Effect of diabetes on metabolic coronary dilatation in the rat

Durante, William; Sunahara, F. A.; Sen, Amar K.

doi:10.1093/cvr/23.1.40

Cited by 30 publications

(20 citation statements)

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“…The current results are in contrast with several observations in animal models for diabetes [9,10] that studied the responsiveness of the heart and coronary vasculature to adenosine. We cannot exclude the possibility that diabetes mellitus differentially affects the coronary and forearm vascular bed in humans.…”

Section: Discussioncontrasting

confidence: 99%

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Preserved vasodilator response to adenosine in insulin‐dependent diabetes mellitus

Rongen¹,

Ginneken²,

Thien³

et al. 1996

Eur J Clin Investigation

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Section: Discussioncontrasting

confidence: 99%

“…Interestingly, an impaired responsiveness to the vasodilator effect of adenosine has been observed in animal models of diabetes mellitus [9,10]. Several mechanisms may be responsible for this reduced responsiveness to adenosine.…”

Section: Introductionmentioning

confidence: 99%

Preserved vasodilator response to adenosine in insulin‐dependent diabetes mellitus

Rongen¹,

Ginneken²,

Thien³

et al. 1996

Eur J Clin Investigation

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“…Such an impairment of metabolic microvascular coronary vasodilation as been shown in diabetic rat hearts (19) and in diabetic patients in response to atrial pacing by Nasher et al (3). However, in the latter study, other coronary risk factors that could impair microvascu- CPT and coronary vasomotion.…”

Section: Discussionmentioning

confidence: 68%

Impairment of Coronary Microvascular Dilation in Response to Cold Pressor–Induced Sympathetic Stimulation in Type 2 Diabetic Patients With Abnormal Stress Thallium Imaging

Nitenberg

Ledoux

Valensi³

et al. 2001

Diabetes

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Coronary microcirculation dysfunction may be associated with myocardial perfusion defects on thallium imaging in diabetic patients without coronary artery stenosis. Microvascular coronary adaptation to increased myocardial oxygen demand in response to sympathetic stimulation evoked by the cold pressor test was examined in 22 type 2 diabetic patients with thallium imaging defects and in 15 control subjects. Both the diabetic patients and control subjects had angiographically normal coronary arteries and no other risk factors. Despite a similar increase in the rate-pressure product in the two groups (22.6 ؎ 12.4% in diabetic patients and 31.8 ؎ 8.2% in control subjects, NS), coronary blood flow increase in the left anterior descending artery (mean flow velocity measured by intracoronary Doppler multiplied by the cross-sectional area measured by digital angiography) was significantly lower in diabetic patients than in control subjects (14.7 ؎ 19.8 vs. 75.5 ؎ 13.5%, respectively; P ‫؍‬ 0.0001). In addition, when there was a positive correlation between the two parameters in control subjects (r ‫؍‬ 0.651, P < 0.01), there was no relationship in diabetic patients (r ‫؍‬ 0.054). In conclusion, vasodilation of the coronary microcirculation in response to sympathetic stimulation evoked by the cold pressor test is impaired in type 2 diabetic patients without epicardial artery lesions. This microvascular impairment during sympathetic stimulation may explain exercise-induced myocardial perfusion abnormalities observed in these patients and may impair microcirculatory coronary vasodilation during current life stress episodes such as exercise, mental stress, or cold exposition. Diabetes 50:1180 -1185, 2001 I t has been shown that endothelium-dependent epicardial coronary artery vasodilation in response to acetylcholine (1) or physiological stimuli (2) is impaired in diabetic patients with angiographically normal coronary arteries. Microvascular functional abnormalities have also been reported by Nasher et al. (3), who have shown that metabolic vasodilation of coronary microcirculation evoked by atrial pacing is reduced in diabetic patients. Similar impairment has also been reported in hypertensive patients with angiographically normal coronary arteries (4) and by Zeiher et al., who showed that coronary blood flow failed to increase during exercise (5) or during the cold pressor test (CPT) in patients with early atherosclerosis (6) and without significant coronary artery stenosis, suggesting that the endothelial function is impaired at the microvascular level. Such coronary microcirculation dysfunction may be associated with myocardial perfusion defects on 99m Tc sestamibi single photon emission computed tomography (SPECT) imaging in humans with angina and minimally obstructive coronary artery disease (7) and might contribute to myocardial ischemia when myocardial oxygen demand is increased, even in the absence of coronary artery stenosis.In diabetes, it has been suggested that coronary functional abnormalities and microvas...

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“…Several animal and human studies have shown that coronary metabolic vasodilation is impaired in diabetes. In diabetic rats, coronary blood flow increase in response to norepinephrine infusion and to pacing was significantly lower than that in control rats (26). In diabetic dogs, coronary arterioles did not dilate when coronary perfusion pressure was decreased (27).…”

Section: Discussionmentioning

confidence: 76%

Coronary Microvascular Adaptation to Myocardial Metabolic Demand Can Be Restored by Inhibition of Iron-Catalyzed Formation of Oxygen Free Radicals in Type 2 Diabetic Patients

Nitenberg¹,

Ledoux²,

Valensi³

et al. 2002

Diabetes

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Dilation of coronary vessels is impaired in diabetic patients when myocardial metabolic demand is increased. Deferoxamine (DFX) restores a normal dilation of epicardial coronary arteries. To assess the effects of DFX on metabolic coronary microvascular dilation in type 2 diabetic patients, coronary blood flow was measured using intracoronary Doppler and quantitative angiography in 17 type 2 diabetic patients with normal coronary arteries and without any other coronary risk factors. Measurements were made at baseline and during a cold pressor test (CPT), before and after intravenous administration of DFX. With a similar ratepressure product (RPP) increase during CPT before and after DFX (؉21.1 ؎ 8.7 vs. ؉20.5 ؎ 8.9%, respectively), coronary blood flow increase was significantly enhanced after DFX (؉31.8 ؎ 16.7 vs. ؉6.3 ؎ 12.9% before DFX, P < 0.001). Moreover, coronary resistance increased during CPT before DFX and decreased after DFX (؉14.8 ؎ 21.9 vs. ؊7.9 ؎ 10.9%, respectively, P < 0.001). Lastly, the negative relationship between coronary blood flow and RPP before DFX (R ‫؍‬ 0.546, P < 0.05) was changed in a positive relationship after DFX (R ‫؍‬ 0.518, P < 0.05). In conclusion, in type 2 diabetic patients, inhibition of iron-catalyzed oxidative reactions by DFX restored dilation of the coronary microcirculation and a normal matching between myocardial metabolic demand and coronary blood flow. Diabetes 51:813-818, 2002 R ecent studies have shown that in diabetic patients coronary blood flow is unable to match myocardial metabolic demand increase evoked by either atrial pacing or sympathetic stimulation by the cold pressor test (CPT) (1,2). It has been suggested that coronary microvascular functional abnormalities might contribute to the development of left ventricular dysfunction through episodes of silent myocardial ischemia when myocardial oxygen demand is increased and might explain the high frequency of exercise thalliumimaging defects (3-6).Impairment of dilation of the coronary microcirculation in diabetic patients has been proposed to be related to the degree of sympathetic nerve dysfunction (7). On the other hand, it is well established that oxygen-derived free radical production, which is increased in diabetes (8,9), could impair endothelium-dependent vasodilation since it has been proved that superoxide anions could inactivate nitric oxide (10). Lastly, several studies have shown that nitric oxide production was reduced in diabetes in both peripheral and coronary vascular beds (11,12).We had previously demonstrated that a low dose of deferoxamine (DFX), an iron chelator that prevents ironcatalyzed generation of hydroxyl radicals, restored normal dilation of epicardial coronary arteries in diabetic patients, suggesting that inactivation of nitric oxide by oxygen species may play a role in impairment of coronary vasomotion (13). Similar results have been obtained in peripheral circulation by antioxidant therapy (14 -17).The purpose of the present study was to determine whether impaired coronary microva...

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Effect of diabetes on metabolic coronary dilatation in the rat

Cited by 30 publications

References 0 publications

Preserved vasodilator response to adenosine in insulin‐dependent diabetes mellitus

Preserved vasodilator response to adenosine in insulin‐dependent diabetes mellitus

Impairment of Coronary Microvascular Dilation in Response to Cold Pressor–Induced Sympathetic Stimulation in Type 2 Diabetic Patients With Abnormal Stress Thallium Imaging

Coronary Microvascular Adaptation to Myocardial Metabolic Demand Can Be Restored by Inhibition of Iron-Catalyzed Formation of Oxygen Free Radicals in Type 2 Diabetic Patients

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