Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Vasodilators during cerebral aneurysm surgery

  • 538 Accesses

  • 14 Citations

Abstract

The objective of this review is to review the anaesthetic implications of vasoactive compounds particularly with regard to the cerebral circulation and their clinical importance for the practicing anaesthetist. Material was selected on the basis of validity and application to clinical practice and animal studies were selected only if human studies were lacking. Hypotensive drugs have been used to induce hypotension and in the treatment of intraoperative hypertension during cerebral aneurysm surgery. After subarachnoid haemorrhage, cerebral blood flow is reduced and cerebral vasoreactivity is disturbed which may lead to brain ischaemia. Also, cerebral arterial vasospasm decreases cerebral blood flow, and may lead to delayed ischaemic brain damage which is a major problem after subarachnoid haemorrhage. Recently, the use of induced hypotension has decreased although it is still useful in patients with intraoperative aneurysm rupture, giant cerebral aneurysm, fragile aneurysms and multiple cerebral aneurysms. In this review, a variety of vasodilating agents, prostaglandin E1 sodium nitroprusside, nitroglycerin,’ trimetaphan, adenosine, calcium antagonists, and inhalational anaesthetics, are discussed for their clinical usefulness. Sodium nitroprusside, nitroglycerin and isoflurane are the drugs of choice for induced hypotension. Prostaglandin E1, nicardipine and nitroglycerin have the advantage that they do not alter carbon dioxide reactivity. Local cerebral blood flow is increased with nitroglycerin, decreased with trimetaphan and unchanged with prostaglandin E1. Intraoperative hypertension is a dangerous complication occurring during cerebral aneurysm surgery, but its treatment in association with subarachnoid haemorrhage is complicated in cases of cerebral arterial vasospasm because fluctuations in cerebral blood flow may be exacerbated. Hypertension should be treated immediately to reduce the risk of rebleeding and intraoperative aneurysmal rupture and the choice of drugs is discussed. Although the use of induced hypotension has declined, the control of arterial blood pressure with vasoactive drugs to reduce the risk of intraoperative cerebral aneurysm rupture is a useful technique. Intraoperative hypertension should be treated immediately but the cerebral vascular effects of each vasodilator should be understood before their use as hypotensive agents.

Résumé

L’objectif de cet article est de revoir les implications anesthésiques des composés vasoactifs particulièrement en rapport avec la circulation cérébrale ainsi que leur importance clinique pour l’anesthésiste. Les agents ont été choisis sur la base de leur validité et de leur application à la pratique clinique et des études animales ont été choisies seulement en l’absence d’étude sur l’homme. Les agents hypotenseurs ont été utilisés pour induire de l’hypotension et pour traiter l’hypertension preopératoire pendant la chirurgie d’anévrisme cérébrale. Après une hémorragie sous-arachnoidienne, le débit sanguin cérébrale réduit et la vasomotricité cérébrale perturbée peuvent entraîner une ischémie cérébrale. Ainsi, le vasospasme artériel cérébral diminue le débit sanguin cérébral et peut conduire à des dommages cérébraux retardés d’ischémie, problème majeur après une hémorragie sous-arachnoïdienne. Récemment, l’utilisation de l’hypotension contrôlée s’est raréfiée bien qu’elle soit encore utile chez les patients avec une rupture peropératoire d’anévrisme, en cas d’anévrisme cérébral géant, d’anévrismes fragiles et d’anévrismes cérébraux multiples. Dans cet article, une variété de vasodilatateurs, le prostaglandine E1 le nitroprussiate de sodium, la nitroglycérine, le trimétaphan, l’adénosine, les antagonistes calciques et les agents d’inhalation son discutés pour leur utilité clinique. Le nitroprussiate de sodium, la nitroglycérine et l’isoflurane sont les agents de choix pour l’hypotension contrôlée. La prostaglandine E1 la nicardipine et la nitroglycérine ont l’avantage de ne pas altérer la réactivité au dioxyde de carbone. Le débit sanguin cérébral local est augmenté avec la nitroglycérine, diminué avec le trimétaphan et inchangé avec la prostaglandine E1. L’hypertension peropératoire est une complication dangereuse aux cours d’une chirurgie d’anévrisme cérébral, mais son traitement lors d’hémorragie sousarachnoïdienne se complique dans les cas de vasospasme artériel cérébral parce que les fluctuations du débit sanguin cérébral peuvent s’exacerber. L’hypertension devrait être traitée immédiatement pour réduire le risque de resaignement et de rupture peropératoire de l’anévrisme. Le choix des agents est discuté. Bien que l’utilisation de l’hypotension contrôlée est moins fréquente, le contrôle de la pression artérielle avec des agents vasoactifs dans le but de réduire le risque de rupture peropératoire d’anévrisme cérébral est une technique courante. L’hypertension peropératoire devrait être traitée immédiatement mais tes effets vasculaires cérébraux de chaque vasodilatateurs devraient être compris avant qu’ils soient utilisés comme agents hypotenseurs.

References

  1. 1

    Lam AM. Induced hypotension. Can Anaesth Soc J 1984; 31: S56-S62.

  2. 2

    Grubb RL Jr, Raichle ME, Eichling JO, Gado MH. Effects of subarachnoid hemorrhage on cerebral blood volume, blood flow, and oxygen utilization in humans. J Neurosurg 1977; 46: 446–53.

  3. 3

    Batjer HH, Frankfurt AI, Purdy PD, Smith SS, Samson DS. Use of etomidate, temporary arterial occlusion, and intraoperative angiography in surgical treatment of large and giant cerebral aneurysms. J Neurosurg 1988; 68: 234–40.

  4. 4

    Symon L. Disordered cerebro-vascular physiology in aneurysmal subarachnoid haemorrhage. Acta Neurochir (Wien) 1978; 41: 7–22.

  5. 5

    McDowall DG. Induced hypotension and brain ischaemia. Br J Anaesth 1985; 57: 110–9.

  6. 6

    Hunt WE, Kosnik EJ. Timing and perioperative care in intracranial aneurysm surgery. Clin Neurosurg 1974; 21: 78–89.

  7. 7

    Disney L, Weir B, Grace M. Factors influencing the outcome of aneurysm rupture in poor grade patients: a prospective series. Neurosurgery 1988; 23: 1–9.

  8. 8

    Dorsch NWC, Branston NM, Harris RJ, Bentivoglio P, Symon L. An experimental study of the effect of nimodipine in primate subarachnoid haemorrhage. Acta Neurochir (Wien) 1989; 99: 65–75.

  9. 9

    Adams HP Jr, Kassell NF, Tomer JC, Haley EC Jr. Predicting cerebral ischemia after aneurysmal subarachnoid hemorrhage: influences of clinical condition, CT results, and antifibrinolytic therapy. A report of the Cooperative Aneurysm Study. Neurology 1987; 37: 1586–91.

  10. 10

    Fein JM. Cerebral energy metabolism after subarachnoid hemorrhage. Stroke 1975; 6: 1–8.

  11. 11

    Graff-Radford NR, Tomer J, Adams HP, Kassell NF. Factors associated with hydrocephalus after subarachnoid hemorrhage. A report of the Cooperative Aneurysm Study. Arch Neurol 1989; 46: 744–52.

  12. 12

    Mohr G, Ferguson G, Khan M, et al. Intraventricular hemorrhage from ruptured aneurysm. J Neurosurg 1983; 58: 482–7.

  13. 13

    Ishii R. Regional cerebral blood flow in patients with ruptured intracranial aneurysms. J Neurosurg 1979; 50: 587–94.

  14. 14

    Powers WJ, Grubb RL Jr, Baker RP, Mintun MA, Raichle ME. Regional cerebral blood flow and metabolism in reversible ischemia due to vasospasm. J Neurosurg 1985; 62: 539–46.

  15. 15

    Weir B, Menon D, Overton T. Regional cerebral blood flow in patients with aneurysms: estimation by Xenon 133 inhalation. Can J Neurol Sci 1978; 5: 301–5.

  16. 16

    Mountz JM, McGillicuddy JE, Wilson MW, Bartold SP, Siegal EM. Preand post-operative cerebral blood flow changes in subarachnoid haemorrhage. Acta Neurochir (Wien) 1991; 109: 30–3.

  17. 17

    Voldby B, Enevoldsen EM, Jensen FT. Regional CBF, intraventricular pressure, and cerebral metabolism in patients with ruptured intracranial aneurysms. J Neurosurg 1985; 62: 48–58.

  18. 18

    Menon D, Weir B, Overton T. Ventricular size and cerebral blood flow following subarachnoid hemorrhage. Journal of Computer Assisted Tomography 1981; 5: 328–33.

  19. 19

    Mathew NT, Meyer JS, Hartmann A. Diagnosis and treatment of factors complicating subarachnoid hemorrhage. Neuroradiology 1974; 6: 237–45.

  20. 20

    Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968; 28: 14–20.

  21. 21

    Jennett B, Bond M. Assessment of outcome after severe brain damage. Lancet 1975; 1: 480–4.

  22. 22

    Alvord EC Jr, Loeser JD, Bailey WL, Copass MK. Subarachnoid hemorrhage due to ruptured aneurysms. A simple method of estimating prognosis. Arch Neurol 1972; 27: 273–84.

  23. 23

    Archer DP, Shaw DA, Leblanc RL, Tranmer BI. Haemodynamic considerations in the management of patients with subarachnoid haemorrhage. Can J Anaesth 1991; 38: 454–70.

  24. 24

    Ljunggren B, Brandt L Kågström E, Sundbärg G. Results of early operations for ruptured aneurysms. J Neurosurg 1981; 54: 473–9.

  25. 25

    Kassell NF, Tomer JC, Haley EC Jr, Jane JA, Adams HP, Kongable GL. The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg 1990; 73: 18–36.

  26. 26

    Haley EC Jr, Kassell NF, Tomer JC. The International Cooperative Study on The Timing of Aneurysm Surgery. The North American experience. Stroke 1992; 23: 205–14.

  27. 27

    Kassell NJ, Torner JC. Aneurysmal rebleeding: a preliminary report from the Cooperative Aneurysm Study. Neurosurgery. 1983; 13: 479–81.

  28. 28

    Kassell NF, Sasaki T, Colohan ART, Nazar G. Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Stroke 1985; 16: 562–72.

  29. 29

    Graf CJ, Nibbelink DW. Cooperative study of intracranial aneurysms and subarachnoid hemorrhage. Report on a randomized treatment study III. Intra-cranial surgery. Stroke 1974; 5: 559–610.

  30. 30

    Kwak R, Niizuma H, Ohi T, Suzuki J. Angiographic study of cerebral vasospasm following rupture of intracranial aneurysms: Part 1. Time of the appearance. Surg Neurol 1979; 11: 257–62.

  31. 31

    Weir B, Grace M, Hansen J, Rothberg C. Time course of vasospasm in man. J Neurosurg 1978; 48: 173–8.

  32. 32

    Heros RC, Zervas NT, Varsos V. Cerebral vasospasm after subarachnoid hemorrhage: an update. Ann Neurol 1983; 14: 599–608.

  33. 33

    Carpenter DA, Grubb RL Jr, Tempel LW, Powers WJ. Cerebral oxygen metabolism after aneurysmal subarachnoid hemorrhage. J Cereb Blood Flow Metab 1991; 11: 837–44.

  34. 34

    Öhman J, Heiskanen O. Effect of nimodipine on the outcome of patients after aneurysmal subarachnoid hemorrhage and surgery. J Neurosurg 1988; 69: 683–6.

  35. 35

    Petruk KC, West M, Mohr G et al. Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter double-blind placebo-controlled trial. J Neurosurg 1988; 68: 505–17.

  36. 36

    Philippon J, Grob R, Dagreou F, Guggiari M, Rivierez M, Viars P. Prevention of vasospasm in subarachnoid haemorrhage. A controlled study with nimodipine. Acta Neurochir (Wien) 1986; 82: 110–4.

  37. 37

    Allen GS, Ahn HS, Preziosi TJ et al. Cerebral arterial vasospasm — a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983; 308: 619–24.

  38. 38

    Origitano TC, Wascher TM, Reichman OH, Anderson DE. Sustained increased cerebral blood flow with prophylactic hypertensive hypervolemic hemodilution (“triple-H” therapy) after subarachnoid hemorrhage. Neurosurgery 1990; 27: 729–39.

  39. 39

    Olesen J. Quantitive evaluation of normal and pathologic cerebral blood flow regulation to perfusion pressure changes in man. Arch Neurol 1973; 28: 143–9.

  40. 40

    Enevoldsen EM, Jensen FT. Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury. J Neurosurg 1978; 48: 689–703.

  41. 41

    Paulson OB. Cerebral apoplexy (stroke): pathogenesis, pathophysiology and therapy as illustrated by regional blood flow measurements in the brain. Stroke 1971; 2: 327–60.

  42. 42

    Schalén W, Messeter K, Nordstrom C. Cerebral vasoreactivity and the prediction of outcome in severe traumatic brain lesions. Acta Anaesthesiol Scand 1991; 35: 113–22.

  43. 43

    Voldby B, Enevoldsen EM, Jensen FT. Cerebrovascular reactivity in patients with ruptured intracranial aneurysms. J Neurosurg 1985; 62: 59–67.

  44. 44

    Artru AA, Colley PS. Cerebral blood flow responses to hypocapnia during hypotension. Stroke 1984; 15: 878–83.

  45. 45

    Abe K, Demizu A, Mima T, Kamada K, Yoshiya I. Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery. Can J Anaesth 1992: 39: 253–9.

  46. 46

    Abe K, Iwanaga H, Yoshiya I. Carbon dioxide reactivity and local cerebral blood flow during prostaglandin E1 or nitroglycerine-induced hypotension. Can J Anaesth 1992; 39: 799–804.

  47. 47

    Abe K, Shimada Y, Iwanaga H, Yoshiya I. Effect of nicardipine on local cerebral blood flow, carbon dioxide reactivity and blood flow velocity of internal carotid artery during cerebral aneurysm surgery. Anesth Anal (in press).

  48. 48

    Nornes H. The role of intracranial pressure in the arrest of hemorrhage in patients with ruptured intracranial aneurysm. J Neurosurg 1973; 51: 226–34.

  49. 49

    Farrar JK, Gamache FW Jr, Ferguson GG, Barker J, Varkey GP, Drake CG. Effects of profound hypotension on cerebral blood flow during surgery for intracranial aneurysms. J Neurosurgery 1981; 55: 857–64.

  50. 50

    Messeter K, Brandt L, Ljunggren B, et al. Prediction and prevention of delayed ischemic dysfunction after aneurysmal subarachnoid haemorrhage and early operation. Neurosurgery 1987; 20: 548–53.

  51. 51

    Cold GE, Jensen FT. Cerebral autoregulation in unconscious patients with brain injury. Acta Anaesthesiol Scand 1978; 22: 270–80.

  52. 52

    Muizelaar JP, Ward JD, Marmarou A, Newlon PG, Wachi A. Cerebral blood flow and metabolism in severely head-injured children. Part 2: Autoregulation. J Neurosurg 1989; 71: 72–6.

  53. 53

    Smith DR, Jacobson J, Kobrine AI, Rizzoli HV. Regional cerebral blood flow with intracranial mass lesions. Part II: Autoregulation in localized mass lesions. Surg Neurol 1977; 7: 238–40.

  54. 54

    Dernbach PD, Little JR, Jones SC, Ebrahim ZY. Altered cerebral autoregulation and CO2 reactivity after aneurysmal subarachnoid hemorrhage. Neurosurgery 1988; 22: 822–6.

  55. 55

    Obrist WD, Thompson HK Jr, King CH, Wang HS. Determination of regional cerebral blood flow by inhalation of 133-Xenon. Circ Res 1967; 20: 124–35.

  56. 56

    Lassen NA, Ingvar DH. Regional cerebral blood flow measurement in man. Arch Neurol 1963; 9: 615–22.

  57. 57

    Olsen TS, Larsen B, Skriver EB, Heming M, Enevoldsen E, Lassen NA. Focal cerebral hyperemia in acute stroke. Incidence, pathophysiology and clinical significance. Stroke 1981; 12: 598–607.

  58. 58

    Yonas H, Wolfson SK Jr, Gur D, et al. Clinical experience with the use of xenon-enhanced CT blood flow mapping in cerebral vascular disease. Stroke 1984; 15: 443–9.

  59. 59

    Powers WJ, Raichle MW. Positron emission tomography and its application to the study of cerebrovascular disease in man. Stroke 1985; 16: 361–76.

  60. 60

    Aukland K, Bower BF, Berliner RW. Measurement of local blood flow with hydrogen gas. Circ Res 1964; 14: 164–87.

  61. 61

    Young W. H2 clearance measurement of blood flow: a review of technique and polarographic principles. Stroke 1980; 11: 552–64.

  62. 62

    Pickard JD, Matheson M, Patterson J, Wyper D. Prediction of late ischemic complications after cerebral aneurysms surgery by the intraoperative measurement of cerebral blood flow. J Neurosurg 1980; 63: 305–8.

  63. 63

    Bell BA, Symon L, Branston NM. CBF and time thresholds for the formation of ischemic cerebral edema, and effect of reperfusion in baboons. J Neurosurg 1985; 62: 31–41.

  64. 64

    Abe K, Demizu A, Kamada K, Morimoto T, Sakaki T, Yoshiya I. Local cerebral blood flow with prostaglandin E1 or trimethaphan during cerebral aneursym clip ligation. Can J Anaesth 1991; 38: 831–6.

  65. 65

    Aaslid R, Huber P, Nornes H. Evaluation of cerebrovascular spasm with transcranial Doppler ultrasound. J Neurosurg 1984; 60: 37–42.

  66. 66

    Seiler RW, Grolimund P, Aaslid R, Huber R, Nornes H. Cerebral vasospasm evaluated by transcranial ultrasound correlated with clinical grade and CT-visualized subarachnoid hemorrhage. J Neurosurg 1986; 64: 594–600.

  67. 67

    Sloan MA, Haley EC Jr, Kassett NF, et al. Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage. Neurology 1989; 39: 1514–8.

  68. 68

    Caplan LR, Brass LM, De Witt LD, et al. Transcranial Doppler ultrasound: present status. Neurology 1990; 40: 696–700.

  69. 69

    Davis SM, Andrews JT, Lichtenstein M, Rossiter SC, Kaye AH, Hopper J. Correlations between cerebral arterial velocities, blood flow, and delayed ischemia after subarachnoid hemorrhage. Stroke 1992; 23: 492–7.

  70. 70

    Giannotta SL, Oppenheimer JH, Levy ML Zelman V. Management of intraoperative rupture of aneurysm without hypotension. Neurosurgery 1991; 28: 531–6.

  71. 71

    Hitchcock ER, Tsementzis SA, Dow AA. Shortand long-term prognosis of patients with subarachnoid haemorrhage in relation to intraoperative period of hypotension. Acta Neurochir 1984; 70: 235–41.

  72. 72

    Lam AM, Manninen PH. Induced hypotension for cerebral aneurysm — isoflurane or sodium nitroprusside? Can J Anaesth 1987; 34: S121-S122.

  73. 73

    Batjer H, Samson D. Intraoperative aneurysmal rupture: incidence, outcome and suggestions for surgical management. Neurosurgery 1986; 18: 701–17.

  74. 74

    Ausman JI, Diaz FG, Malik GM, Fielding AS, Son CS. Current management of cerebral aneurysms: is it based on facts or myths? Surg Neurol 1985; 24: 625–35.

  75. 75

    Calhoun DA, Oparil S. Treatment of hypertensive crisis. N Engl J Med 1990; 223: 1177–83.

  76. 76

    Carbon LA, Ekelund L-G, Orö L. Circulatory and respiratory effects of different doses of prostaglandin E1 in man. Acta Physiol Scand 1969; 75: 161–9.

  77. 77

    D’Ambra MN, LaRaia PJ, Philbin DM, Watkins WD, Hilgenberg AD, Buckley MJ. Prostaglandin E1. A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement. J Thorac Cardiovasc Surg 1985; 89: 567–72.

  78. 78

    Goto F, Otani E, Fujita T. Antihypertensive activity and metabolic rate of prostaglandin E1 in surgical patients under general anesthesia. Prostaglandins Leukot Essent Fatty Acid 1985; 18: 359–66.

  79. 79

    Sinha AK, Colman RW. Prostaglandin E1 inhibits platelet aggregation by a pathway independent of adenosine 3′, 5′monophosphate. Science 1978; 200: 202–3.

  80. 80

    Carlson LA, Irion E, Orö L. Effect of infusion of prostaglandin E1 on the aggregation of blood platelets in man. Life Sci 1968; 7: 85–90.

  81. 81

    Woodside J, Garner L, Bedford RF, et al. Captopril reduces the dose requirement for sodium nitroprusside induced hypotension. Anesthesiology 1984; 60: 413–7.

  82. 82

    Marsh ML Shapiro HM, Smith RW, Marshall LF. Changes in neurologic status and intracranial pressure associated with nitroprusside administration. Anesthesiology 1979; 51: 336–8.

  83. 83

    Cottrell JE, Gupta B, Rappaport H, Tumdorf H, Ransohoff J, Flamm ES. Intracranial pressure during nitroglycerin-induced hypotension. J Neurosurg 1980; 53: 309–11.

  84. 84

    Rogers MC, Traystman RJ. Cerebral hemodynamic effects of nitroglycerin and nitroprusside. Acta Neurol Scand Suppl 1979; 62: 600–1.

  85. 85

    Pinaud M, Souron R, Lelausque JN, Gazeau M-F, Lajat Y, Dixneuf B. Cerebral blood flow and cerebral oxygen consumption during nitroprusside-induced hypotension to less than 50 mmHg. Anesthesiology 1989; 70: 255–60.

  86. 86

    Hines R, Barash PG. Infusion of sodium nitroprusside induces platelet dysfunction in vitro. Anesthesiology 1989; 70: 611–5.

  87. 87

    Larsen R, Teichmann J, Hilfiker O, Busse C, Sonntag H. Nitroprusside-hypotension: cerebral blood flow and cerebral oxygen consumption in neurosurgical patients. Acta Anaesthesiol Scand 1982; 26: 327–30.

  88. 88

    Newman B, Gelb AW, Lam AM. The effect of isofluraneinduced hypotension on cerebral blood flow and cerebral metabolic rate for oxygen in humans. Anesthesiology 1986; 64: 307–10.

  89. 89

    Sollevi A, Lagerkranser M, Irestedt L, Gordon E, Lindquist C. Controlled hypotension with adenosine in cerebral aneurysm surgery. Anesthesiology 1984; 61: 400–5.

  90. 90

    Winn HR, Welsh JE, Rubio R, Berne RM. Brain adenosine production in rat during sustained alteration in systemic blood pressure. Am J Physiol 1980; 239: H636-H641.

  91. 91

    Öwall A, Gordon E, Lagerkranser M, Lindquist C, Rudehill A, Sollevi A. Clinical experience with adenosine for controlled hypotension during cerebral aneurysm surgery. Anesth Analg 1987; 66: 229–34.

  92. 92

    Öwall A, Lagerkranser M, Sollevi A. Effects of adenosineinduced hypotension on myocardial hemodynamics and metabolism during cerebral aneurysm surgery. Anesth Analg 1988; 67: 228–32.

  93. 93

    Lagerkranser M, Bergstrand G, Gordon E, et al. Cerebral blood flow and metabolism during adenosine-induced hypotension in patients undergoing cerebral aneurysm surgery. Acta Anaesthesiol Scand 1989; 33: 15–20.

  94. 94

    Zäll, S, Edén E, Winsö I, Volkmann R, Sollevi A, Ricksten SE. Controlled hypotension with adenosine or sodium nitroprusside during cerebral aneurysm surgery: effects on renal hemodynamics, excretory function, and renin release. Anesth Analg 1990; 71: 631–6.

  95. 95

    Murad F. Cyclic guanosine monophosphate as a mediator of vasodilation. J Clin Invest 1986; 78: 1–5.

  96. 96

    Ignarro LJ, Lippton H, Edwards JC, et al. Mechanism of vascular smooth muscle relaxation by organic nitrates, nitrites, nitroprusside and nitric oxide: evidence for the involvement of S-nitrosothiols as active intermediates. J Pharmacol Exp Ther 1981; 218: 739–49.

  97. 97

    Langerkranser M. Effects of nitroglycerin on intracranial pressure and cerebral blood flow. Acta Anaesthesiol Scand 1992; Suppl 36: 34–6.

  98. 98

    Maktabi M, Warner D, Sokoll M, et al. Comparison of nitroprusside, nitroglycerin, and deep isoflurane anesthesia for induced hypotension. Neurosurgery 1986; 19: 350–5.

  99. 99

    Larson AG. Deliberate hypotension. Anesthesiology 1964; 24: 682–706.

  100. 100

    Miller ED Jr. Deliberate hypotension.In: Miller RDJr (Ed.). Anesthesia, 2nd ed, New York: Churchill Livingstone, 1986; 1949–70.

  101. 101

    Knight PR, Lane GA, Hensinger RN, Bolles RS, Bjoraker DG. Catecholamine and resin-angiotensin response during hypotensive anesthesia induced by sodium nitroprusside or trimethaphan camsylate. Anesthesiology 1983; 59: 248–53.

  102. 102

    Turner JM, Powell D, Gibson RM, McDowall DG. Intracranial pressure changes in neurosurgical patients during hypotension induced with sodium nitroprusside or trimetaphan. Br J Anaesth 1977; 49: 419–25.

  103. 103

    Reves JG, Kissin I, Lell WA, Tosone S. Calcium entry blockers: uses and implications for anesthesiologists. Anesthesiology 1982; 57; 504–18.

  104. 104

    Opie LH. Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. Cardiovascular Drugs and Therapy 1988; 1: 625–56.

  105. 105

    Zimpfer M, Fitzal S, Tonczar L. Verapamil as a hypotensive agent during neuroleptanaesthesia. Br J Anaesth 1981; 53: 885–9.

  106. 106

    Bernard JM, Pinaud M, Carteau S, Hubert C, Souron R. Hypotensive actions of diltiazem and nitroprusside compared during fentanyl anaesthesia for total hip arthroplasty. Can Anaesth Soc J 1986; 33: 308–14.

  107. 107

    Hof RP. Calcium antagonists and the peripheral circulation: differences and similarities between PY 108–068, nicardipine, verapamil and diltiazem. Br J Pharmacol 1983; 78: 375–94.

  108. 108

    Sorkin EM, Clissold SP. Nicardipine. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy, in the treatment of angina pectoris, hypertension and related cardiovascular disorders. Drugs 1987; 33: 296–345.

  109. 109

    Milde LN, Milde JH, Michenfelder JD. Delayed treatment with nimodipine improves cerebral blood flow after complete cerebral ischaemia in the dog. J Cereb Blood Flow Metab 1986; 6: 332–7.

  110. 110

    Pearce WJ, Bevan JA. Diltiazem and autoregulation of canine cerebral blood flow. J Pharmacol Exp Ther 1987; 242: 812–7.

  111. 111

    Frishman WH. New therapeutic modalities in hypertension: focus on a new calcium antagonist-nicardipine. J Clin Pharmacol 1989; 29: 481–7.

  112. 112

    Yamamoto M, Ohta T, Toda N. Mechanisms of relaxant action of nicardipine, a new Ca++-agonist, on isolated dog cerebral and mesenteric arteries. Stroke 1983; 14: 270–5.

  113. 113

    Norman J. The IV administration of drugs (Editorial). Br J Anaesth 1983; 55: 1049–52.

  114. 114

    Bertel O, Conen D, Radü EW, Müller J, Lang C, Dubach UC. Nifedipine in hypertensive emergencies. BM J 1983; 286: 19–21.

  115. 115

    Pool PE, Massie BM, Venkataraman K, et al. Diltiazem as monotherapy for systemic hypertension: a multicenter, randomized, placebo-controlled trial. Am J Cardiol 1986; 57: 212–7.

  116. 116

    Weber MA, Cheung DG, Graettinger WF, Lipson JL. Characterization of antihypertensive therapy by whole-day blood pressure monitoring. JAMA 1988; 259: 3281–5.

  117. 117

    Onoyama K, Omae T, Ilmura O, et al. Effects of a drip infusion of intravenous diltiazem on severe systemic hypertension. Current Therapeutic Research 1988; 43: 361–8.

  118. 118

    Mullen JC, Miller DR, Weisel RD, et al. Postoperative hypertension: a comparison of diltiazem, nifedipine, and nitroprusside. J Thorac Cardiovasc Surg 1988; 96: 122–32.

  119. 119

    Godet G, Coriat P, Baron JF, et al. Prevention of intraoperative myocardial ischemia during noncardiac surgery with intravenous diltiazem: a randomized trial versus placebo. Anesthesiology 1987; 66: 241–5.

  120. 120

    Bevan JA. Selective action of diltiazem on the cerebral vascular smooth muscle in the rabbit: antagonism of extrinsic but not intrinsic maintained tone. Am J Cardiol 1982; 49: 519–24.

  121. 121

    Bevan JA, Bevan RD, Frazee JG. Experimental chronic cerebrovascular spasm in the monkey: an assessment of the functional changes in the cerebral arteries and their protection by diltiazem. Am J Cardiol 1985; 56: 15H-20H.

  122. 122

    Lam AM, Gelb AW. Cardiovascular effects of isofluraneinduced hypotension for cerebral aneurysm surgery. Anesth analg 1983; 62: 742–8.

  123. 123

    Nicholas JF, Lam AM. Isofurane-induced hypotension does not cause impairment in pulmonary gas exchange. Can Anaesth Soc J 1984; 31: 352–8.

  124. 124

    Roth S, Jones SC, Ebrahim ZY, Friel H, Little JR. Local cortical blood flow and oxygen consumption during isoflurane-induced hypotension. Results in patients undergoing intracranial aneurysm clipping. Clevel Clin J Med 1989; 56: 766–70.

  125. 125

    Haraldstedt VY, Asmussen J, Herlevsen P, Cold GE. Cerebral arteriovenous difference of oxygen during gradual and sudden increase of the concentration of isoflurane for induction of deliberate hypotension. Acta Anaesthesiol Scand 1992; 36: 142–44.

  126. 126

    Grosslight K, Foster R, Colohan AR, Bedford RF. Isoflurane for neuroanesthesia: risk factors for increases in intracranial pressure. Anesthesiology 1985; 65: 533–6.

  127. 127

    Macnab MSP, Manninen PH, Lam AM, Gelb AW The stress response to induced hypotension for cerebral aneurysm surgery: a comparison of two hypotensive techniques. Can J Anaesth 1988; 35: 111–5.

  128. 128

    Blaise G, Still JC, Nugent M, Van Dyke RA, Vanhoutte PM. Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries. Anesthesiology 1987; 67: 513–7.

  129. 129

    Stone DJ, Johns RA. Endothelium-dependent effects of halothane, enflurane and isoflurane on isolated rat aortic vascular rings. Anesthesiology 1989; 71: 126–32.

  130. 130

    James DJ, Bedford RF. Hydralazine for controlled hypotension during neurosurgical operations. Anesth Analg 1982; 61: 1016–9.

  131. 131

    Gerber JG, Nies AS. Antihypertensive agents and the drug therapy of hypertension.In: Gilman AG (Ed.). The Pharmacological Basis of Therapeutics. 8th ed. New York: Pergamon Press, 1990; 784–813.

  132. 132

    Orlowski JP, Shiesley D, Vidt DG, Barnett GH, Little JR. Labetalol to control blood pressure after cerebrovascular surgery. Crit Care Med 1988; 16: 765–8.

  133. 133

    Muzzi DA, Black S, Losasso TJ, Cucchiara RF. Labetalol and esmolol in the control of hypertension after intracranial surgery. Anesth Analg 1990; 70: 68–71.

  134. 134

    Chong KY, Gelb AW. Management of intracranial aneurysms and subarachnoid hemorrhage. Current Opinion in Anaesthesiology 1992; 5: 620–5.

  135. 135

    Bauer JH, Reams GP. The role of calcium entry blockers in hypertensive emergencies. Circulation 1987; 75: V174-V180.

Download references

Author information

Correspondence to Kazuo Abe.

Rights and permissions

Reprints and Permissions

About this article

Cite this article

Abe, K. Vasodilators during cerebral aneurysm surgery. Can J Anaesth 40, 775–790 (1993). https://doi.org/10.1007/BF03009775

Download citation

Key words

  • isoflurane
  • hypotension
  • hypotension
  • blood flow
  • carbon dioxide tension
  • prostaglandin E1
  • ganglionic blockade
  • trimetaphan
  • adenosine
  • nitroglycerin
  • nitroprusside
  • calcium channel blockers
  • hydralazine
  • diazoxide
  • labetalol
  • esmolol
  • intraoperative hypertension
  • brain ischaemia
  • rebleeding