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Biomedical subjects

K M Macleod

Publications and source records attributed to K M Macleod.

6 recordsLinked to original sources
PubMed2006

Six months of aerobic exercise does not improve microvascular function in type 2 diabetes mellitus.

AIMS/HYPOTHESIS: Adults with type 2 diabetes mellitus have impaired microvascular function. It has been hypothesised that microvascular function may be restored through regular exercise. The aim of this study was to investigate whether 6 months of regular aerobic exercise would improve microvascular function in adults with type 2 diabetes. MATERIALS AND METHODS: Fifty-nine patients with type 2 diabetes (32 males, age 62.9+/-7.6 years, HbA(1c) 6.8+/-0.9%) were randomised to either a 6-month aerobic exercise programme (30 min, three times a week, 70-80% of maximal heart rate) or a 'standard care' control group. Before and after the intervention period, microvascular function was assessed as the maximum skin hyperaemia to local heating and endothelial and non-endothelial responsiveness following the iontophoretic application of acetylcholine and sodium nitroprusside. Maximal oxygen uptake, as an index of aerobic fitness, was assessed using a maximal exercise test. RESULTS: No significant improvement was seen in the exercise group compared with the control group for any of the variables measured: maximal oxygen uptake (control pre: 1.73+/-0.53 [means+/-SD] vs post: 1.67+/-0.40; exercise pre: 1.75+/-0.56 vs post: 1.87+/-0.62 l/min, p=0.10); insulin sensitivity (insulin tolerance test) (control pre: -0.17+/-0.06 vs post: -0.17+/-0.06; exercise pre: -0.16+/-0.1 vs post: -0.17+/-0.07 mmol l(-1) min(-1), p=0.97); maximal hyperaemia (control pre: 1.49+/-0.43 vs post: 1.52+/-0.57; exercise pre: 1.42+/-0.36 vs post: 1.47+/-0.33 V, p=0.85); peak response to acetylcholine (control pre: 1.37+/-0.47 vs post: 1.28+/-0.37; exercise pre: 1.27+/-0.44 vs post: 1.44+/-0.23 V, p=0.19) or to sodium nitroprusside (control pre: 1.09+/-0.50 vs post: 1.10+/-0.39; exercise pre: 1.12+/-0.28 vs post: 1.13+/-0.40 V, p=0.98). CONCLUSIONS/INTERPRETATION: In this group of type 2 diabetic patients with good glycaemic control a 6-month aerobic exercise programme did not improve microvascular function or aerobic fitness.

Adult↗
PubMed1997

Influence of streptozotocin diabetes on the alpha-1 adrenoceptor and associated G proteins in rat arteries.

Previous studies from this laboratory have demonstrated an enhancement in both the contractile and signaling response to stimulation of either alpha-1 adrenoceptors or guanine nucleotide binding proteins (G proteins) in arteries from male Wistar rats with 12 to 14 weeks of streptozotocin-induced diabetes. The purpose of the present investigation was to determine whether changes in arterial alpha-1 adrenoceptors or the G proteins coupled to them are associated with the enhanced responsiveness of the diabetic arteries. No difference in affinity was detected between control and diabetic aorta or caudal artery membranes in saturation binding of [3H]prazosin to alpha-1 adrenoceptors. However, the alpha-1 adrenoceptor number was significantly decreased in caudal artery but not aorta from diabetic rats. In competition binding experiments, a low-affinity and a high-affinity binding site for norepinephrine were detected in the absence of guanine nucleotides and NaCl in control arteries, whereas only the low-affinity site was detected in diabetic arteries, suggesting that coupling of the alpha-1 adrenoceptor to G proteins is impaired in diabetic aorta and caudal artery. The levels of immunoreactive Gi2,3alpha and Gq/11alpha were not different between control and diabetic aorta or caudal artery. Thus, not only do changes in the number and coupling of the alpha-1 adrenoceptor or level of G proteins not explain the enhanced contractile responses of diabetic arteries to norepinephrine, but also the changes in alpha-1 adrenoceptor binding would counteract the enhancement. Instead, an increase in the activity of the G proteins or phospholipase C-beta coupled to the alpha-1 adrenoceptor may be mediating the enhanced responsiveness elicited by alpha-1 adrenoceptor stimulation in diabetic arteries.

Animals↗
PubMed1994

Psychological and demographic correlates of glycaemic control in adult patients with type 1 diabetes.

The relationship between an objective measure of glycaemic control (glycated haemoglobin (HbA1)) and personality variables was examined in two separate groups of adult Type 1 (insulin-dependent) diabetic patients. Study 1 included 121 patients, all of whom also had subjective self-reporting of treatment compliance assessed, while the first 57 patients had individual differences in intelligence, major dimensions of personality and forgetfulness documented. Study 2 examined 303 patients, all of whom had their major dimensions of personality assessed using a shortened and updated version of the original personality questionnaire. Demographic indices (age, onset-age, duration of diabetes) were assessed in both groups. No significant correlation was found between HbA1 and self-report compliance suggesting that self-reporting may be invalid as a measure of glycaemic control. In study 1 personality and intelligence variables did not correlate significantly with HbA1 values. Older patients with shorter duration of diabetes had significantly better glycaemic control (p < 0.05). A significant correlation was observed between HbA1 concentration and onset-age of diabetes (p < 0.001); the patients who had developed diabetes later in life were achieving better control of their blood glucose. In the larger number of subjects in study 2 no significant correlations were evident between HbA1 and personality variables. It is concluded that the predictors of glycaemic control indexed by HbA1 may be distinct from predictors of self-report compliance and that the latter have limited or no value in providing an assessment of quality of glycaemic control. There is no evidence of an effect of personality on glycaemic control as measured by HbA1.

Adolescent↗
PubMed1984

The interaction of carbachol and forskolin in rabbit papillary muscles.

The ability of the muscarinic agonist, carbachol, to overcome increases in tension and in cAMP produced in response to the adenylate cyclase activator, forskolin, in rabbit papillary muscles was measured. Forskolin alone increased cAMP levels to a much greater extent than did a concentration of isoproterenol that produced an equivalent increase in tension. Carbachol completely overcame the increase in tension, while having no effect on the increase in cAMP, produced by forskolin. The response to carbachol was associated with a significant increase in cGMP levels. It appears that carbachol may block the inotropic response to forskolin by antagonizing the effects of forskolin-induced increases in cAMP.

Animals↗
PubMed1978

Responses of rabbit portal vein to histamine.

1 Histamine produced a dose-dependent contraction of the isolated portal vein of the rabbit. This contraction was not antagonized by atropine, methysergide, indomethacin, cocaine or 6-hydroxy-dopamine, nor by pretreatment of the rabbit with reserpine. 2 The response to histamine was blocked by H1-receptor antagonists only when the blocking agent was used in very high concentrations, and was not antagonized by the H2-receptor blocking agent, metiamide, H1-receptor antagonists did not block the effects of 5-hydroxytryptamine. 3 The contractions elicited by histamine, 5-hydroxytryptamine and noradrenaline were blocked by phentolamine. 4 Desensitization to high doses of 5-hydroxytryptamine caused a concomitant depression in the response to histamine but not to noradrenaline or acetylcholine. 5 The results suggest that the contractions of rabbit portal vein elicited by histamine are not mediated by receptors of the H1- or the H2-type, but may involve an action of histamine at a receptor which is also involved in the action of 5-hydroxytryptamine.

Animals↗