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Background Phaeochromocytomas are rare catecholamine-producing tumours which typically present with comparatively benign symptoms such as headache, palpitations, sweating, hypertension, and insulin resistance. In rare cases, severe cardiac manifestations have been reported. We describe a patient who developed severe hypoglycaemia after an oral glucose tolerance test (OGTT), potentially triggering a phaeochromocytoma crisis and cardiogenic shock. To the best of our knowledge, only four other cases of hypoglycaemia after OGTT have been reported in patients with phaeochromocytoma, of which none developed a phaeochromocytoma crisis. Case summary A 53-year-old woman with hypertension, dyslipidaemia, and prediabetes presented to the Emergency Department with hypoxia, hyperglycaemia, lactic acidosis, severe left ventricular dysfunction, and pulmonary oedema followed by cardiogenic shock. Onset of symptoms was only few hours after an OGTT during which she had developed severe transient hypoglycaemia. Angiography was performed due to elevated troponin levels and showed a midventricular contraction pattern typical of takotsubo. This was subsequently confirmed by cardiac magnetic resonance imaging. The patient’s condition improved during the first 36 h and she was discharged home on Day 7. A positive catecholamine test prompted readmission to the Endocrinology Unit, where computer tomography confirmed the diagnosis of phaeochromocytoma. An adrenalectomy was performed, and the diagnosis was verified histopathologically. Discussion The possibility of a phaeochromocytoma must be considered as a potential triggering factor in patients presenting with takotsubo cardiomyopathy, in particular, when blood glucose levels fluctuate between severe hypo- and hyperglycaemia.

Objective To study whether vascular reactivity as assessed by the methods forearm blood flow (FBF) and postocclusive reactive hyperaemia (PRH) in the nail fold was related as a measure of endothelium-dependent vasodilation in the microcirculation. Methods Microvascular reactivity was assessed in forearm blood flow and in the nail fold by vital capillaroscopy of individual microvessels as postocclusive reactive hyperaemia. Vascular reactivity was assessed at baseline (n = 25) as well as after infusion of acetylcholine and of sodium nitroprusside (n = 13). We also performed a multivariate regression analysis to assess whether forearm blood flow or flow-mediated dilatation related to postocclusive reactive hyperaemia. Results This study showed a distinct microvascular response to both acetylcholine (endothelium-dependent vasodilation) and sodium nitroprusside (endothelium-independent vasodilation) during forearm blood flow assessment and postocclusive reactive hyperaemia assessment in the nail fold (n = 13). These changes were inversely related (r- = -0·57; P Conclusions Forearm blood flow was inversely correlated to postocclusive reactive hyperaemia. Postocclusive reactive hyperaemia was shortened after infusion with both acetylcholine and sodium nitroprusside. This occurred in parallel with the expected increase in forearm blood flow, conceivably reflecting that both methods can be used to assess endothelium-dependent vasodilation in the microcirculation.

Manifestations of vascular disease, including microvascular changes, constitute the major part of the morbidity and mortality in diabetic patients. Oxidative stress has been suggested to play an important role in the vascular dysfunction of diabetic patients. Furthermore, epidemiological observations indicate a beneficial effect of an increased dietary intake of antioxidants. The present study tested the hypothesis that the antioxidant ascorbic acid influences microcirculatory function in patients with Type II diabetes. Patients with Type II diabetes were treated with 1 g of ascorbic acid three times a day for 2 weeks in a randomized placebo-controlled double-blind cross-over design. Microvascular reactivity was assessed by vital capillaroscopy and PRH (post-occlusive reactive hyperaemia). hs-CRP (high-sensitivity C-reactive protein), IL-6 (interleukin-6), IL-1ra (interleukin-1 receptor antagonist) and ox-LDL (oxidized low-density lipoprotein) were analysed. The results showed no significant change in microvascular reactivity assessed after 2 weeks of ascorbic acid treatment. TtP (time to peak) was 12.0±3.3 s before and 11.2±3.5 s after ascorbic acid (n=17). In comparison, TtP was 11.5±2.9 s before and 10.6±2.8 s after placebo (not significant). IL-1ra, IL-6, hs-CRP and ox-LDL did not change significantly after ascorbic acid, neither as absolute or relative values. In conclusion, in contrast with some studies reported previously, we could not demonstrate an effect of continuous oral treatment with ascorbic acid on microvascular reactivity assessed at the level of individual capillaries. Furthermore, we found no indication of an effect on inflammatory cytokines or ox-LDL.

High lipid levels have been shown to coexist with a disturbed vascular endothelial function. Thus, acute lipid lowering could be expected to improve vascular reactivity. Patients with familial hyperlipidemia (FH) have substantial and rapid decreases in lipid levels after low-density lipoprotein apheresis. Thus, an opportunity exists to study acute effects of lipid lowering on vascular reactivity. Flow mediated vasodilation (FMD) is commonly used to assess endothelial function in conduit vessels, whereas vital capillary microscopy during the post-reactive hyperemia (PRH) phase is used to assess response at the microvascular level. It is not known whether endothelial dysfunction is a general phenomenon in all kinds of vessels or if there are differences between micro- and macrovessels. In the present study, we were not able to demonstrate an improved vascular response after acute lipid lowering in FH patients. This was true both in the microcirculation (PRH) and in the conduit vessels (FMD). However, the two methods gave concordant results, demonstrating disturbed vascular reactivity in the patients as compared with healthy subjects. We have found no previous report with parallel assessments at the microcirculatory and macrocirculatory levels.

Objective Exposure to SHS, as by passive smoking, seems to increase the incidence of cardiovascular events. It has been shown that active smoking of a single cigarette causes an immediate and significant decrease in microcirculatory blood flow velocity, whereas the acute effects of exposure to SHS on microcirculatory flow have as yet not been demonstrated. Methods Healthy nonsmoking volunteers of both genders were studied during acute exposure to SHS of two cigarettes burning up to 10 minutes. Microvessels were examined by in vivo vital capillaroscopy (Capiflow®), allowing continuous assessment of CBV. Results CBV decreased from 514 mm/sec (CI 383–646) at baseline to 306 mm/sec (CI 191–420) at end of SHS exposure with a further decrease to a nadir of 240 mm/sec (CI 155–325) four minutes after the end of this exposure (p

Background: Cigarette smoking provokes marked acute changes in the microcirculatory vasculature, including a reduced blood flow velocity. in accordance with the hypothesis that the reduced blood flow is due to an imbalance between pro-oxidants and oxidants, we recently showed that most of the reduction could be reversed by a high dose of vitamin C. Hypothesis: in the present work we tested the hypothesis that N-acetylcysteine, a mucolyticum and an antioxidant, may have an effect on the smoking-induced changes observed by vital capillary microscopy of the nailfold. Methods: in all, 37 healthy volunteers of both genders and with varied smoking habits were treated with N-acetylcysteine 200 mg t.i.d. for 2 weeks. in vivo investigation of the microcirculation by capillaroscopy was performed before and after treatment. Results: Treatment with N-acetylcysteine significantly reduced the smoking-induced relative decrease in capillary blood flow velocity in a group of volunteers with varied smoking habits (p=0.0016). The preventive effect was clearly significant in smokers (p=0.003). Conclusion: Treatment with N-acetylcysteine has a positive impact on microcirculatory flow during smoking, particularly in habitual smokers.

Dietary treatment of rabbits with 1% cholesterol resulted in a transient rise in their plasma nitrate levels. After 3 weeks of treatment the nitrate levels were about 50% higher than those of the controls (p < 0.005). After 10 weeks of treatment the nitrate levels were similar to those at the start of the study. In accordance with previous work (Xiuet al., J. Clin. Invest.,1994,93,2732–2737), the cholesterol treatment led to a decreased blood flow velocity in arterioli of the third order in the conjunctiva, and a decreased diameter of these arterioli. There was a significant correlation between plasma nitrate levels and the two microcirculatory variables (p < 0.0001). Nitrate is the major metabolic end product of nitric oxide (NO), and plasma nitrate levels may be used as an index of the endogenous formation of NO. The present results suggest that dietary cholesterol induces a transient increase in the synthesis of NO. Such an increased synthesis may compensate for part of a cholesterol-induced degradation of NO.

Microcirculation was studied during 10 wk in untreated rabbits (n = 13) and in rabbits treated with dietary addition of 1% cholesterol (n = 13), 1% cholesterol + 1% of the antioxidant BHT (butylated hydroxytoluene) (n = 11), or 1% BHT (n = 5). The studies were performed by direct intravital microscopic imaging of the left and right conjunctivae with the use of a stereo microscope and a high resolution television camera. Microvessel diameter, erythrocyte flow velocity, and microhemorheologic conditions were evaluated quantitatively via a computer-assisted digital image processing system. Significant and marked changes occurred in all the above variables as a consequence of cholesterol feeding. After 3 wk of feeding there was a dramatic decrease (approximately 30%) in blood flow velocity in arterioli of the third order (P < 0.0001), accompanied by aggregation of cells in 40-50% of the smaller conjunctival vessels (P < 0.0001). These changes were enhanced further during the following 7 wk of treatment. All the above changes in the microcirculation were markedly reduced by the addition of BHT treatment. The diameter of the above arterioli decreased in the purely cholesterol-fed group (P < 0.005), whereas this did not occur in the group fed both cholesterol and BHT. In rabbits fed BHT in the absence of cholesterol, there was no significant effect on any assessed microcirculatory variable. In conclusion, the results demonstrate that the antioxidant BHT prevented early cholesterol-induced microcirculatory changes. This prevention occurred in the absence of a reduction of blood lipid levels. The results provide strong support for the hypothesis that a considerable part of the effects on microcirculation in hypercholesterolemia may be due to cholesterol-induced oxidations and not to cholesterol itself. The results are discussed in relation to the previously demonstrated antiatherogenic effect of BHT and the possible use of antioxidants in the therapy and prophylaxis of atherosclerosis.

Endothelial function at the arterial level has been extensively assessed by a non-invasive method using flow-mediated dilatation (FMD) of the brachial artery. Early disturbances have been found in patient groups prone to later development of manifest macrovascular atherosclerosis. A possible non-invasive means of studying blood-flow regulation and function at the microcirculatory level is through videophotometric capillaroscopy. The most stable variable in such an investigation is the time-to-peak (TtP) flow after a brief arterial occlusion. The short-term reproducibility of such assessments is excellent but the coefficient of variation (CV) in long-term studies is reported to be in the order of slightly less than 20%. The aim of the present methodological study was to evaluate different sources of variations in such microcirculatory assessments in order to be able to propose design recommendations that minimize the number of patients and recordings needed to achieve sufficient statistical power in longitudinal studies. We used a symmetric design with 144 recordings of TtP after a one-minute arterial occlusion in healthy volunteers. We did six occlusions each time in the capillaries of two fingers on each occasion, and repeated the procedure three times with an interval of at least one week between each investigation. All recordings were analyzed off-line using a cross-correlation technique with the Capiflow system. Each analysis was performed at least three times, giving a total of slightly less than 500 assessments. In our material (n = 10) TtP had a mean of 6.3 s (95% confidence interval 5.2-7.4). The correlation between repeated measurements in a single capillary during a single session was r0.91 (CV 6%). The between-finger CV was 8% (r = 0.84). The CV of measurements between different days was about 20% when single measurements were compared. However, the CV decreased to less than 13% when the mean of at least two time-to-peak assessments on each occasion was used. In conclusion, the methodological error including day-to-day variation could be minimized using the mean of at least two repeated assessments of post-occlusive hyperemia at each time point in a longitudinal study. This finding should be taken into consideration in the design of future longitudinal studies.

To investigate whether a daily intake of a moderate dose of antioxidants modifies the microcirculatory response to smoking, assuming a major influence of oxidative stress on microcirculation.The microvascular response to smoking was assessed in individual capillaries by capillaroscopy before and after two weeks of treatment with oral antioxidants.Smoking prolonged time to peak (TtP) capillary blood flow velocity in all subjects. When the subjects were pre-treated with ascorbate, TtP was comparable to baseline values of untreated subjects. No significant effect of vitamin E was observed either before or after smoking. Capillary blood flow velocity increased after treatment with ascorbate as well as after vitamin E. However, significant reductions in velocity were still observed in response to smoking even after subjects consumed ascorbate and vitamin E (p0.0004 and p0.000008 respectively).This study focused on individual capillaries, and confirms that smoking has a very pronounced, direct and reproducible microvascular effect possible to demonstrate in vivo in human capillaries. Moderate intake of the antioxidant ascorbate clearly mitigated the effects induced by smoking. TtP after smoking in subjects treated with ascorbate was similar to that observed in untreated subjects before smoking a cigarette. Thus, oxidative stress could be assumed to play a role in the effects of smoking on microcirculation.

To assess the acute effect of a single dose of 10 mg oral micronized 17beta-estradiol on microcirculation in postmenopausal women with and without coronary artery disease and its potential influence on exercise capacity.Postmenopausal women (n=11) with coronary artery disease had symptoms of ischemic heart disease and at least 1 mm ST depression at exercise. Microcirculation was examined by vital microscopy, with and without the acute administration of estrogen in a placebo-controlled cross-over design. Exercise test was performed on bicycle. The microcirculatory findings were contrasted to those in 14 healthy postmenopausal women.17Beta-estradiol in serum and blood flow velocity increased significantly after acute oral estrogen administration both in women with coronary artery disease (p0.001) and in healthy women (p0.0001), with no significant difference between the two groups. No effect on exercise capacity or ST depression at exercise was detected.Previously reported data that a single dose of estrogen administered to postmenopausal women results in positive effects on exercise was not reproduced. An increased peripheral microvascular flow velocity was detected in women with coronary artery disease and this increase was not accompanied by an increased exercise capacity.

We have shown that inclusion of the antioxidant butylated hydroxytoluene (BHT) in the diet protects against development of atherosclerotic lesions in cholesterol-fed rabbits. In parallel, BHT treatment results in increased plasma triglyceride levels. The present study explores the relationship between the triglyceride-inducing and protective effects of BHT in two different studies. The combined material contains 22 rabbits fed cholesterol and 18 rabbits fed cholesterol in combination with 1% BHT. In the BHT group there was an inverse relationship between triglyceride exposure/cholesterol exposure and extent of lesions with r=0.74 (P=0.0005). Our results show that increased triglyceride exposure parallels the anti-atherogenic effect of BHT. There was no significant correlation between atheromatosis and serum BHT levels. beta-very low density lipoprotein (beta-VLDL) from cholesterol and BHT animals was triglyceride-enriched and smaller compared to beta-VLDL from cholesterol-fed animals, but there was no significant association between the anti-atherogenic effect of BHT and particle size or apolipoprotein pattern of LDL or beta-VLDL. LDL isolated from rabbits treated with cholesterol and BHT was less sensitive to oxidative modification than LDL isolated from rabbits treated with cholesterol only. In conclusion, our results demonstrate that the degree of triglyceride exposure may be an important modulator of the anti-atherogenic effect of an antioxidant.