Summary.In a survey of 541 diabetic males, aged 20-59 years, 190 (35%) had erectile impotence. Using linear logistic regression models for analysis the five most significant associations with impotence were age (p < 0.001), treatment with either insulin or oral hypoglycaemic agents (p < 0.001), retinopathy (p < 0.001), symptomatic peripheral neuropathy (p < 0.001) and symptomatic autonomic neuropathy (p < 0.005). The greatest correlations were found in patients with severe microangiopathy, as demonstrated by proliferative retinopathy and symptomatic autonomic neuropathy. In addition the duration of diabetes and the presence of ischaemic heart disease, nephropathy and poor diabetic control may also be associated with diabetic impotence. It is concluded that diabetic impotence is still a common problem and may have a multifactorial aetiology.Key words: Diabetic impotence, prevalence, aetiological factors.The increased frequency of impotence in the diabetic male has long been recognised [7]. Despite improvement in the treatment of diabetes since the early insulin era there has been no decrease in recent reports of the frequency of diabetic impotence [7,10,14]. Thus the prevalence of impotence with increasing age in diabetic men aged between 20-60 years is still approximately 18-71% [19] and considerably greater than 0.1-18.4% for the corresponding normal male population [13].There has been no previous extensive survey of the prevalence of diabetic impotence in the United Kingdom. The aim of the present study was therefore to ascertain the prevalence in males attending a large U. K. diabetic clinic. An assessment was also made of possible contributing factors involved in the aetiology of diabetic impotence. Materials and MethodsDuring a nine month period 563 males attending the Diabetic Out-Patient Department were interviewed. A total of 132 clinics were covered and at each clinic every male aged between 20-59 years was included. After three months an initial non-randomised group of 319 men (Group 1) had been interviewed. At this time it was decided to interview a random group of approximately 100 men to exclude the possibility of bias in the original group. The total clinic male population aged 20-59 years was 887 and from the remaining 568, a random sample of 101 men (Group 2) was drawn who were subsequently interviewed over a six month period. Over this latter period a second non-random group of 121 men (Group 3) who were attending the clinic and not included in the random sample were also interviewed.The total number of men included for study was thus 541, representing 61% of the male clinic population aged between 20-59 years. A further 22 who were unable to give satisfactory interviews were omitted: in the two non-random groups (Groups 1 and 3) 9 were mentally defective, 2 had cerebrovascular accidents with dysphasia and 2 were unable to speak English; in the random group (Group 2) 5 had recently left the area, 1 was hospitalised elsewhere, 2 were mentally defective and 1 had a cerebrovascular accident.A deta...

Autonomic mechanisms underlying the initial heart rate response to standing were analyzed in nine normal subjects. The normal pattern of response was altered by atropine to a small and gradual R-R interval shortening over 30 beats, with no rebound R-R interval lengthening. With additional propranolol, R-R interval shortening was even less and confined to the first 15-20 beats, whereas propranolol alone did not affect the normal response pattern, showing that this is under vagal control with increased cardiac sympathetic activity occurring only if the vagus is blocked. The response was reproducible in 23 normal subjects. Heart rate variation during quiet standing was almost completely abolished by atropine, but unaffected by propranolol, confirming that it is also under vagal control. In four normal subjects no rebound R-R interval lengthening occurred during either "fast" or "slow" tilt, whereas it was present during both "slow" and "fast" standing. The rebound R-R interval lengthening is determined by the muscular activity involved in standing up, rather than by the speed of the maneuver.

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The Cenozoic development of the North Atlantic province has been dramatically influenced by the behaviour of the Iceland Plume, whose striking dominance is manifest by long-wavelength free-air gravity anomalies and by oceanic bathymetric anomalies. Here, we use these anomalies to estimate the amplitude and wavelength of present-day dynamic uplift associated with this plume. Maximum dynamic support in the North Atlantic is 1.5–2 km at Iceland itself. Most of Greenland is currently experiencing dynamic support of 0.5–1 km, whereas the NW European shelf is generally supported by <0.5 km. The proto-Iceland Plume had an equally dramatic effect on the Early Cenozoic palaeogeography of the North Atlantic margins, as we illustrate with a study of plume-related uplift, denudation and sedimentation on the continental shelf encompassing Britain and Ireland. We infer that during Paleocene time a hot subvertical sheet of asthenosphere welled up beneath an axis running from the Faroes through the Irish Sea towards Lundy, generating a welt of magmatic underplating of the crust which is known to exist beneath this axis. Transient and permanent uplift associated with this magmatic injection caused regional denudation, and consequently large amounts of clastic sediment have been shed into surrounding basins during Cenozoic time. Mass balance calculations indicate agreement between the volume of denuded material and the volume of Cenozoic sediments deposited offshore in the northern North Sea Basin and the Rockall Trough. The volume of material denuded from Britain and Ireland is probably insufficient to account for the sediment in the Faroe-Shetland Basin and an excess of sediment has been supplied to the Porcupine Basin. We emphasize the value of combining observations from both oceanic and continental realms to elucidate the evolution of the Iceland Plume through space and time.

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