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EFFECT OF PROSTAGLANDIN E1-INDUCED HYPOTENSION ON CARBON DIOXIDE REACTIVITY AND LOCAL CEREBRAL BLOOD FLOW AFTER SUBARACHNOID HAEMORRHAGE
British Journal of Anaesthesia 1992; 68: 268-271
EFFECT OF PROSTAGLANDIN E^INDUCED HYPOTENSION ON CARBON DIOXIDE REACTIVITY AND LOCAL CEREBRAL BLOOD FLOW AFTER SUBARACHNOID HAEMORRHAGE K. ABE, A. DEMIZU AND I. YOSHIYA
The effect of prostaglandin E, (PGE,) on local cerebral blood flow (LCBF) and carbon dioxide reactivity (CO2R) was studied during cerebral aneurysm surgery for subarachnoid haemorrhage in 24 patients under neuroleptanaesthesia. Eleven patients had good neurological status (Hunt and Kosnik grade I: group A) and 13 patients poor status (grades II-IV: group B). Arterial hypotension was induced with PGE, 0.1 ng kg-' min~' initially and adjusted to maintain mean arterial pressure at about 70 mm Hg. PGE, was discontinued at the completion of aneurysm clipping. LCBF and CO2R were measured during and after administration of PGE,. LCBF was unchanged and C02R preserved in both groups. The carbon dioxide response was better in group A than in group B (P < 0.01). PGE, may be a suitable agent for hypotensive anaesthesia in these patients. KEY WORDS
an appropriate relative. Twenty-four patients undergoing craniotomy for cerebral aneurysm surgery were admitted to the study. The patients were allocated to two groups according to neurological status, using the Hunt and Kosnik scale [9] (table I) at the time of admission to the operating theatre: group A (11 patients) had good neurological status (grade I); group B (13 patients) had poor neurological status (grades II-IV). Subarachnoid haemorrhage was confirmed by lumbar puncture or computed tomographic scanning. Conventional angiography was performed a few hours to a few days after subarachnoid haemorrhage to confirm the presence of a cerebral aneurysm. Outcome was graded by the Glasgow Outcome Scale at discharge [10]. Atropine 0.5 mg and phenobarbitone 100 mg were given i.m. 1 h before surgery. Anaesthesia was induced with thiopentone 4mgkg~1. Tracheal intubation was performed with cricoid pressure and facilitated by pancuronium 0.1 mg kg"1. The lungs were ventilated mechanically with 70 % nitrous oxide
Brain: blood flow, carbon dioxide tension. Surgery: neurological. Pharmacology: prostaglandin E,. TABLE I. Hunt and Kosnik classification of patients with intracranial amurysms according to surgical risk [9]
Deliberate hypotension is used commonly in cerebral aneurysm surgery to reduce the risk of premature rupture and facilitate surgery [1-3]. Patients who have had a subarachnoid haemorrhage frequently develop abnormal cerebrovascular reactivity and impaired autoregulation [4], which may lead to postoperative neurological deficits [5]. Trimetaphan, nitroglycerine, adenosine triphosphate and sodium nitroprusside have been used to decrease arterial pressure, but have disadvantages such as increasing intracranial pressure, rebound hypertension and toxic metabolites. Prostaglandin E, (PGE,) has been advocated as a suitable hypotensive agent, but there is little information on its cerebral vascular effects [6-8]. We therefore studied local cerebral blood flow (LCBF) and carbon dioxide reactivity (CO2R) during PGE^induced hypotension in patients during cerebral aneurysm surgery.
Grade O I
la
II
III IV
V
Characteristics Unruptured aneurysm Asymptomatic, or minimal headache and slight nuchal rigidity No acute meningeal or brain reaction, but with fixed neurological deficit Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy Drowsiness, confusion, or mild focal deficit Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity, and vegetative disturbances Deep coma, decerebrate rigidity, moribund appearance
PATIENTS AND METHODS
The study was approved by the Subcommittee on Human Studies of the Osaka Police Hospital and informed consent was obtained from each patient or
KAZUO ABE, M.D. ; AKIRA DEMIZU, M.D.; IKUTO YOSHIYA, M.D. ;
Department of Anaesthesiology, Osaka Police Hospital, 10-31 Kitayamacho Tennoujiku Osaka 543, Japan. Accepted for Publication: September 19, 1991.
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on March 18, 2015
SUMMARY
CEREBRAL BLOOD FLOW AND PGE,
269
TABLE II. Details of patients studied. AcomA = Anterior communicating artery ; ICA = internal carotid artery ; PCA = posterior communicating artery; AchA = anterior choroidal artery; OphA = ophthalmic artery; MCA = middle cerebral artery; BA = basilar artery. * Outcome was graded by Glasgow outcome scale from V = death to I = good recovery ; there was a significant difference between groups (P < 0.05, chi-square test). + Hunt and Kosnik scale (table I) No.
Age (yr)
Aneurysm location
Outcome*
F F F M F M M M M M F
r. MCA r. IC-AchA BA AcomA AcomA 1. IC-AchA r. IC-AchA r. MCA r. MCA 1. MCA AcomA
I I IV I I II I I I I I
M F M F F F F M F F F F F
1. IC-AchA 1. IC-top AcomA 1. IC-PCA 1. IC-AchA AcomA AcomA r. MCA 1. MCA 1. MCA r. MCA 1. IC-OphA 1. IC-PCA
I I I II I I I III I IV IV IV III
— —, 00
Neurological statusf
Tj- 00 ->
o* S oo r~ in
oo oi in
I I I I
II II II II II II II II III IV IV IV IV
in oxygen. Anaesthesia was maintained with fentanyl 2 ng kg' 1 h"1 and droperidol 0.1 mg kg"1. Continuous arterial pressure recordings and intermittent arterial blood samples were obtained via a cannula placed in the radial artery. End-tidal carbon dioxide wa (PECO,) s monitored in all patients. A venous cannula was placed into the femoral vein for infusion of PGE,. Mean arterial pressure (MAP) and heart rate were monitored. After the dura mater was opened, the probe of a thermal gradient blood flow meter (Biomedical Science Co., Tokyo, Japan) was placed on the middle frontal gyrus, some distance from the point of intended brain retraction. This instrument measures changes in heat conductivity of the tissue in response to altered blood flow. The thermal gradient is maximal when no blood is passing through the cerebral cortex (Vo). As cortical blood flow increases, the temperature difference decreases in proportion to the flow. LCBF was calculated from the following formula, using the output (V) of the thermocouple generated by temperature changes: LCBF = 6 ( 1 / F - l / F o ) where k is a constant [11-12]. Control measurements were made just before the start of PGE, administration. The initial dose of PGE, was 0.1 ug kg"1 min"1, which was adjusted to maintain MAP at about 70 mm Hg. LCBF was measured at 10, 30 and 60 min after the start of infusion of PGE,, before aneurysm clipping and at 10, 30 and 60 min after
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Group A 1 50 2 41 3 61 4 21 5 76 6 48 7 44 8 55 9 56 10 55 11 26 Mean 48.6 Group B 1 80 47 2 3 60 4 68 59 5 6 81 7 26 8 48 9 76 10 41 11 41 12 55 13 44 Mean 55.5
Sex
270
discontinuation of PGEX at the completion of cerebral aneurysm clip ligation. CO2R was defined as LCBF changes in response to alterations in PaCOt and was defined as the unit change in LCBF per unit change in PaCOj (ml min"1/100 g mm Hg"1). CO,R was calculated just before the start of PGE13 60 min later and 60 min after its discontinuation.
after its discontinuation (table III). No significant changes occurred in heart rate. LCBF did not change significantly throughout the study (table III). COjR was significantly better in group A compared with group B throughout the study, and did not change in either group throughout the study (table IV). There was a close correlation between presurgical neurological status and COSR (r, = -0.549, P<0.01) (fig. 1). DISCUSSION
In this study, local cerebral blood flow and CO2 reactivity were preserved during PGE^induced hypotension for cerebral aneurysm surgery as measured by the thermal gradient method. The advantages of this method are simplicity, lack of radioactivity and ability to measure change in LCBF RESULTS rapidly and continuously. The values in this study were comparable to those of previous reports using Table II shows clinical details of the patients studied. other methods [13, 14]. The probe was placed on the The outcome of group A patients was significantly middle frontal gyrus and LCBF was measured in a better than that of group B (P < 0.05). After the start boundary zone between the territories of the anterior of administration of PGE U MAP decreased imand middle cerebral arteries where perfusion was mediately in both groups, and was still decreased 1 h least [15]. Cerebral blood flow measurements in this study may have been from regions different from TABLE IV. Mean (sz>) carbon dioxide reactivity (CO,R). PGE, = those supplied by the vessels subjected to surgery. Prostaglandin E,. * P < 0.05; ** P < 0.01 compared with group A PGEi administration was discontinued at com(ANOVA and Bonferroni) pletion of the clipping procedure, but the hypoCO.R (ml min-7100 g mm Hg-1) tensive effects and its effect on LCBF persisted for 1 h in spite of its short elimination half-time. Goto, Just before 60 min after 60 min after Otani and Fujita [16] also reported a prolongation PGE, end PGE, start of hypotensive effect under general anaesthesia, 1.46(0.64) 1.35(0.57) Group A 1.39(0.69) although the blood concentration of PGE, had 0.69 (0.28)** 0.81 (0.29)* Group B 0.84 (0.37)* declined to the pre-administration value within about 10 min after discontinuation. The prolonged effect of PGE! remains unexplained. The study also confirmed the relationship between preoperative neurological status and clinical outcome and showed 3 a relationship between preoperative status and reactivity to carbon dioxide. It is controversial if intraoperative hypotension should be used during aneurysm surgery. It is well known that subarachnoid haemorrhage causes a CD X significant decrease in cerebral blood flow [17, 18]. E For this reason, a major concern with the use of E 2 induced hypotension is that cerebral blood flow may CD O decrease to a critically low level and result in O ischaemic brain damage. c It would seem important, therefore, to preserve E LCBF and CO2R if hypotensive drugs are used to facilitate cerebral aneurysm surgery [19, 20]. PaulCM 1 son, Olesen and Christensen studied autoregulation ! ! o of cerebral blood flow by hypocapnia and concluded that restoration of autoregulation during hypocapnia may protect the brain against oedema formation and may therefore be of therapeutic value [21]. Trimetaphan (TMP) reduces CO2R in animals [22] and may induce cerebral vasoconstriction in man [23]. Sodium nitroprusside also impairs COSR [22], but IV has been shown to preserve cerebral blood flow Status better than TMP [15]. Nitroglycerin increased FIG. 1. Individual values for carbon dioxide reactivity (CO,R) and intracranial pressure in one study [24] and ATP presurgical neurological status (Status) (Hunt and Kosnik scale induced cerebral vasodilatation and impaired auto[9]) during hypotension induced by prostaglandin E,. n = 24; regulation in man [25]. None of the agents used r, = -0.549; P < 0 . 0 1 .
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on March 18, 2015
Statistical analysis Comparison of Glasgow Outcome Scale was performed with a chi-square test. Analysis of variance (ANOVA) and Bonferroni test were used to define differences within and between groups. The correlation between presurgical neurological status and CO2R was performed with the Spearman Rank correlation test. P < 0.05 was considered statistically significant.
BRITISH JOURNAL OF ANAESTHESIA
CEREBRAL BLOOD FLOW AND previously would appear to be ideal for inducing hypotension in patients following subarachnoid haemorrhage, and PGEj may be preferable. ACKNOWLEDGEMENTS We thank Dr Kitaro Kamada and Professor Toshisuke Sakaki for technical advice.
12. Carter LP, Erspamer RBS, White WL, Yamagata S. Cortical blood flow during craniotomy for aneurysm. Surgical Neurology 1982; 17: 204-208. 13. Merory J, Thomas DJ, Humphrey PRD, Du Boulay GH, Marshall J, Russel RWR, Symon L, Zilkha E. Cerebral blood flow after surgery for recent subarachnoid haemorrhage. Journal of Neurology, Neurosurgery and Psychiatry 1980; 4 3 :
214-221. 14. Olesen J, Paulson OB, Lassen NA. Regional cerebral blood flow in man determined by the initial slope of the clearance of intra-arterial injections of lMXc. Stroke 1971; 2: 519-540. 15. McDowall DG. Induced hypotension and brain ischaemia. British Journal of Anaesthesia 1985; 57: 110-119. 16. Goto F, Otani E, Fujita T. Antihypertensive activity and metabolic rate of prostaglandin E, in surgical patients under general anesthesia. Prostaglandins, Leukotrienes, and Essential
17. 18. 19. 20.
21. 22. 23. 24. 25.
Fatty Acids 1985; 18: 359-366. Parkes JD, James IM. Electroencephalographic and cerebral blood flow changes following spontaneous subarachnoid haemorrhage. Brain 1971; 94: 69-76. Berergvall U, Steiner L, Forster DMC. Early pattern of cerebral circulatory disturbances following subarachnoid haemorrhage. Neuroradiology 1973; 5: 24-32. Ishii R. Regional cerebral bloodflowin patients with ruptured intracranial aneurysm. Journal of Neurosurgery 1979; 50: 587-594. Voldby B, Enevoldsen EM, Jensen FT. Regional cerebral blood flow, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms. Journal of Neurosurgery 1985; 62: 59-67. Paulson OB, Olesen J, Christensen MS. Restoration of autoregulation of cerebral blood flow by hypocapnia. Neurology 1972; 22: 286-293. Artru AA, Colley PS. Cerebral blood flow responses to hypocapnia during hypotension. Stroke 1984; 15: 878-883. Harp JR, Wollmann H. Cerebral metabolic effects of hyperventilation and deliberate hypotension. British Journal of Anaesthesia 1973; 45: 256-260. Cottrell JE, Gupta B, Rappaport H, Turndorf H. Intracranial pressure during nitroglycerin-induced hypotension. Journal of Neurosurgery 1980; 53: 309-311. Lagerkranser M, Bergstrand G, Gordon E, Ircstedt L, Lindquist C, Stange K, Sollevi A. Cerebral blood flow and metabolism during adcnosine-induced hypotension in patients undergoing cerebral aneurysm surgery. Ada Anaesthesiologica Scandinavica 1989; 33: 15—20.
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on March 18, 2015
REFERENCES 1. Griffiths DPG, Cummins BF, Greenbaum R. Cerebral blood flow and metabolism during hypotension induced with sodium nitroprusside. British Journal of Anaesthesia 1974; 46: 671-679. 2. Aitken RR, Drake CG. A technique of anesthesia with induced hypotension for surgical correction of intracranial aneurysms. Clinical Neurosurgery 1974; 21: 107-114. 3. Yashon D, Magncss AP n, Vise WM. Systemic hypotension in neurosurgery. Journal of Neurosurgery 1975; 43: 579—589. 4. Grubb RL, Raichle ME, Eichling JO. Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. Journal of Neurosurgery 1977; 46: 446-153. 5. Pickard JD, Matheson M, Patterson J. Prediction of late ischemic complications after cerebral aneurysm surgery by the intraoperative measurement of cerebral blood flow. Journal of Neurosurgery 1980; 53: 305-308. 6. Horton EW. Hypothesis on physiological roles of prostaglandins. Physiological Reviews 1989; 49: 123-161. 7. Steiner L, Forster DMC, Bergvall U, Carlson LA. Effects of prostaglandin El on cerebral circulatory disturbances following subarachnoid haemorrhage in man. Neuroradiology 1972;4: 20-24. 8. Olesen J. Effect of intracarotid prostaglandin El on regional cerebral blood flow in man. Stroke 1976; 7: 566-569. 9. Hunt WE, Kosnik EJ. Timing and perioperauve care in intracranial aneurysm surgery. Clinical Neurosurgery 1974; 21: 79-89. 10. Jennett B, Bond M. Assessment of outcome after severe brain injury. Lancet 1975; 1: 480-484. 11. Carter LP, Erspamer R, Bro WJ. Cortical blood flow: thermal diffusion vs isotope clearance. Stroke 1981; 12: 513-518.
271
EFFECT OF PROSTAGLANDIN E^INDUCED HYPOTENSION ON CARBON DIOXIDE REACTIVITY AND LOCAL CEREBRAL BLOOD FLOW AFTER SUBARACHNOID HAEMORRHAGE K. ABE, A. DEMIZU AND I. YOSHIYA
The effect of prostaglandin E, (PGE,) on local cerebral blood flow (LCBF) and carbon dioxide reactivity (CO2R) was studied during cerebral aneurysm surgery for subarachnoid haemorrhage in 24 patients under neuroleptanaesthesia. Eleven patients had good neurological status (Hunt and Kosnik grade I: group A) and 13 patients poor status (grades II-IV: group B). Arterial hypotension was induced with PGE, 0.1 ng kg-' min~' initially and adjusted to maintain mean arterial pressure at about 70 mm Hg. PGE, was discontinued at the completion of aneurysm clipping. LCBF and CO2R were measured during and after administration of PGE,. LCBF was unchanged and C02R preserved in both groups. The carbon dioxide response was better in group A than in group B (P < 0.01). PGE, may be a suitable agent for hypotensive anaesthesia in these patients. KEY WORDS
an appropriate relative. Twenty-four patients undergoing craniotomy for cerebral aneurysm surgery were admitted to the study. The patients were allocated to two groups according to neurological status, using the Hunt and Kosnik scale [9] (table I) at the time of admission to the operating theatre: group A (11 patients) had good neurological status (grade I); group B (13 patients) had poor neurological status (grades II-IV). Subarachnoid haemorrhage was confirmed by lumbar puncture or computed tomographic scanning. Conventional angiography was performed a few hours to a few days after subarachnoid haemorrhage to confirm the presence of a cerebral aneurysm. Outcome was graded by the Glasgow Outcome Scale at discharge [10]. Atropine 0.5 mg and phenobarbitone 100 mg were given i.m. 1 h before surgery. Anaesthesia was induced with thiopentone 4mgkg~1. Tracheal intubation was performed with cricoid pressure and facilitated by pancuronium 0.1 mg kg"1. The lungs were ventilated mechanically with 70 % nitrous oxide
Brain: blood flow, carbon dioxide tension. Surgery: neurological. Pharmacology: prostaglandin E,. TABLE I. Hunt and Kosnik classification of patients with intracranial amurysms according to surgical risk [9]
Deliberate hypotension is used commonly in cerebral aneurysm surgery to reduce the risk of premature rupture and facilitate surgery [1-3]. Patients who have had a subarachnoid haemorrhage frequently develop abnormal cerebrovascular reactivity and impaired autoregulation [4], which may lead to postoperative neurological deficits [5]. Trimetaphan, nitroglycerine, adenosine triphosphate and sodium nitroprusside have been used to decrease arterial pressure, but have disadvantages such as increasing intracranial pressure, rebound hypertension and toxic metabolites. Prostaglandin E, (PGE,) has been advocated as a suitable hypotensive agent, but there is little information on its cerebral vascular effects [6-8]. We therefore studied local cerebral blood flow (LCBF) and carbon dioxide reactivity (CO2R) during PGE^induced hypotension in patients during cerebral aneurysm surgery.
Grade O I
la
II
III IV
V
Characteristics Unruptured aneurysm Asymptomatic, or minimal headache and slight nuchal rigidity No acute meningeal or brain reaction, but with fixed neurological deficit Moderate to severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy Drowsiness, confusion, or mild focal deficit Stupor, moderate to severe hemiparesis, possibly early decerebrate rigidity, and vegetative disturbances Deep coma, decerebrate rigidity, moribund appearance
PATIENTS AND METHODS
The study was approved by the Subcommittee on Human Studies of the Osaka Police Hospital and informed consent was obtained from each patient or
KAZUO ABE, M.D. ; AKIRA DEMIZU, M.D.; IKUTO YOSHIYA, M.D. ;
Department of Anaesthesiology, Osaka Police Hospital, 10-31 Kitayamacho Tennoujiku Osaka 543, Japan. Accepted for Publication: September 19, 1991.
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on March 18, 2015
SUMMARY
CEREBRAL BLOOD FLOW AND PGE,
269
TABLE II. Details of patients studied. AcomA = Anterior communicating artery ; ICA = internal carotid artery ; PCA = posterior communicating artery; AchA = anterior choroidal artery; OphA = ophthalmic artery; MCA = middle cerebral artery; BA = basilar artery. * Outcome was graded by Glasgow outcome scale from V = death to I = good recovery ; there was a significant difference between groups (P < 0.05, chi-square test). + Hunt and Kosnik scale (table I) No.
Age (yr)
Aneurysm location
Outcome*
F F F M F M M M M M F
r. MCA r. IC-AchA BA AcomA AcomA 1. IC-AchA r. IC-AchA r. MCA r. MCA 1. MCA AcomA
I I IV I I II I I I I I
M F M F F F F M F F F F F
1. IC-AchA 1. IC-top AcomA 1. IC-PCA 1. IC-AchA AcomA AcomA r. MCA 1. MCA 1. MCA r. MCA 1. IC-OphA 1. IC-PCA
I I I II I I I III I IV IV IV III
— —, 00
Neurological statusf
Tj- 00 ->
o* S oo r~ in
oo oi in
I I I I
II II II II II II II II III IV IV IV IV
in oxygen. Anaesthesia was maintained with fentanyl 2 ng kg' 1 h"1 and droperidol 0.1 mg kg"1. Continuous arterial pressure recordings and intermittent arterial blood samples were obtained via a cannula placed in the radial artery. End-tidal carbon dioxide wa (PECO,) s monitored in all patients. A venous cannula was placed into the femoral vein for infusion of PGE,. Mean arterial pressure (MAP) and heart rate were monitored. After the dura mater was opened, the probe of a thermal gradient blood flow meter (Biomedical Science Co., Tokyo, Japan) was placed on the middle frontal gyrus, some distance from the point of intended brain retraction. This instrument measures changes in heat conductivity of the tissue in response to altered blood flow. The thermal gradient is maximal when no blood is passing through the cerebral cortex (Vo). As cortical blood flow increases, the temperature difference decreases in proportion to the flow. LCBF was calculated from the following formula, using the output (V) of the thermocouple generated by temperature changes: LCBF = 6 ( 1 / F - l / F o ) where k is a constant [11-12]. Control measurements were made just before the start of PGE, administration. The initial dose of PGE, was 0.1 ug kg"1 min"1, which was adjusted to maintain MAP at about 70 mm Hg. LCBF was measured at 10, 30 and 60 min after the start of infusion of PGE,, before aneurysm clipping and at 10, 30 and 60 min after
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Group A 1 50 2 41 3 61 4 21 5 76 6 48 7 44 8 55 9 56 10 55 11 26 Mean 48.6 Group B 1 80 47 2 3 60 4 68 59 5 6 81 7 26 8 48 9 76 10 41 11 41 12 55 13 44 Mean 55.5
Sex
270
discontinuation of PGEX at the completion of cerebral aneurysm clip ligation. CO2R was defined as LCBF changes in response to alterations in PaCOt and was defined as the unit change in LCBF per unit change in PaCOj (ml min"1/100 g mm Hg"1). CO,R was calculated just before the start of PGE13 60 min later and 60 min after its discontinuation.
after its discontinuation (table III). No significant changes occurred in heart rate. LCBF did not change significantly throughout the study (table III). COjR was significantly better in group A compared with group B throughout the study, and did not change in either group throughout the study (table IV). There was a close correlation between presurgical neurological status and COSR (r, = -0.549, P<0.01) (fig. 1). DISCUSSION
In this study, local cerebral blood flow and CO2 reactivity were preserved during PGE^induced hypotension for cerebral aneurysm surgery as measured by the thermal gradient method. The advantages of this method are simplicity, lack of radioactivity and ability to measure change in LCBF RESULTS rapidly and continuously. The values in this study were comparable to those of previous reports using Table II shows clinical details of the patients studied. other methods [13, 14]. The probe was placed on the The outcome of group A patients was significantly middle frontal gyrus and LCBF was measured in a better than that of group B (P < 0.05). After the start boundary zone between the territories of the anterior of administration of PGE U MAP decreased imand middle cerebral arteries where perfusion was mediately in both groups, and was still decreased 1 h least [15]. Cerebral blood flow measurements in this study may have been from regions different from TABLE IV. Mean (sz>) carbon dioxide reactivity (CO,R). PGE, = those supplied by the vessels subjected to surgery. Prostaglandin E,. * P < 0.05; ** P < 0.01 compared with group A PGEi administration was discontinued at com(ANOVA and Bonferroni) pletion of the clipping procedure, but the hypoCO.R (ml min-7100 g mm Hg-1) tensive effects and its effect on LCBF persisted for 1 h in spite of its short elimination half-time. Goto, Just before 60 min after 60 min after Otani and Fujita [16] also reported a prolongation PGE, end PGE, start of hypotensive effect under general anaesthesia, 1.46(0.64) 1.35(0.57) Group A 1.39(0.69) although the blood concentration of PGE, had 0.69 (0.28)** 0.81 (0.29)* Group B 0.84 (0.37)* declined to the pre-administration value within about 10 min after discontinuation. The prolonged effect of PGE! remains unexplained. The study also confirmed the relationship between preoperative neurological status and clinical outcome and showed 3 a relationship between preoperative status and reactivity to carbon dioxide. It is controversial if intraoperative hypotension should be used during aneurysm surgery. It is well known that subarachnoid haemorrhage causes a CD X significant decrease in cerebral blood flow [17, 18]. E For this reason, a major concern with the use of E 2 induced hypotension is that cerebral blood flow may CD O decrease to a critically low level and result in O ischaemic brain damage. c It would seem important, therefore, to preserve E LCBF and CO2R if hypotensive drugs are used to facilitate cerebral aneurysm surgery [19, 20]. PaulCM 1 son, Olesen and Christensen studied autoregulation ! ! o of cerebral blood flow by hypocapnia and concluded that restoration of autoregulation during hypocapnia may protect the brain against oedema formation and may therefore be of therapeutic value [21]. Trimetaphan (TMP) reduces CO2R in animals [22] and may induce cerebral vasoconstriction in man [23]. Sodium nitroprusside also impairs COSR [22], but IV has been shown to preserve cerebral blood flow Status better than TMP [15]. Nitroglycerin increased FIG. 1. Individual values for carbon dioxide reactivity (CO,R) and intracranial pressure in one study [24] and ATP presurgical neurological status (Status) (Hunt and Kosnik scale induced cerebral vasodilatation and impaired auto[9]) during hypotension induced by prostaglandin E,. n = 24; regulation in man [25]. None of the agents used r, = -0.549; P < 0 . 0 1 .
Downloaded from http://bja.oxfordjournals.org/ at University of Iowa Libraries/Serials Acquisitions on March 18, 2015
Statistical analysis Comparison of Glasgow Outcome Scale was performed with a chi-square test. Analysis of variance (ANOVA) and Bonferroni test were used to define differences within and between groups. The correlation between presurgical neurological status and CO2R was performed with the Spearman Rank correlation test. P < 0.05 was considered statistically significant.
BRITISH JOURNAL OF ANAESTHESIA
CEREBRAL BLOOD FLOW AND previously would appear to be ideal for inducing hypotension in patients following subarachnoid haemorrhage, and PGEj may be preferable. ACKNOWLEDGEMENTS We thank Dr Kitaro Kamada and Professor Toshisuke Sakaki for technical advice.
12. Carter LP, Erspamer RBS, White WL, Yamagata S. Cortical blood flow during craniotomy for aneurysm. Surgical Neurology 1982; 17: 204-208. 13. Merory J, Thomas DJ, Humphrey PRD, Du Boulay GH, Marshall J, Russel RWR, Symon L, Zilkha E. Cerebral blood flow after surgery for recent subarachnoid haemorrhage. Journal of Neurology, Neurosurgery and Psychiatry 1980; 4 3 :
214-221. 14. Olesen J, Paulson OB, Lassen NA. Regional cerebral blood flow in man determined by the initial slope of the clearance of intra-arterial injections of lMXc. Stroke 1971; 2: 519-540. 15. McDowall DG. Induced hypotension and brain ischaemia. British Journal of Anaesthesia 1985; 57: 110-119. 16. Goto F, Otani E, Fujita T. Antihypertensive activity and metabolic rate of prostaglandin E, in surgical patients under general anesthesia. Prostaglandins, Leukotrienes, and Essential
17. 18. 19. 20.
21. 22. 23. 24. 25.
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