We studied 424 adults with falciparum malaria admitted over 28 months. They were divided into three groups: cerebral malaria (n = 214); severe non-cerebral malaria (n = 58); and uncomplicated malaria (n = 152). Fundus examination was done daily from admission to discharge, and weekly thereafter in those with persistent changes. All patients were treated by a protocol based on WHO guidelines. Ophthalmoscopic abnormalities were: retinal haemorrhages, 40 (9.43%) (25 cerebral malaria, 10 severe non-cerebral and five uncomplicated malaria); papilloedema, 17 (7.94%) cerebral malaria and two uncomplicated malaria; blurring of disc margins, 25 (11.68%) cerebral and seven non-cerebral; retinal oedema, six (2.80%) cerebral and five non-cerebral malaria; disc pallor, five patients all with cerebral malaria; vitreous haemorrhage and hard exudate in one patient each, both cerebral malaria. Retinal haemorrhage was associated with cerebral malaria and severe non-cerebral malaria, especially with severe anaemia (p < 0.001), as compared to uncomplicated malaria (p < 0.01). The association of papilloedema and cerebral malaria was highly significant compared to severe non-cerebral malaria (p < 0.001). None of these findings was associated with statistically significant mortality, except disc pallor in cerebral malaria (p < 0.05). (+info)
(2/956) Endothelial function in Marfan syndrome: selective impairment of flow-mediated vasodilation.
BACKGROUND: The cardiovascular complications of Marfan syndrome arise due to alterations in the structural and functional properties of fibrillin, a constituent of vascular connective tissues. Fibrillin-containing microfibrils are closely associated with arterial endothelial cells, indicating a possible functional role for fibrillin in the endothelium. Plasma concentrations of endothelial cell products are elevated in Marfan subjects, which indirectly indicates endothelial dysfunction. This study directly assessed flow- and agonist-mediated endothelium-dependent brachial artery reactivity in Marfan subjects. METHODS AND RESULTS: In 20 Marfan and 20 control subjects, brachial artery diameter, blood flow, and blood pressure were measured by ultrasonic wall tracking, Doppler ultrasound, and photoplethysmography, respectively. Measurements were taken during hand hyperemia (a stimulus for endothelium-derived nitric oxide [NO] release in the upstream brachial artery) and after sublingual administration of the endothelium-independent vasodilator nitroglycerin. In 9 Marfan and 6 control subjects, the above parameters were also assessed during intra-arterial infusions of acetylcholine and bradykinin (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO production). Flow-mediated responses differed markedly between Marfan and control subjects (-1.6+/-3.5% versus 6. 50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7% versus 15.2+/-7.8%; P=NS). Agonist-induced vasodilation to incremental intra-arterial infusions of acetylcholine and bradykinin were not significantly different between Marfan and control subjects, and intra-arterial L-NMMA produced similar reductions in brachial artery diameter in both groups. CONCLUSIONS: These data demonstrate impaired flow-mediated but preserved agonist-mediated endothelium-dependent vasodilation in Marfan subjects and suggest preservation of basal NO release. Selective loss of flow-mediated dilation suggests a role for fibrillin in endothelial cell mechanotransduction. (+info)
(3/956) Trigeminal and carotid body inputs controlling vascular resistance in muscle during post-contraction hyperaemia in cats.
1. In anaesthetized cats, the effects of stimulation of the receptors in the nasal mucosa and carotid body chemoreceptors on vascular resistance in hindlimb skeletal muscle were studied to see whether the responses were the same in active as in resting muscle. The measurements of vascular resistance were taken, first, in resting muscle, and second, in the immediate post-contraction hyperaemic phase that followed a 30 s period of isometric contractions. 2. Stimulation of the receptors in the nasal mucosa caused reflex apnoea and vasoconstriction in muscle. The latter response was attenuated when the test was repeated during post-contraction hyperaemia. 3. Stimulations of the carotid bodies were made during a period of apnoea evoked reflexly by electrical stimulation of both superior laryngeal nerves. This apnoea prevented any effects of changes in respiration on the carotid body reflex vascular responses. Stimulation of the carotid bodies evoked hindlimb muscle vasoconstriction. In the post-contraction hyperaemic period, the response was reduced or abolished. A similar attenuation of the reflex vasoconstrictor responses occurred in decentralized muscles stimulated through their motor roots in the cauda equina. 4. Evidence is presented that the attenuation of the vasoconstrictor responses evoked by the two reflexes is a phenomenon localized to the contracting muscles themselves resulting from an interaction between sympathetic neuronal activity and the local production of metabolites. 5. The results are discussed in relation to the metabolic needs of tissues in relation to asphyxial defence mechanisms such as occur in the diving response. (+info)
(4/956) Neurogenic origin of articular hyperemia in early degenerative joint disease.
It has been speculated that joint instability resulting from anterior cruciate ligament (ACL) rupture could be exacerbated by changes in vasomotor activity in the remaining supporting structures. In this study, the effect of ACL transection on medial collateral ligament (MCL) basal perfusion and its responsiveness to calcitonin gene-related peptide (CGRP) and sympathetic adrenergic influences was examined. Using urethan-anesthetized rabbits, we tested the effects of CGRP and its antagonist CGRP-(8-37) by topical application of these agents to the exposed knee while sympathetic influences were tested by electrically stimulating the saphenous nerve. It was found that MCL basal perfusion was elevated in ACL-sectioned joints; however, this effect was abrogated by prior resection of the articular nerve supply. At the doses tested, the normal vasodilator response to CGRP was abolished in ACL-sectioned joints, whereas the response to CGRP-(8-37) was attenuated. Even under the influence of increased constrictor tone, MCL and capsule blood vessels still showed substantially reduced responses to exogenous CGRP administration. By contrast, nerve-mediated constrictor responses were mostly unaffected by joint instability. This study suggests that posttraumatic knee joint hyperemia is neurogenically mediated, possibly by increased secretion of CGRP. (+info)
(5/956) Endothelial function is impaired in fit young adults of low birth weight.
OBJECTIVE: Non-insulin-dependent diabetes, hypertension and ischaemic heart disease, with insulin resistance, are associated with low birth weight (the 'Small Baby Syndrome'). Common to these adult clinical conditions is endothelial dysfunction. We tested the hypothesis that endothelial dysfunction could precede their development in those of low birth weight. METHODS: Endothelial function was measured by ultrasonic 'wall-tracking' of flow-related brachial artery dilatation in fit 19-20 year old subjects randomly selected (blind to the investigators throughout the study) from low (< 2.5 kg) and normal (3.0-3.8 kg) birth weight subjects in the 1975-7 cohort of the Cardiff Births Survey and with no known cause for endothelial dysfunction. RESULTS: Flow-related dilatation was impaired in low birth weight relative to normal birth weight subjects (median 0.04 mm [1.5%] [n = 22] cf. 0.11 mm [4.1%] [n = 17], p < 0.05; 0.04 mm [1.5%] [n = 15] cf. 0.12 mm [4.4%] [n = 12], p < 0.05 after exclusion of inadvertently included ever-smokers). CONCLUSION: The findings suggest that endothelial dysfunction is a consequence of foetal malnutrition, consistent with contributing to the clinical features of the 'Small Baby Syndrome' in later adult life. (+info)
(6/956) The association between laser Doppler reactive hyperaemia curves and the distribution of peripheral arterial disease.
OBJECTIVES: To determine whether postocclusive laser Doppler fluxmetry (LDF) curves can be related to the arteriographic distribution of disease. DESIGN: Prospective study. MATERIALS: Sixty-nine patients with symptomatic peripheral ischaemia and 15 healthy subjects. METHODS: Laser Doppler fluxmetry (LDF) was monitored on the dorsum of the symptomatic foot following 2 min of arterial occlusion at the ankle. During reperfusion three patterns of LDF were identified (types I-III). All patients subsequently underwent arteriography which was reported independent of LDF results. The distribution of disease, particularly patency of below-knee vessels, was related to the type of LDF curve observed during reactive hyperaemia. RESULTS: Type I curves were observed in all healthy subjects and 75% of patients with a single arterial lesion. Type II curves were found in 78% of patients with multiple lesions above the knee. The presence of either a type I or II curve was associated with a continuous vessel from knee to ankle (positive predictive value 83%, p < 0.01), whilst type III curve was associated with discontinuous infrapopliteal run-off (positive predictive value 86%, p < 0.01). CONCLUSIONS: This pilot study suggests that post-occlusive LDF curves may identify the distribution of arterial disease and may be useful in the non-invasive management of peripheral ischaemia. (+info)
(7/956) Inhibition of phospholipase A2 attenuates functional hyperemia in the hamster cremaster muscle.
Arachidonic acid (AA) is the common precursor for several vasodilatory factors involved in the local control of blood flow. This study was designed to determine the role of phospholipase A2 (PLA2) and AA release in functional hyperemia in the hamster cremaster muscle. The muscle was prepared for in vivo microscopy and subjected to electrical field stimulation for 1 min. First- and second-order arterioles dilated in response from a mean diameter of 66 +/- 5 to 88 +/- 7 micrometer (n = 6). PLA2 was then inhibited with quinacrine (3 x 10(-6) M) for 60 min. PLA2 inhibition was verified by an attenuation of thrombin-induced vasodilation (2 U/ml). Quinacrine had no effect on resting arteriolar diameter but completely abolished functional hyperemia. Quinacrine also had no effect on dilation induced by superfusion of the preparation with 3 x 10(-6)-10(-5) M AA, 10(-6)-10(-4) M adenosine, or 10(-6)-10(-4) M sodium nitroprusside, ruling out nonspecific effects of quinacrine on smooth muscle contractility. These results indicate that functional hyperemia in the hamster cremaster muscle is dependent on PLA2 activation and the availability of AA. (+info)
(8/956) Abnormalities of vascular endothelial function may contribute to increased coronary heart disease risk in UK Indian Asians.
OBJECTIVE: To test the hypothesis that abnormalities of endothelial function are present in Indian Asians and may contribute to their increased coronary heart disease risk. SETTING: Single centre in west London. PATIENTS: 26 Indian Asian and 18 European white healthy male subjects, aged 35 to 61 years recruited from general practice lists. DESIGN: Brachial artery diameter responses to reactive hyperaemia and sublingual glyceryl trinitrate were compared using high resolution ultrasound. RESULTS: Mean (SEM) flow mediated, endothelium dependent dilatation was reduced in Indian Asians compared with European whites, at 3.2 (0.8)% v 5.9 (1.0)%, p = 0.03. In contrast, there were no significant differences in baseline brachial arterial diameter (4.6 (0.1) v 4.6 (0.1) mm, p = 0.65) or glyceryl trinitrate induced dilatation (18.8 (1.5)% v 18.5 (1.7)%, p = 0.90) between Indian Asians and European whites, respectively. Univariate analysis showed that Indian Asian race was significantly associated with impaired flow mediated dilatation (regression coefficient = -2.8 (1.3)%, p = 0.03), and in multivariate analysis, this relation was independent of both conventional coronary heart disease risk factors and markers of insulin resistance. CONCLUSIONS: Endothelial function is impaired in healthy UK Indian Asians compared with European whites, and the defect is not accounted for by major coronary heart disease risk factors. Endothelial function may be modulated by novel risk factors in Indian Asians. (+info)