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S T McCarthy

Publications and source records attributed to S T McCarthy.

26 records · Page 2Linked to original sources

Glucose control of basal insulin secretion in diabetes.

The plasma insulin response to both a small increase and decrease in the plasma glucose has been studied in normal and diabetic, non-obese subjects. In a second investigation the plasma insulin concentrations were measured during a gradual reduction of the raised fasting plasma glucose of diabetes to normal levels. In both studies, diabetic patients were found to have a markedly impaired response of the fasting plasma insulin to small changes in plasma glucose. These results do not support the suggestion that stimulated and not basal insulin secretion is impaired in diabetes. Both modes of secretion are probably via the same B-cell release mechanism, which is deficient in diabetes. There was a gradation of response between maturity onset and juvenile onset diabetics.

Aged↗

Beta-cell function improved by supplementing basal insulin secretion in mild diabetes.

Insulin supplements, predominantly as a constant basal fish insulin infusion, were given to patients with mild diabetes to reduce the overnight fasting glucose level to normal. The basal plasma human insulin levels were reduced to subnormal levels by the infusion, and the insulin response to intravenous glucose was enhanced. The beta-cell in diabetes seems to be in a vicious circle in which an impaired insulin response to glucose produces hyperglycaemia, which stresses beta-cell function, making it more inefficient. A constant basal insulin supplement to induce basal normoglycaemia may benefit beta-cell function in diabetes.

Blood Glucose↗

Diabetic autonomic neuropathy: the prevalence of impaired heart rate variability in a geographically defined population.

The prevalence of diabetic autonomic neuropathy and its relationship with other diabetic complications were studied in a geographically defined population. Heart rate variability was measured by a computerized technique at rest and in response to both a single deep breath and a Valsalva manoeuvre. Among 43 Type 1 (insulin-dependent) and 202 Type 2 (non-insulin-dependent) patients results below the 2.5 centile for age-related normal ranges occurred in 9 Type 1 and 32 Type 2 patients (16.7, 95% Cl 12.6 to 21.9, %). Symptomatic autonomic neuropathy was uncommon but was significantly more frequent in Type 1 than Type 2 patients (5 Type 1, 1 Type 2, p less than 0.001 Fisher's exact test). In Type 1 diabetes, cardiovascular autonomic dysfunction was significantly associated with impaired vibration perception and a higher logarithmic urinary albumin concentration and, in Type 2 diabetes, it was associated with a significantly higher body mass index, systolic blood pressure, and logarithm of the urinary albumin and fasting insulin concentrations. The aggregation of these factors with cardiovascular autonomic dysfunction suggests that mortality might be increased in Type 2 patients with asymptomatic autonomic neuropathy.

Adult↗

Analysis of the gamma ray spectra recorded in the use of Xenon-133 for cerebral blood flow studies.

A problem in the measurement of cerebral blood flow with 133Xenon is the presence of extra-cerebral counts in the total counts recorded with a collimated gamma ray detector looking at the brain. A method of studying qualitatively the contribution of this extra-cranial component in patients is described. This entails the sequential accumulation of gamma ray spectra recorded during the clearance phase of 133Xenon from the brain. It is shown that different CBF indices are obtained for various regions of the recorded gamma ray spectra. The principal component of the extra-cerebral counts at 15 minutes postinjection appears to be intra-cranial, and not the scalp as assumed previously in the spectrum subtraction method.

Brain↗

Circadian variation of abnormal heart beats in an elderly population and their relation to sudden cardiac death.

The relationships between the circadian variation of abnormal heart beats and the circadian variation in sudden cardiac death warrant further discussion for the high correlations demonstrated here are difficult to ignore. In the healthy group abnormal beats showed a high correlation of their circadian variation with that of sudden cardiac death which is independent of heart rate. As a result the conclusion that the relationship of the circadian variations of abnormal heart beats and sudden cardiac death is merely dependent on a mutual dependence on activity is not supported here. The present data illustrates a strong association between arrhythmias and sudden cardiac death. The relationship of sudden cardiac death with abnormal heart beats demonstrated here, however, cannot confirm a causal role of the latter on the former for both may be responding to circadian variations of some underlying mechanism such as ischemia. Additionally the population studied here, although relatively comparable in terms of living conditions and other significant factors, was not strictly age-matched with those from the sudden cardiac death study warranting further caution in interpreting the association demonstrated here. The results from the unhealthy group, although somewhat limited, indicate that cardiovascular morbidity may alter the relationship of sudden cardiac death and abnormal heart beats. Such a result could be explained by the presence of other forms of heart disease which could be responsible for sudden cardiac death in the unhealthy group. An interesting question to ask concerning the data presented above is whether or not significant circadian variations in in the frequency of abnormal heart beats could have been demonstrated when exogenous factors such as meal times and activity were altered. The data on in hospital sudden cardiac death indicates that the circadian variation in sudden cardiac death is significantly altered by the radical changes in routine which accompany hospitalization. If the relationship between the circadian variation of sudden cardiac death and abnormal heart beats is as strong as the results presented here indicate, it is likely that the alteration of such exogenous factors would also change the circadian variation of abnormal heart beats. The results of the present study indicate that both the circadian variation in abnormal heart beats, and its relationship to sudden cardiac death, warrant further study.

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