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Re: Effects of glyceryl trinitrate on cerebrovascular autoregulation
- Iain K Moppett, Ravi P. Mahajan (20 July 2008)
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Effects of glyceryl trinitrate on cerebrovascular autoregulation
- Luzius A. Steiner, [David Pfister], [Stephan P. Strebel] (9 May 2008)
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Vasoactive drugs and cerebral circulation: authors' reply
- Iain K Moppett (29 February 2008)
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Vasoactive drugs and cerebral circulation.
- Hari Krovvidi (12 February 2008)
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Iain K Moppett University of Nottingham, Ravi P. Mahajan
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We thank Dr Steiner and his colleagues for his interest and thoughtful comments on our study. In response to the end-tidal CO2 values, the individual changes in 'resting' end-tidal values with and without GTN were mostly less than 0.3kPa, and occured in both directions. We cannot exclude undetected changes in PaCO2 due to GTN effects on pulmonary blood flow. We would therefore suggest that, within the limits of the study, any effects of changes in end-tidal CO2 were small and unlikely to affect autoregulation significantly. We agree with Dr Steiner that the decrease in flow velocity in parallel with a GTN induced decrease in arterial pressure can be interpreted as a reduction in static autoregulation. However, two factors suggest that this may not be the case. First, neither we1, nor other authors2, found changes in tests of dynamic autoregulation, and it would be an interesting finding to demonstrate significant uncoupling of dynamic and static tests of autoregulation. Secondly, GTN vasodilates the basal cerebral arteries3, which will result in lower flow velocities for the same cerebral blood flow. The theoretical advantage of dynamic techniques is that the confounding effects of GTN are present throughout the test thereby avoiding this problem. We would therefore caution against claiming changes in static autoregulation without confirmatory evidence that cerebral blood flow has in fact decreased4. Iain Moppett & Ravi Mahajan 1 Moppett IK, Sherman RW, Wild MJ, Latter JA, Mahajan RP. Effects of norepinephrine and glyceryl trinitrate on cerebral haemodynamics: transcranial Doppler study in healthy volunteers Br. J. Anaesth. 2008; 100: 240-244 2 Endoh H, Honda T, Ohashi S, Hida S, Shibue C, Komura N. The influence of nitroglycerin and prostaglandin E1 on dynamic cerebral autoregulation in adult patients during propofol and fentanyl anaesthesia. Anaesthesia 2001; 56: 947–52 3 Dahl A, Russell D, Nyberg-Hansen R, Rootwelt K. Effect of nitroglycerin on cerebral circulation measured by transcranial Doppler and SPECT. Stroke 1989; 20: 1733–6 4 Willmot M, Ghadami A, Whysall B, Clarke W, Wardlaw J, Bath PMW. Transdermal glyceryl trinitrate lowers blood pressure and maintains cerebral blood flow in recent stroke. Hypertension 2006; 47: 1209–15 Conflict of Interest:None declared |
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Luzius A. Steiner Department of Anaesthesia, University Hospital Basel, [David Pfister], [Stephan P. Strebel]
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Editor - We have read the article by Moppett et al.1 with great interest. There is a paucity of data on cerebrovascular effects of vasoactive drugs in awake patients without intracranial pathology and we are grateful to the authors for providing such data. However, we would like to highlight two aspects regarding the glyceryl trinitrate part of their study. First, the CO2-reactivities measured in this study are very high. We would expect reactivities in the range of 15-30%/kPa.2 Such high CO2- reactivities make the study of changes in blood flow velocity in response to changes in arterial pressure very difficult as already small changes in CO2 will have marked effects on the flow velocities. Table 1 suggests that a shift to a lower end-tidal CO2 occurred between the measurements performed before and during infusion of glyceryl trinitrate. This would have led to improved autoregulation. Second, assuming intact autoregulation, the decrease in flow velocity in response to the blood pressure decrease induced by glyceryl trinitrate is surprisingly large. If the static rate of autoregulation3 is calculated based on the median given in Table 1 the result is 37%, i.e. in contrast to the measurements of dynamic autoregulation performed by the authors static autoregulation is clearly disturbed. This discrepancy is unexpected in the investigated group of patients. In our opinion, based on the presented data, it cannot be concluded that glyceryl trinitrate did not affect cerebrovascular autoregulation in this study. David Pfister1 Stephan P. Strebel2 Luzius A. Steiner2* 1Zürich, Switzerland 2Basel, Switzerland *E-mail: lsteiner@uhbs.ch References: 1. Moppett IK, Sherman RW, Wild MJ, Latter JA, Mahajan RP. Effects of norepinephrine and glyceryl trinitrate on cerebral haemodynamics: transcranial Doppler study in healthy volunteers. Br J Anaesth 2008; 100: 240-4 2. Joshi S, Ornstein E, Young WL, Cerebral and spinal cord blood flow, in Anesthesia and Neurosurgery, J.E. Cottrell , D.S. Smith, Editors. 2001, Mosby: St. Louis. p. 19-67 3. Tiecks FP, Lam AM, Aaslid R, Newell DW. Comparison of Static and Dynamic Cerebral Autoregulation Measurements. Stroke 1995; 26: 1014-9 Conflict of Interest:None declared |
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Iain K Moppett
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Dear Editor, We would like to thank Dr Krovvidi for his interest in our paper. We agree that the effects we observed apply to volunteers with no known intracranial pathology as stated in the article summary and discussed in the paper itself. In order to define the abnormal it is important to know what is normal. We therefore chose to study healthy subjects without any concommittant disease or drugs. What happens in subjects with acute brain injury is not clear. Although some areas of the blood-brain-barrier may be disrupted, as Dr Krovvidi correctly points out, this is not necessarily a global nor constant phenomenon and some areas of the brain may have an intact blood- brain-barrier at different times after injury. (1,2,) < Iain Moppett 1) Baskaya MK, Rao AM, Dogan A, Donaldson D, Dempsey RJ. The biphasic opening of the blood–brain barrier in the cortex and hippocampus after traumatic brain injury in rats Neuroscience Letters 1997;226:33-6 2) Nagaraja TN, Karki K, Ewing JR, Croxen RL, Knight RA. Identification of Variations in Blood-Brain Barrier Opening After Cerebral Ischemia by Dual Contrast-Enhanced Magnetic Resonance Imaging and T1sat Measurements. Stroke. 2008;39:427-32 Conflict of Interest:None declared |
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Hari Krovvidi, SPR,Anaesthetics Queen Elizabeth Hospital,Univeristy Hospitals of Birmingham,Birmingham
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We read with great interest the study by Moppet et al (1),about the effects of vasoactive drugs on cerebral haemodyanimics. We congratulate the authors for proposing the more reliable parameters to measure cerebral blood flow like effective cerebral perfusion pressure (eCPP) and zero flow pressure (ZFP). It will be interesting to see the results when these parameters are measured in pathological conditions. However the authors comments ‘the change in eCPP may or may not follow the change in MAP induced by a vasoactive agent’ in the introduction did not make it clear weather this is true in healthy volunteers or injured brains. It is well known fact that intact blood brain barrier (BBB) will form an anatomical and chemical barrier for many systemic drugs, which is also true for catecholamines (2). So the effects of systemic noradrenaline in healthy individuals with intact blood brain barrier, on cerebral hemodyanims may be minimal. This was demonstrated in the author’s study results which showed minimal changes in estimated CPP even with statistically significant changes in MAP. However on injured brains with disrupted BBB the effects of noradrenaline may be different, a median increase in MAP by 46% is associated with 36% decrease in CBF with noradrnaline infusion (3). The authors would have made clear in conclusion or introduction that the minimal changes in CPP with noradrenaline is more true in healthy individuals rather in injured brains. References: (1).Moppett K et al. Br J Anaesth 2008; 100:240-4. (2).MacKenzie ET et al. Am J Physiol 1976;231:483-88. (3).Moller K et al. Crit Care Med 2002; 28:1027-32. Conflict of Interest:None declared |
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