The Effect of Inhalation of Different Mixtures of O2and CO2on Ocular Fundus Pulsations

Schmetterer, Leopold; Lexer, Franz; Findl, Oliver; Graselli, Ursula; Eichler, Hans‐Georg; Wolzt, Michael

doi:10.1006/exer.1996.0125

Cited by 59 publications

(35 citation statements)

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“…Oxygen breathing has been reported to decrease retinal blood flow by 30% using Heidelberg Retina Flowmeter (Sternn et al, 1997), 36% using blue-field entoptic technique (Fallon et al, 1985), and 60% using LDF (Trokel, 1965;Eperson et al, 1975;Riva et al, 1983). In contrast, inhalation of oxygen has little or no effect on choroidal blood flow in the macular region (Riva et al, 1994;Schmetterer et al, 1995;Schmetterer et al, 1996). Taken together, the measured blood-flow changes by MRI are nonetheless sensitive to changes in retinal vasculature, although basal blood flow is weighted heavily by the high basal blood flow in the choroid which does not vasoreacts to hyperoxia.…”

Section: Hyperoxiamentioning

confidence: 99%

Blood-flow magnetic resonance imaging of the retina

Cheng

Duong

2008

NeuroImage

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This study describes a novel MRI application to image basal blood flow, physiologically induced blood-flow changes, and the effects of isoflurane concentration on blood flow in the retina. Continuous arterial-spin-labeling technique with a separate neck coil for spin labeling was used to image blood flow of the rat retina at 90×90×1500-μm resolution. The average blood flow of the whole retina was 6.3±1.0 ml/g/min under 1% isoflurane, consistent with the high blood flow in the retina reported using other techniques. Blood flow is relatively constant along the length of the retina, except it dipped slightly around the optic nerve head and dropped significantly at the distal edges where the retina terminates. Hyperoxia (100% O 2 ) decreased blood flow 25± 6% relative to baseline (air) due to vasoconstriction. Hypercapnia (5% CO 2 +21% O 2 ) increased blood flow 16±6% due to vasodilation. Increasing isoflurane (a potent vasodilator) concentration to 1.5% increased blood flow to 9.3±2.7 ml/g/min. Blood-flow signals were confirmed to be genuine by repeating measurements after the animals were sacrificed in the MRI scanner. This study demonstrates a proof of concept that quantitative blood flow of the retina can be measured using MRI without depth limitation. Bloodflow MRI has the potential to provide unique insights into retinal physiology, serve as an early biomarker for some retinal diseases, and could complement optically based imaging techniques.

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Section: Hyperoxiamentioning

confidence: 99%

Blood-flow magnetic resonance imaging of the retina

Cheng

Duong

2008

NeuroImage

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“…Using a single mode laser diode the distance changes between cornea and Study protocol retina during the cardiac cycle can be assessed with high accuracy [13]. These changes depend on the pulsatile Study 1 After an overnight fast, all subjects rested for at inflow of arterial blood into the choroidal vasculature of least 20 min in a sitting position to establish a stable the eye [14,15]. The maximum distance change between baseline.…”

Section: G -mentioning

confidence: 99%

Pharmacokinetic‐pharmacodynamic profile of systemic nitric oxide‐synthase inhibition with L‐NMMA in humans

Mayer¹,

Mensik²,

Krishnaswami

et al. 1999

Brit J Clinical Pharma

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Aims It has been demonstrated that inhibition of endothelium derived nitric oxide with N G -monomethyl-l-arginine (l-NMMA) results in a different cardiac and peripheral vascular response. The purpose of this study was to investigate the pharmacokinetic-pharmacodynamic profile of l-NMMA and pharmacokinetic interactions with l-arginine in healthy subjects. Methods Plasma pharmacokinetics were analysed from two different studies: In study 1, 3 mg kg −1 l-NMMA was administered i.v. over 5 min and systemic haemodynamics, cardiac output (CO), fundus pulsation amplitude (FPA), and NO-exhalation (exhNO) were measured at baseline and 15, 65, 95, 155, and 305 min after start of drug administration (n=7). In study 2, 17 mg kg −1 min −1 of the physiologic substrate for nitric oxide synthase, l-arginine, was coinfused i.v. over 30 min with a primed constant infusion of 50 mg kg , drug effects over time were in good agreement with an E max model (r 2 >0.98 each), which also suggested that concentrations producing half-maximum effects were higher for FPA than for CO and exhNO. The coinfusion with l-arginine caused a nearly two-fold increase in plasma l-NMMA levels, indicating a pharmacokinetic interaction. Conclusions In the absence of a systemic hypertensive response, l-NMMA significantly decreased CO, exhNO, and FPA. The concentration calculated to produce a half maximal effect was equivalent for exhNO and CO, but markedly higher for FPA. Furthermore, measurement of FPA is susceptible to changes in l-NMMA levels at small plasma concentrations.

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“…FPA was calculated as the mean of at least five cardiac cycles. To obtain information on the choroidal blood flow, the macula, where the retina lacks vasculature, was chosen for measurements [22].…”

Section: Methodsmentioning

confidence: 99%

Ocular hyperperfusion following onset of intensified insulin therapy is inversely correlated with plasma endothelin-1 in Type I diabetes

et al. 2002

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Aims/hypothesis. It has been reported that improvement of metabolic control by intensified insulin therapy in patients with Type I (insulin-dependent) diabetes mellitus is associated with alterations in ocular blood flow. We hypothesized that these changes in ocular blood flow could be associated with alterations of plasma insulin, glucose or endothelin concentration. Methods. In 16 patients with Type I diabetes ocular haemodynamic parameters were assessed daily during the first 5 days of institution of intensified insulin therapy and plasma concentrations of glucose, insulin, and endothelin-1 plasma were measured. Retinal white blood cell flux was estimated with the blue field entoptic technique. Pulsatile choroidal blood flow was assessed by laser interferometric measurement of fundus pulsation amplitude. Results. Retinal white blood cell flux (p=0.0015) and ocular fundus pulsation amplitude (p<0.001) increased during institution of strict metabolic control. Changes in ocular haemodynamic variables were inversely correlated with concentrations of plasma ET-1, but not with that of insulin or glucose. Conclusions/interpretation. These data indicate that institution of improved metabolic status is paralleled by rapid changes in the production of ET-1, which could in turn affect ocular perfusion. [Diabetologia (2002) aimed to achieve glycaemic control as close as possible to the non-diabetic range [1]. Moreover, the DCCT showed that total lifetime exposure to glycaemia is the principal determinant of the risk of retinopathy [2]. However, shortly after the institution of strict diabetic control some patients show progression of diabetic retinopathy [1,3]. Previous studies indicate that this progression of diabetic retinopathy is associated with changes in retinal blood flow [4,5,6].The reasons for these immediate changes in retinal blood flow and their role in the development of retinopathy are not clear. On the one hand alterations in concentrations of plasma insulin and plasma glucose could affect ocular vascular tone, because insulin and glucose induce vasodilation at the level of the ocular vasculature [7,8,9,10,11,12]. Alternatively the institution of strict metabolic control could exert effects The Diabetes Control and Complications Trial (DCCT) demonstrated a reduction in the development and progression of the long-term complications of Type I diabetes with intensive insulin therapy

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The Effect of Inhalation of Different Mixtures of O2and CO2on Ocular Fundus Pulsations

Cited by 59 publications

References 0 publications

Blood-flow magnetic resonance imaging of the retina

Blood-flow magnetic resonance imaging of the retina

Pharmacokinetic‐pharmacodynamic profile of systemic nitric oxide‐synthase inhibition with L‐NMMA in humans

Ocular hyperperfusion following onset of intensified insulin therapy is inversely correlated with plasma endothelin-1 in Type I diabetes

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