Michael Johnstone
Manchester Royal Infirmary
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Featured researches published by Michael Johnstone.
Anaesthesia | 1976
Michael Johnstone
The arterial hypertension of ketamine is prevented by verapamil, a calcium ion antagonist. This indicates that ketamine is a direct myocardial stimulant acting by increasing the availability of calcium across the cell membranes of the myocardial and the Purkinjé systems. The positive chronotropic action of ketamine is not reversed by verapamil. Both the chronotropic and the inotropic effects of ketamine are prevented by halothane which acts partly by increased vagal tone and partly by what appears to be a verapamil-like depression of calcium availability. Ketamine blocks the reflex sympathetic response of the peripheral blood vessels to surgical stimuli. The site of the block within the sympathetic reflex arc has not been identified. It is not at the alpha adrenoceptor level. The clinical implications of the findings have been discussed.
Anaesthesia | 1976
Michael Johnstone
Volume-pulse digital plethysmography performed under ideal conditions on relatively fit adults has shown that lorazepam 4 mg intravenously abolishes the vasoconstriction of fear and restores the digital vasodilatation of the tranquil mind. The sedative effect of the drug is prolonged and is associated with several hours of anterograde amnesia from the time of its administration. The drug has no effect on the vasoconstrictor reaction to cold, pain, noise or other forms of adrenergic stimuli. Lorazepam seems to modify or prevent the psychomotor reactions which may complicate ketamine anaesthesia.
Anaesthesia | 1967
Michael Johnstone
Sedation in the presence of trouble may be described as a state of consciousness in which anxiety is absent and the critical sense is present. The preservation of the critical sense distinguishes sedation from euphoria in which the ability to appraise intelligently a difficult situation is either diminished or lost. The distortion of the intellect by psychotropic and addictive drugs is not sedation, nor is it analgesia. Neither anxiety nor sedation can as yet be measured. At the present time many drugs are being used more or less arbitrarily in surgical patients to produce what is loosely described as pre-operative sedation. The effects of these drugs, short of narcosis and stupor, are assessed mainly by their ability to induce what appears to be an anxiety-free state as judged by the patient’s appearance and comments, neither of which can be regarded as a source of reliable information. The relative advantages and disadvantages of the various drugs are determined to a large extent by their unwanted effects on the respiratory, gastro-intestinal and other functions that are open to direct measurement. The problems of the study of sedation, apart from those dictated by pathological expediency, are: 1 To provide objective evidence of the presence of anxiety. 2 To show whether the evidence is modified by drug therapy. There is reason to believe that anxiety in healthy subjects may be revealed by plethysmography. Digital plethysmography in man and in animals has shown that anxiety, pain, cold and mental concentration cause peripheral vasoconstriction and a considerable reduction in the blood flow in the finger, whereas mental tranquillity in comfortable surroundings produces vasodilatation with an increased blood flow in the finger1~2~3~4~5. It was observed that changes in the calibre of the digital blood vessels in response to emotional stimuli cause a wide range of alterations in the blood flow in the finger with comparatively little changes in the pulse rate or the blood
Anaesthesia | 1956
Michael Johnstone
Anaesthesia | 1959
Michael Johnstone
Anaesthesia | 1963
Michael Johnstone
Anaesthesia | 1958
Michael Johnstone
Anaesthesia | 1980
Michael Johnstone; T.B. Boulton
Anaesthesia | 1967
Michael Johnstone
Anaesthesia | 1958
Michael Johnstone