreated control rats. Arterial blood gases and blood pressure were unchanged. Naloxone (1 mg/kg) given at the time of TGI or as late as 60 minutes post-TGI and every 2 hours thereafter for 24 hours or bilateral cervical vagotomy prevented the depression in cardiac output and blocked the hyperemic-oligemic cerebral blood flow pattern that was predictive of stroke in this rat model. Changes in cardiac output after TGI in this model appear to be mediated by parasympathetic pathways to the heart from the brain stem. Opiate receptor blockade probably blocks endogenous opioid peptide stimulation of these brain-stem circulatory centers, which results in inhibition of parasympathetic activity and improvement in cardiac output. The usefulness of naloxone in the treatment of experimental stroke may be a function of its ability to improve cerebral perfusion in pressure-passive cerebrovascular territories. Variations in cardiac output during experimental stroke may explain the dissimilar responses to naloxone treatment reported by other investigators of experimental stroke.

Intraoperative complications in aneurysm surgery: a prospective national study

2002 ◽  
Vol 96 (3) ◽  
pp. 515-522 ◽  
Author(s):  
Steen Fridriksson ◽  
Hans Säveland ◽  
Karl-Erik Jakobsson ◽  
Göran Edner ◽  
Stefan Zygmunt ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intraoperative Complications ◽  
Aneurysm Rupture ◽  
Arterial Blood Flow ◽  
National Study ◽  
Aneurysm Surgery ◽  
Content Type ◽  
Poor Outcome ◽  
Arterial Blood ◽  
Fine Print

Object. With increasing use of endovascular procedures, the number of aneurysms treated surgically will decline. In this study the authors review complications related to the surgical treatment of aneurysms and address the issue of maintaining quality standards on a national level. Methods. A prospective, nonselected amalgamation of every aneurysm case treated in five of six neurosurgical centers in Sweden during 1 calendar year was undertaken (422 patients; 7.4 persons/100,000 population/year). The treatment protocols at these institutions were very similar. Outcome was assessed using clinical end points. In this series, 84.1% of the patients underwent surgery, and intraoperative complications occurred in 30% of these procedures. Poor outcome from technical complications was seen in 7.9% of the surgically treated patients. Intraoperative aneurysm rupture accounted for 60% and branch sacrifice for 12% of all technical difficulties. Although these complications were significantly related to aneurysm base geometry and the competence of the surgeon, problems still occurred apparently at random and also in the best of hands (17%). The temporary mean occlusion time in the patients who suffered intraoperative aneurysm rupture was twice as long as the temporary arrest of blood flow performed to aid dissection. Conclusions. The results obtained in this series closely reflect the overall management results of this disease and support the conclusion that surgical complications causing a poor outcome can be estimated on a large population-based scale. Intraoperative aneurysm rupture was the most common and most devastating technical complication that occurred. Support was found for a more liberal use of temporary clips early during dissection, regardless of the experience of the surgeon. Temporary regional interruption of arterial blood flow should be a routine method for aneurysm surgery on an everyday basis. A random occurrence of difficult intraoperative problems was clearly shown, and this factor of unpredictability, which is present in any preoperative assessment of risk, strengthens the case for recommending neuroprotection as a routine adjunct to virtually every aneurysm operation, regardless of the surgeon's experience.

Transesophageal Doppler Measurement of Renal Arterial Blood Flow Velocities and Indices in Children

2012 ◽  
Vol 114 (6) ◽  
pp. 1277-1284 ◽  
Author(s):  
Luis Zabala ◽  
Sana Ullah ◽  
Carol DʼAnn Pierce ◽  
Nischal K. Gautam ◽  
Michael L. Schmitz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Blood Flow ◽  
Doppler Measurement ◽  
Arterial Blood ◽  
Blood Flow Velocities ◽  
Transesophageal Doppler ◽  
Flow Velocities

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

1998 ◽  
Vol 89 (3) ◽  
pp. 448-453 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nitric Oxide Synthesis ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. Methods. The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-l-arginine methyl ester (l-NAME) and in nine control animals. The l-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the l-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). Conclusions. These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury

1978 ◽  
Vol 48 (5) ◽  
pp. 689-703 ◽  
Author(s):  
Erna M. Enevoldsen ◽  
Finn T. Jensen
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Severely Injured ◽  
Content Type ◽  
Cerebrovascular Autoregulation ◽  
Decerebrate Rigidity ◽  
Arterial Blood ◽  
Fine Print

✓ Regional cerebral blood flow (rCBF), cerebral intraventricular pressure (IVP), systemic arterial blood pressure, and cerebral ventricular fluid (CSF) lactate and pH were studied repeatedly in 23 patients during the acute phase of severe brain injury lasting from 3 to 21 days after the trauma. Cerebrovascular autoregulation was tested repeatedly by means of angiotensin infusion in 21 of the patients, and CO2 response in 14 by means of passive hyperventilation. The pressure in the brain ventricles was measured continuously in all patients and kept below 45 mm Hg during the study. If the IVP increased more than 10 mm Hg during the angiotensin infusion (as in one case), the autoregulation test was considered contraindicated and the angiotensin infusion was discontinued. Dissociation between cerebrovascular autoregulation and CO2 response was a common phenomenon. Typically, autoregulation appeared preserved in the most severely injured areas of the cerebral cortex when the patient was deeply comatose, but deteriorated concomitantly with recovery; by the time the patient became alert, the autoregulation was always impaired. The CO2 response was impaired only in patients who were deeply comatose and had attacks of decerebrate rigidity; during recovery the CO2 response became normal. Thus, preserved autoregulation associated with impaired CO2 response indicated very severe brain damage, whereas impaired autoregulation associated with preserved CO2 response suggested moderate or severe brain damage in recovery. These paradoxical observations raise the question whether the preserved autoregulation seen in severely injured brain tissue is a true autoregulation caused by an active vasoconstrictor response to an increase in blood pressure.

Dimethyl sulfoxide in experimental brain injury, with comparison to mannitol

1980 ◽  
Vol 53 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Frederick D. Brown ◽  
Lydia M. Johns ◽  
Sean Mullan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Brain Injury ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Missile Injury ◽  
Fine Print

✓ The effects of dimethyl sulfoxide therapy were studied in rhesus monkeys following a standardized occipitofrontal missile injury. This therapy resulted in substantially higher blood pressure, cerebral perfusion pressure, blood flow, and oxidative metabolism than those of a group of monkeys that had been treated similarly with mannitol, and than those of an untreated group.

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