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PERIPHERAL VASOMOTOR DISORDERS IN MIGRAINE
1211 of vitamin A is apparently required to maintain epithelia in their normal state. Leereported a seasonal variation in the clinical onset of leukaemia in young people, but the observation seems to have little relevance to the seasonal birth date of persons with carcinoma of the bronchus. Clearly Dijkstra’s finding must be studied further. a
critical
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PERIPHERAL VASOMOTOR DISORDERS IN MIGRAINE
MIGRAINE is an episodic vasomotor disorder. If patients with migraine were found to have a generalised abnormality of vasomotor response, this might account for some of the extracranial symptoms. Several workers have claimed to demonstrate a generalised change. Appenzeller et al .6have examined the reflex response of blood-flow in the hands of migraineurs. They found that in such subjects warmth applied to the chest led to no vasodilatation in the hand. A vasodilator response is normal,’ and was in fact obtained by Appenzeller and his colleagues in a small control group of subjects without migraine. Reflex vasoconstriction, in so far as it was tested, seemed to be the same in both groups. These findings could support the view that some general abnormality of vasomotor response does exist in migraine. It will be of considerable interest to see whether the observations are confirmed. ALCOHOL AND ASTHMA
IN a previous issue Salter8 noted that alcohol might relieve an asthmatic attack, but after a century information Now Herxheimer and on this point is still scanty. Stresemann 9 report the effects of alcohol on the vital capacities of 6 healthy people and 23 chronic asthmatics (19 males and 4 females). The subjects were given 40-80 ml. (usually 40 ml.) of brandy or vodka containing 38-40% ethanol. The vital capacity was recorded at five-minute intervals. In the normal subjects the vital capacity remained unchanged, but in 20 of the 23 asthmatics it increased by 6-38% (mean 13%), and the increase was usually accompanied by subjective improvement. The increase began about ten minutes after ingestion of the alcohol, reached its peak after twenty-five to thirty minutes, and began to decline after about an hour. Owing to the difficulty of disguising the flavour and effects of alcoholic drinks, placebos were not used for control experiments; but the authors point out that psychological factors are unlikely to have caused the increase since it did not reach its peak until about half an hour after ingestion of the dose. Moreover, administration of pure ethanol to 2 patients in a dose equivalent to that given in vodka or
brandy produced comparable improvement. Herxheimer and Stresemann 10 draw attention to another effect of alcohol in asthmatics. In experimental work the administration of bradykinin by aerosol had been found to produce a slight increase in bronchospasm, but in 1 patient it caused an explosive asthmatic attack. Subsequent inquiry revealed that the patient before presenting himself had taken 8 or 9 glasses of schnaps (though not apparently with any thought of improving his vital capacity). The 5. Lee, J. A. H. Brit. med. J. 1962, 6. Appenzeller, O., Davidson, K.,
i, 1737. Marshall, J. J. Neurol. Neurosurg. Psychiat. 1963, 26, 447. 7. Kirslche, D. Mk., Cooper, K. E. Clin. Sci. 1950, 9, 31. 8. Salter, H. H. Lancet, 1863, ii, 558. 9. Herxheimer, H., Stresemann, E. Arch. int. Pharmacodyn. 1963, 144, 310. 10. Herxheimer, H., Stresemann, E. ibid. p. 315.
possibility that alcohol might intensify the bradykinin effect was therefore investigated. 6 healthy persons and 15 asthmatics were first given 0’5% bradykinin aerosol to ascertain the extent of their reactions; and after the effect, if any, had passed off, they were each given 10-140 ml. (mostly 40 ml.) of brandy or vodka containing 38-40% ethanol. Twenty-five to thirty minutes later, at the peak of the alcohol effect, they were given the same amount of bradykinin as before. Bradykinin alone reduced the vital capacity of only 1 of the 6 healthy subjects: after alcohol had been given, bradykinin produced a greater reduction in this subject, and also a reduction in 2 of the others. Bradykinin alone reduced the vital capacity in all 15 asthmatics: after alcohol it reduced the vital capacity by a still greater margin in 9 instances; and in 5 of these 9 patients bronchospasm was severe. So far Herxheimer and Stresemann cannot explain why alcohol usually tends to relieve bronchospasm in asthma but often intensifies the bronchospastic effect of bradykinin. GASTROINTESTINAL PACING
AFTER most abdominal operations, intestinal motility is abolished for some hours or even for a day or two,1but the condition may become self-perpetuating as increasing distension from accumulation of intestinal secretions and swallowed and bacterial gas aggravates the paresis and establishes a vicious circle. The management of postoperative ileus has generally been accepted as calling for suction drainage and intravenous fluid therapy (since suction removes large quantities of salt and water from the body) until the bowel resumes tone and activity. Though regarded as essential by many surgeons and therefore tolerated by most patients, an indwelling gastric tube undoubtedly contributes to postoperative discomfort, increases the risk of pulmonary complications, and, if used for a long time, may damage the lower oesophagus either directly or from reflux of acid-pepsin, because of impaired efficiency of the oesophago-gastric junction. Reassessment of the need for these measures is certainly overdue; for much has recently been added to knowledge of the extent and severity of small-bowel paralysis after abdominal surgery. Wangensteen2 has emphasised that the term paralytic ileus is ill-fitted to describe the meteorism and motor inactivity, and other observers 34 have provided evidence that the bowel is inhibited rather than paralysed and can still respond to stimulation. A recent paper by Lillehei et al. adds further support to this view, and describes a method of treatment by direct electrical stimulation of the gastrointestinal tract by means of a specially designed electronic pacemaker. Impressed with the success of the cardiac pacemaker in complete heart-block and arguing from the observation that a stimulus applied to the small bowel, besides causing local contraction, can also induce a peristaltic rush, the American workers designed experiments in dogs to determine the best types of current and sites for stimulation. The results, tested and modified in man, showed that a current of 7-10 mA with an impulse frequency of 50 cycles per second given for 5 seconds was sufficient to induce peristalsis judged by barium examination of healthy subjects, and later by direct observation of the bowel at laparotomy. A pacemaker area has been des1. 2. 3. 4. 5.
Wakim, K. G., Mann, F. C. Gastroenterology, 1943, 1, 513. Wangensteen, O. H. Intestinal Obstruction. Springfield, Ill., 1955. Frey, S. Arch. klin. Chir. 1926, 142, 445. Hotz, G. Cited by Bilgutay et al. (ref. 5) Bilgutay, A. M., Winrove, R., Griffen, W. O., Bonnabeau, R. C., Lillehei, C. W. Ann. Sure. 1963, 158, 338.
critical
amount
PERIPHERAL VASOMOTOR DISORDERS IN MIGRAINE
MIGRAINE is an episodic vasomotor disorder. If patients with migraine were found to have a generalised abnormality of vasomotor response, this might account for some of the extracranial symptoms. Several workers have claimed to demonstrate a generalised change. Appenzeller et al .6have examined the reflex response of blood-flow in the hands of migraineurs. They found that in such subjects warmth applied to the chest led to no vasodilatation in the hand. A vasodilator response is normal,’ and was in fact obtained by Appenzeller and his colleagues in a small control group of subjects without migraine. Reflex vasoconstriction, in so far as it was tested, seemed to be the same in both groups. These findings could support the view that some general abnormality of vasomotor response does exist in migraine. It will be of considerable interest to see whether the observations are confirmed. ALCOHOL AND ASTHMA
IN a previous issue Salter8 noted that alcohol might relieve an asthmatic attack, but after a century information Now Herxheimer and on this point is still scanty. Stresemann 9 report the effects of alcohol on the vital capacities of 6 healthy people and 23 chronic asthmatics (19 males and 4 females). The subjects were given 40-80 ml. (usually 40 ml.) of brandy or vodka containing 38-40% ethanol. The vital capacity was recorded at five-minute intervals. In the normal subjects the vital capacity remained unchanged, but in 20 of the 23 asthmatics it increased by 6-38% (mean 13%), and the increase was usually accompanied by subjective improvement. The increase began about ten minutes after ingestion of the alcohol, reached its peak after twenty-five to thirty minutes, and began to decline after about an hour. Owing to the difficulty of disguising the flavour and effects of alcoholic drinks, placebos were not used for control experiments; but the authors point out that psychological factors are unlikely to have caused the increase since it did not reach its peak until about half an hour after ingestion of the dose. Moreover, administration of pure ethanol to 2 patients in a dose equivalent to that given in vodka or
brandy produced comparable improvement. Herxheimer and Stresemann 10 draw attention to another effect of alcohol in asthmatics. In experimental work the administration of bradykinin by aerosol had been found to produce a slight increase in bronchospasm, but in 1 patient it caused an explosive asthmatic attack. Subsequent inquiry revealed that the patient before presenting himself had taken 8 or 9 glasses of schnaps (though not apparently with any thought of improving his vital capacity). The 5. Lee, J. A. H. Brit. med. J. 1962, 6. Appenzeller, O., Davidson, K.,
i, 1737. Marshall, J. J. Neurol. Neurosurg. Psychiat. 1963, 26, 447. 7. Kirslche, D. Mk., Cooper, K. E. Clin. Sci. 1950, 9, 31. 8. Salter, H. H. Lancet, 1863, ii, 558. 9. Herxheimer, H., Stresemann, E. Arch. int. Pharmacodyn. 1963, 144, 310. 10. Herxheimer, H., Stresemann, E. ibid. p. 315.
possibility that alcohol might intensify the bradykinin effect was therefore investigated. 6 healthy persons and 15 asthmatics were first given 0’5% bradykinin aerosol to ascertain the extent of their reactions; and after the effect, if any, had passed off, they were each given 10-140 ml. (mostly 40 ml.) of brandy or vodka containing 38-40% ethanol. Twenty-five to thirty minutes later, at the peak of the alcohol effect, they were given the same amount of bradykinin as before. Bradykinin alone reduced the vital capacity of only 1 of the 6 healthy subjects: after alcohol had been given, bradykinin produced a greater reduction in this subject, and also a reduction in 2 of the others. Bradykinin alone reduced the vital capacity in all 15 asthmatics: after alcohol it reduced the vital capacity by a still greater margin in 9 instances; and in 5 of these 9 patients bronchospasm was severe. So far Herxheimer and Stresemann cannot explain why alcohol usually tends to relieve bronchospasm in asthma but often intensifies the bronchospastic effect of bradykinin. GASTROINTESTINAL PACING
AFTER most abdominal operations, intestinal motility is abolished for some hours or even for a day or two,1but the condition may become self-perpetuating as increasing distension from accumulation of intestinal secretions and swallowed and bacterial gas aggravates the paresis and establishes a vicious circle. The management of postoperative ileus has generally been accepted as calling for suction drainage and intravenous fluid therapy (since suction removes large quantities of salt and water from the body) until the bowel resumes tone and activity. Though regarded as essential by many surgeons and therefore tolerated by most patients, an indwelling gastric tube undoubtedly contributes to postoperative discomfort, increases the risk of pulmonary complications, and, if used for a long time, may damage the lower oesophagus either directly or from reflux of acid-pepsin, because of impaired efficiency of the oesophago-gastric junction. Reassessment of the need for these measures is certainly overdue; for much has recently been added to knowledge of the extent and severity of small-bowel paralysis after abdominal surgery. Wangensteen2 has emphasised that the term paralytic ileus is ill-fitted to describe the meteorism and motor inactivity, and other observers 34 have provided evidence that the bowel is inhibited rather than paralysed and can still respond to stimulation. A recent paper by Lillehei et al. adds further support to this view, and describes a method of treatment by direct electrical stimulation of the gastrointestinal tract by means of a specially designed electronic pacemaker. Impressed with the success of the cardiac pacemaker in complete heart-block and arguing from the observation that a stimulus applied to the small bowel, besides causing local contraction, can also induce a peristaltic rush, the American workers designed experiments in dogs to determine the best types of current and sites for stimulation. The results, tested and modified in man, showed that a current of 7-10 mA with an impulse frequency of 50 cycles per second given for 5 seconds was sufficient to induce peristalsis judged by barium examination of healthy subjects, and later by direct observation of the bowel at laparotomy. A pacemaker area has been des1. 2. 3. 4. 5.
Wakim, K. G., Mann, F. C. Gastroenterology, 1943, 1, 513. Wangensteen, O. H. Intestinal Obstruction. Springfield, Ill., 1955. Frey, S. Arch. klin. Chir. 1926, 142, 445. Hotz, G. Cited by Bilgutay et al. (ref. 5) Bilgutay, A. M., Winrove, R., Griffen, W. O., Bonnabeau, R. C., Lillehei, C. W. Ann. Sure. 1963, 158, 338.