Effect of aspirin and indomethacin on exercise-induced changes in blood pressure and limb blood flow in normal volunteers

Cowley, Alison; Stainer, K.; Rowley, J M; Wilcox, Rosalinde G.

doi:10.1093/cvr/19.3.177

Cited by 29 publications

(26 citation statements)

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“…This is consistent with the findings of other studies in which a COX inhibitor (aspirin, indomethacin, or ibuprofen) was given systemically (4,21,34). By contrast, when indomethacin or aspirin was directly infused into the forearm circulation, baseline FVC decreased and venous efflux of PGI 2 and PGE 2 decreased, indicating a tonic dilator influence of PGs (6,38).…”

Section: Effects Of Aspirinsupporting

confidence: 90%

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Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia

Win

Marshall²

2005

Journal of Applied Physiology

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In 11 healthy volunteers, we evaluated, in a double-blind crossover study, whether the vasodilation that follows isometric contraction is mediated by prostaglandins (PGs) and/or is O2 dependent. Subjects performed isometric handgrip for 2 min at 60% maximal voluntary contraction (MVC), after pretreatment with placebo or aspirin (600 mg orally), when breathing air or 40% O2. Forearm blood flow was measured in the dominant forearm by venous occlusion plethysmography. Arterial blood pressure was also recorded, allowing calculation of forearm vascular conductance (FVC; forearm blood flow/arterial blood pressure). During air breathing, aspirin significantly reduced the increase in FVC that followed contraction at 60% MVC: from a baseline of 0.09 +/- 0.011 [mean +/- SE, conductance units (CU)], the peak value was reduced from 0.24 +/- 0.03 to 0.14 +/- 0.01 CU. Breathing 40% O2 similarly reduced the increase in FVC relative to that evoked when breathing air; the peak value was 0.24 +/- 0.03 vs. 0.15 +/- 0.02 CU. However, after aspirin, breathing 40% O2 had no further effect on the contraction-evoked increase in FVC (the peak value was 0.15 +/- 0.02 vs. 0.16 +/- 0.02 CU). Thus the present study indicates that prostaglandins make a substantial contribution to the peak of the vasodilation that follows isometric contraction of forearm muscles at 60% MVC. Given that hyperoxia similarly reduced the vasodilation and attenuated the effect of aspirin, we propose that the stimulus for prostaglandin synthesis and release is hypoxia of the endothelium.

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Section: Effects Of Aspirinsupporting

confidence: 90%

“…More recently, both indomethacin and aspirin substantially reduced the increase in calf blood flow and decrease in vascular resistance that occurred following a 30-min period of treadmill exercise (4). In this study, a placebo or one of the COX inhibitors was given on different experimental days in randomized order.…”

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confidence: 98%

Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia

Win

Marshall²

2005

Journal of Applied Physiology

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“…We have confirmed that vasodilatory prostanoids are important in determining the response to ACh in both diabetic (4) and nondiabetic subjects (11,12). We have also demonstrated that, in the absence of pretreatment with a cyclo-oxygenase inhibitor, endothelium-dependent vasodilation is not impaired in type 1 diabetic patients who have no evidence of additional macrovascular risk.…”

Section: Prostaglandin-mediated Vasodilation In Type 1 Diabetessupporting

confidence: 70%

“…There is evidence that vasodilatory prostanoids may be important in determining responses to ACh in both diabetic (4) and nondiabetic subjects (11,12), their effects being mediated through an increase in cyclic AMP. We hypothesized that increased prostaglandin-mediated vasodilation might compensate for decreased activity of the NO pathway in type 1 diabetes.…”

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confidence: 99%

Effects of cyclo-oxygenase inhibition on vasodilatory response to acetylcholine in patients with type 1 diabetes and nondiabetic subjects.

Meeking

Browne²,

Allard³

et al. 2000

Diabetes Care

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OBJECTIVE -Studies examining vasodilatory responses to acetylcholine (ACh) and its derivatives have been conflicting. Enhanced activation of the cyclo-oxygenase pathway and increased availability of vasodilatory prostanoids may occur in type 1 diabetes, and this may compensate for the observed reduction in nitric oxide (NO) activity. We examined the role of cyclo-oxygenase inhibition on vasodilatory responses in 12 healthy normotensive type 1 diabetic adults and 12 nondiabetic control subjects of similar age, sex, and BMI.RESEARCH DESIGN AND METHODS -Forearm blood flow was measured using a venous occlusion plethysmography technique at baseline and after brachial artery infusions of ACh (7.5, 15, and 30 µg/min). Forearm blood flow at baseline and after ACh was then reexamined after local intra-arterial infusion of indomethacin (0.3 mg/100 ml forearm volume), a cyclo-oxygenase inhibitor.RESULTS -Baseline blood flow in the diabetic and control groups were similar (2.65 ± 0.26 vs. 2.59 ± 0.20 ml/min per 100 ml, respectively; P = 0.4). After indomethacin infusion, the vasodilatory responses to all doses of ACh were reduced in both the diabetic (by 25.30 ± 4.90%) and control group (by 11.23 ± 5.45%). However, the reduction in blood flow response to ACh after indomethacin was greater in diabetic patients compared with control subjects (P = 0.03).CONCLUSIONS -Our findings suggest that vasodilatory prostanoids are important in determining endothelial response to ACh in diabetic and nondiabetic subjects. Increased prostaglandin-mediated vasodilation may compensate for attenuated responses to NO previously reported in diabetic subjects. These findings may partly explain the conflicting reports of endothelial dysfunction in patients with type 1 diabetes.

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“…3233 Although Stassen et al 33 found no increase in systemic vascular resistance after treatment with indomethacin, Cowley et al 32 found that calf blood flow measured immediately postexercise was attenuated by about 40%. However, oral administration of indomethacin may have minimized the drug's effectiveness, since intravenous injection of indomethacin has been shown to augment vascular resistance in dynamically contracting dog skeletal muscle.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

Stebbins¹,

Maruoka

Longhurst

1986

Circulation Research

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The purpose of this study was to determine the contribution of prostaglandins to the reflex cardiovascular responses induced by static contraction of the hind limb in cats, i.e., the exercise reflex. To accomplish this, the cardiovascular responses to hind limb contraction induced by electrical stimulation of spinal cord ventral roots L^ and S, were compared before and after inhibition of prostaglandin synthesis (indomethacin, 2-6 mg/kg i.v., n = 5, or sodium meclofenamate, 2-6 mg/kg i.v., n = 5) or after injection of prostaglandin E 2 into the hind limb arterial blood supply. Treatment with indomethacin attenuated the contraction-induced increase in mean arterial pressure and left ventricular dP/dt by 76% and 86%, respectively. Heart rate and average developed triceps surae muscle tension were unchanged. After administering sodium meclofenamate, the reflex response was attenuated to a similar degree. In the indomethacin-treated animals, injection of exogenous prostaglandin E 2 (PGE 2 ) partially restored the pressor and myocardial contractile responses. In 6 animals, treatment with exogenous PGE 2 without prior inhibition of prostaglandin synthesis did not significantly augment the contraction-induced cardiovascular response. Using the radioactive microsphere technique, we measured skeletal muscle blood flow during contraction before and after treatment with indomethacin (n = 6) to determine if an indomethacin-induced alteration in blood flow could account for the attenuated contraction-induced cardiovascular response. Blood flow during static muscle contraction was not significantly altered by indomethacin. We conclude that prostaglandins contribute to the exercise reflex through an action on afferent nerve endings rather than through a regional vascular effect. (Circulation Research 1986;59:645-654)

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Effect of aspirin and indomethacin on exercise-induced changes in blood pressure and limb blood flow in normal volunteers

Cited by 29 publications

References 0 publications

Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia

Contribution of prostaglandins to the dilation that follows isometric forearm contraction in human subjects: effects of aspirin and hyperoxia

Effects of cyclo-oxygenase inhibition on vasodilatory response to acetylcholine in patients with type 1 diabetes and nondiabetic subjects.

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

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