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Biomedical subjects

M J Stevens

Publications and source records attributed to M J Stevens.

103 records · Page 6Linked to original sources
PubMed1983

Facilitatory prejunctional beta-adrenoceptors in human arteries and veins.

The effects of beta-adrenoceptor agonists and antagonists on both the transmitter outflow and the associated pressure response produced by perivascular nerve stimulation have been studied in human digital arteries and metatarsal veins, in which transmitter stores were labelled with [3H]noradrenaline. Both isoprenaline in arteries, and salbutamol in arteries and veins, at concentrations of 10(-8) - 10(-6) mol/l significantly enhanced stimulation-induced tritium outflow. These two agonists were approximately equipotent. Salbutamol also potentiated pressure responses to stimulation, and propranolol prevented the enhancement of stimulation-induced tritium outflow by salbutamol. Adrenaline, at a concentration of 10(-8) mol/l, but not lower concentrations, significantly enhanced stimulation-induced tritium outflow in arteries. Propranolol, however, had no effect on stimulation-induced transmitter outflow, even when the arteries were either perfused throughout the experiment with a low concentration of adrenaline, or when the arteries were preincubated in a high concentration of adrenaline as well as perfused throughout with a low concentration of adrenaline. It is concluded that facilitatory prejunctional beta-adrenoceptors (probably of the beta 2-subtype) are present in human arteries and veins, but that under the conditions of these experiments, neither transmitter noradrenaline, nor adrenaline that has been incorporated into transmitter stores with noradrenaline, activate these prejunctional beta-adrenoceptors. They may, however, be activated under conditions of enhanced adrenomedullary secretion.

Adrenergic beta-Agonists↗
PubMed1981

Personality evaluation of doctoral applicants: a survey of clinical psychology training directors.

The growing dissatisfaction with traditional criteria used to select doctoral applicants has led clinical faculties to consider alternative selection criteria, including the use of a formal personality evaluation. A survey of training directors of APA-approved clinical psychology programs was conducted to assess their opinions with regard to this proposal. The results showed that 75.3% of the respondents opposed the use of a personality evaluation. Opposition was based primarily on the applicant's right to privacy and the inadequacies of assessment alternatives.

Education, Graduate↗
PubMedDate not supplied

Diabetic autonomic neuropathy.

One of the earliest manifestations of diabetic neuropathy is denervation of the cardiovascular system; loss of heart rate variability may have a prevalence as high as 21.5% in diabetic patients, and declines at 1 beat/min/year, which is 3 times faster than in normal subjects. The cause of this neuropathy is unknown: attempts at decreasing the excess quantities of sorbitol, glucose and fructose in nerve tissue have lead to little functional improvement in man. Nerve ischaemia and immunological damage have stimulated increased interest lately, the latter particularly because of the structural homology of nerve growth factor and insulin. Symptoms from autonomic neuropathy are rare. When present they may well be intermittent, but never remit; they rarely progress or become disabling. One uncommon consequente of loss of sympathetic vascular tone is postural hypotension. This may result from failure of splanchnic vasoconstriction on standing. Food and insulin can greatly exacerbate the postural blood pressure fall. Reduced vascular tone in the neuropathic foot leads to increased arterio-venous shunt flow. The local reflex control of this shunt flow is also abnormal: paradoxical vasoconstriction occurs in response to local skin heating and postural reflexes are reduced. This high shunt flow together with its abnormal vascular control may be important in the pathogenesis of neuroarthropathy and foot ulceration. The prognosis of patients with autonomic neuropathy is better than previously reported. Abnormal heart rate variability alone is of no prognostic value. The presence of symptoms, in particular postural hypotension, significantly reduces survival. The majority of deaths however, result from concurrent renal disease and macrovessel atheroma.

Cardiovascular System↗
PubMedDate not supplied

Are neuronal uptake mechanisms responsible for the difference in sensitivity to noradrenaline between human arteries and veins?

1. The sensitivity of human metacarpal veins and digital arteries obtained post-mortem to noradrenaline and phenylephrine has been tested. 2. pED50 values for noradrenaline were significantly higher in the veins (6.99, s.e.m. = 0.08) than in the arteries (6.56, s.e.m. = 0.09), whereas pED50 values for phenylephrine in the two tissues were not significantly different (arteries: 6.24, s.e.m. = 0.09; veins: 6.26, s.e.m. = 0.05). 3. The addition of propranolol (4 x 10(-6) mol/l) alone, or in combination with hydrocortisone (4 x 10(-5) mol/l), did not affect the responses to either noradrenaline or phenylephrine. The further addition of cocaine (3 x 10(-5) mol/l) slightly shifted the noradrenaline and phenylephrine concentration-effect curves to the left in both arteries and veins, but veins were still found to be more sensitive than arteries to noradrenaline whilst there was still no difference in the sensitivity of veins and arteries to phenylephrine. 4. Cocaine also slightly potentiated responses to barium chloride, potassium chloride and serotonin. 5. It is concluded that the difference in sensitivity to noradrenaline between arteries and veins cannot be explained by differences in neuronal uptake and it is possible that there may be differences in the properties of the postsynaptic alpha-adrenoreceptors of the two tissues. It is also concluded that the potentiation of the contractile effect of noradrenaline produced by cocaine is not solely due to inhibition of neuronal uptake of amines.

Arteries↗
PubMedDate not supplied

Paradoxical blood flow responses in the diabetic neuropathic foot: an assessment of the contribution of vascular denervation and microangiopathy.

Blood flow is abnormal in the diabetic neuropathic foot, and this may be of importance in the pathogenesis of complications. Arteriovenous shunting is increased, and blood flow through these channels may paradoxically decrease in response to local heating. Peak skin blood flow is also reduced in these patients. It is not known whether these blood flow abnormalities may reflect diabetic microangiopathy, or whether they simply reflect vascular denervation. The skin blood flow response to a local thermal stimulus was studied in four non-diabetic patients with a unilateral traumatic neuropathy and foot ulceration. All showed a decrease in skin blood flow (to 68% of basal) at the great toe during local heating in the neuropathic limb, in contrast to the normal limb, in which blood flow increased to 180% of basal. Peak skin blood flow was also greatly reduced in the neuropathic limb, being only 29% of the normal limb. Neuropathy alone can be responsible for abnormal skin blood flow responses in the neuropathic foot.

Adolescent↗