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Biomedical subjects

M Wolzt

Publications and source records attributed to M Wolzt.

At least 55 records · Page 3Linked to original sources
PubMed1999

Systemic NO synthase inhibition blunts the chronotropic, but not the inotropic response to isoprenaline in man.

There is evidence that nitric oxide (NO) is involved in the chronotropic, the inotropic, and the vasodilator response to beta-adrenoceptor agonists. In the present study we hypothesized that inhibition of NO synthase may modulate the systemic vascular and cardiac effects of isoprenaline, a beta-adrenoceptor agonist, in healthy subjects. Subjects received stepwise increasing doses of isoprenaline (0.1-0.8 microg/min) in the absence or presence of systemic NO-synthase inhibition using two intravenous doses of N-monomethyl-L-arginine (L-NMMA; dosage 1, 3.0 mg/kg over 5 min, followed by 30 microg/kg/min over 75 min; dosage 2, 6.0 mg/kg over 5 min, followed by 60 microg/kg/min over 75 min) or peripheral vasoconstriction using exogenous endothelin-1 (ET-1; 5.0 ng/kg/min for 80 min). The chronotropic (RR interval) and the inotropic (QS2c) responses were assessed by noninvasive measurement of systolic time intervals. L-NMMA alone did not influence QS2c, but did increase the RR interval (P < 0.001) and the mean arterial blood pressure (P = 0.003). L-NMMA did not attenuate the blood pressure and the QS2c responses to isoprenaline, but significantly and dose-dependently blunted the heart rate response to beta-adrenoceptor stimulation (P = 0.029). ET-1 decreased the RR interval (P < 0.001) and increased the mean arterial blood pressure (P = 0.028). Our results indicate that beta-adrenoceptor mediated effects on the heart rate are much more susceptible to NOS inhibition than inotropic responses. This indicates that NO has an important role in heart rate control during beta-adrenoceptor stimulation.

Adult↗
PubMed1999

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

AIMS: It has been demonstrated that inhibition of endothelium derived nitric oxide with NG-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 microg kg-1 min-1 L-NMMA (n=8). RESULTS: Bolus infusion of L-NMMA resulted in a maximum plasma concentration of 12. 9+/-3.4 microg ml-1 (mean+/-s.d.) with elimination half-life of 63. 5+/-14.5 min and clearance of 12.2+/-3.5 ml min-1 kg-1 and caused a small hypertensive response, decreased CO by 13%, FPA by 26%, exhNO by 46% and increased systemic vascular resistance by 16% (P<0.05 each) 15 min after start of drug administration. Although only limited data points were available in the L-NMMA plasma concentration range between 0 and 4 microg ml-1, drug effects over time were in good agreement with an Emax model (r2>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.

Adult↗
PubMed1999

Renal hemodynamic effects of L-arginine and sodium nitroprusside in heart transplant recipients.

BACKGROUND: Long-term treatment with cyclosporine A (CsA) induces vasoconstriction in the kidney and causes renal impairment. An altered L-arginine (L-Arg)/nitric oxide (NO) pathway may play a key role in CsA nephrotoxicity. METHODS: We studied the effect of L-Arg (dosage, 17 mg/kg/min over 30 min), the precursor of NO synthesis, and sodium nitroprusside (SNP; dosage, 1.0 microgram/kg/min over 30 min) on renal hemodynamics in a double-blind, placebo-controlled, randomized, three-way cross-over study comprising 12 stable cardiac transplant recipients on long-term CsA treatment, 10 patients with chronic nephropathy not receiving CsA, and 13 healthy controls. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were measured by paraaminohippurate (PAH) and the inulin clearance method, respectively. RESULTS: In healthy subjects, L-Arg induced an increase in RPF (P = 0.009) and GFR (P = 0.001). By contrast, L-Arg did not induce renal hemodynamic effects in heart transplant patients or patients with chronic nephropathy. SNP reduced RPF (P = 0.050) and GFR (P = 0.005) in patients with chronic nephropathy but did not affect renal hemodynamics in heart transplant recipients or in healthy subjects. CONCLUSIONS: These data indicate that L-Arg cannot be used to reverse CsA-induced renal vasoconstriction in heart transplant recipients under long-term CsA treatment, although these patients have a normal renal response to SNP.

Aged↗
PubMed1999

Large amounts of vascular endothelial growth factor at the site of hemostatic plug formation in vivo.

Vascular endothelial growth factor (VEGF) is important for the proliferation, differentiation, and survival of microvascular endothelial cells. It is a potent angiogenic factor and a specific endothelial cell mitogen that increases fenestration and extravasation of plasma macromolecules. Recently, large quantities of VEGF were detected in human megakaryocytes. Incubation of human platelets with thrombin in vitro resulted in the release of large amounts of VEGF. To investigate whether VEGF is released from platelets during coagulation activation in vivo, we measured in human subjects VEGF at the site of plug formation, ie, in blood emerging from a standardized injury made to determine bleeding time (shed blood). VEGF was also determined in the same volunteers after treatment with the specific thrombin inhibitor recombinant hirudin (r-hirudin). In a double-blind, randomized, crossover study, 17 healthy male volunteers (aged 20 to 35 years) were investigated. VEGF concentrations were measured in venous blood and in shed blood by the use of an immunoassay 10 minutes after intravenous administration of r-hirudin (0.35 mg/kg of body weight) or physiological saline. Prothrombin fragment f1.2 (f1.2) and beta-thromboglobulin (beta-TG) were determined as indicators of coagulation and platelet activation, respectively. Concentrations of VEGF, f1.2, and beta-TG in shed blood 4 minutes after injury were significantly higher than in venous blood (VEGF, 55.8+/-9.2 versus <20 pg/mL, P<0.001; f1.2, 71.3+/-10.4 versus 0.78+/-0.03 nmol/L, P<0. 001; beta-TG, 2290+/-170 versus 53.2+/-14.0 ng/mL, P<0.001). Administration of r-hirudin caused a >50% inhibition of the beta-TG and f1.2 levels in shed blood. In a similar manner, much lower amounts of VEGF were detectable at the site of plug formation after r-hirudin treatment (69.0+/-9.5 versus 37.8+/-2.6 pg/mL per minute; P=0.0015). Our data indicate that substantial quantities of VEGF are released from platelets during the interaction with the injured vessel wall in vivo. This finding may be relevant with respect to wound healing and tissue repair, tumor vascularization, or arterial thrombus formation.

Adult↗
PubMed1998

Effect of pituitary adenylate cyclase activating polypeptide 1-27 on ocular, cerebral and skin blood flow in humans.

The aim of the study was to assess the effects of a neuropeptide, pituitary adenylate cyclase activating polypeptide 1-27 (PACAP), on ocular, cerebral and skin blood flow in man. PACAP (0.01-10 pmol kg(-1) min(-1)) was administered intravenously to eight healthy male subjects in a placebo-controlled, double-blind dose escalation trial. Fundus pulsation amplitude was measured by laser interferometry, mean blood flow velocity in the ophthalmic artery and the middle cerebral artery measured by Doppler sonography, and regional blood flow of the skin was estimated by laser Doppler flowmetry. Infusion of PACAP at the highest dose of 10 pmol kg(-1) min(-1) induced a significant increase in fundus pulsation amplitude (+83.4%), mean flow velocity in the ophthalmic artery (+91.9%) and regional skin blood flow (+260.3%, P<0.01, ANOVA; each parameter). In contrast, PACAP did not cause any change in middle cerebral artery blood flow velocity or systemic hemodynamics. Our findings indicate that the vasculatures of the eye and the skin are particularly sensitive to PACAP and may implicate a potential role for this peptide in the regulation of blood flow in these vascular beds.

Adult↗
PubMed1998

Pharmacokinetics of tamsulosin in subjects with normal and varying degrees of impaired renal function: an open-label single-dose and multiple-dose study.

OBJECTIVE: This study was performed to estimate whether the pharmacokinetics and safety of tamsulosin, and alpha(1A)-adrenoceptor antagonist for the treatment of symptomatic benign prostatic hyperplasia (BPH), are influenced by impaired renal function. METHODS: In an open-label study design, the plasma concentration profile of 0.4 mg tamsulosin p.o. was studied in age-matched groups of male subjects with normal (n = 10), moderately impaired (n = 10), and severely impaired (n = 8) renal function after single-dose administration and in steady state, i.e. after 21 days of multiple-dose administration. RESULTS: The AUC of total, but not of unbound, tamsulosin was correlated to creatinine clearance and alpha(1)-acid glycoprotein plasma levels, and was found to be significantly higher in both groups of subjects with impaired renal function than in controls after single- and multiple-dose administration. However, the pharmacokinetics of total and unbound tamsulosin were comparable for both trail periods. CONCLUSIONS: Impaired renal function increases total tamsulosin plasma concentration by approximately 100% after single-dose administration and in steady state. Since active unbound drug levels are not affected, no dose modification is required in symptomatic BPH patients with renal impairment.

Adrenergic alpha-Antagonists↗
PubMed1998

Topical fundus pulsation measurements in age-related macular degeneration.

BACKGROUND: The purpose of the present study was to investigate regional fundus pulsations in age-related macular degeneration (AMD) patients with subretinal neovascular membranes. METHODS: Local fundus pulsation amplitudes (FPAs) were measured in 12 patients with AMD with classic neovascular membranes. Measurements were performed directly on the membrane and adjacent to the membrane. FPAs were assessed with a recently developed laser interferometric method. FPA measurements were performed in 12 healthy subjects at similar posterior pole locations. RESULTS: In AMD patients FPAs were consistently lower when measured directly on the neovascular membrane ("inside") than at measurement sites around the membrane ("outside"). The difference in FPA was 26 +/- 3% (mean +/- SEM, range 13-40%, P < 0.0001). In healthy subjects, however, FPAs were significantly higher at the measurement points corresponding to "inside" points (15 +/- 4%, P < 0.0006). CONCLUSIONS: We have shown that FPAs are reduced at classic neovascular membranes in patients with AMD. The mechanism behind this finding remains unclear. Hence, future studies have to ascertain whether this observation is associated with changes in fundus layers or with local choroidal perfusion abnormalities.

Aged↗
PubMed1998

Reversal of endothelin-1-induced ocular hemodynamic effects by low-dose nifedipine in humans.

BACKGROUND AND PURPOSE: There is evidence that calcium channel blockers may be useful in patients with normal tension glaucoma and vasospastic reactions. We therefore hypothesized that calcium channel blockers may increase ocular blood flow and that there may be a functional antagonism between endothelin-1 (ET-1) and calcium channel blockers in the ocular vasculature. METHODS: This was a randomized, double-blind, three-way crossover study with respect to ET-1 infusions (placebo, 2 ng/kg/min ET-1, and 4 ng/kg/min ET-1) and a randomized double-blind study in two parallel groups with respect to nifedipine (placebo or 5 mg nifedipine). Ocular hemodynamics in the 12 healthy subjects participating in the study was assessed by laser interferometric measurement of fundus pulsation amplitude (FPA) in the optic disc and two-dimensional scanning laser Doppler flowmetry in the optic disc. RESULTS: ET-1 caused a dose-dependent decrease in FPA and flow. With a dose of 4 ng/kg/min a decrease of -18% +/- 5% (p < 0.001) and -17% +/- 5% (p = 0.023) on FPA and flow, respectively, were observed. This effect was completely reversed by nifedipine compared with placebo (FPA, p < 0.001; flow, p = 0.011). However, nifedipine did not affect ocular hemodynamics after placebo infusion. CONCLUSIONS: These results show that nifedipine does not increase optic nerve head blood flow during baseline conditions but reverses ET-1-induced constriction in ocular vasculature at doses that do not affect systemic hemodynamics. This supports the close relation of the therapeutic effect of calcium channel blockers in patients with normal tension glaucoma to the endothelin system. Moreover, the present study provides a strong rationale for a study of low dose nifedipine as a supplementary medication in glaucoma patients.

Adult↗
PubMed1998

Hemodynamic effects of continuous urodilatin infusion: a dose-finding study.

OBJECTIVE: To evaluate the effects of urodilatin (INN, ularitide) on systemic and renal hemodynamic parameters. METHODS: Twenty healthy male subjects were included in this double-blind, randomized placebo-controlled trial and assigned to receive either continuous intravenous infusion of different doses of 7.5, 15, or 22.5 ng/kg body weight/min urodilatin or placebo over 300 minutes. Cardiac performance, systolic time intervals, and airway function were measured noninvasively. The effects on renal hemodynamic values were assessed with para-aminohippurate and inulin clearance techniques. RESULTS: Urodilatin was well tolerated by all subjects at doses of 7.5 and 15 ng/kg/min. Infusion was stopped prematurely for the group that received 22.5 ng/kg/min urodilatin group because of systemic hypotensive responses with nausea and dizziness. Infusion of 15 ng/kg/min urodilatin significantly increased urine flow by a maximum of 165%, filtration fraction by 46%, renal resistance by 49%, and systemic vascular resistance by 45%. It decreased renal plasma flow by a maximum of 31% from baseline value. No change in cardiac inotropic function was detectable, but cardiac output decreased in all dose groups. Effects on glomerular filtration rate, forced expiratory volume, blood pressure, and pulse were not different from those with placebo. CONCLUSION: Continuous infusion of 7.5 ng/kg/min and 15 ng/kg/min urodilatin exerts a significant increase in systemic and renal vascular resistance. Results of our experiments suggested that the therapeutic window for continuous urodilatin infusion is small and that doses higher than approximately 20 ng/kg/min urodilatin carry high risk for adverse drug reactions.

Adult↗
PubMed1998

Role of nitric oxide in exercise-induced vasodilation in man.

Nitric oxide (NO) is a potent endothelium-derived vasodilator, which is known to play an important role in the regulation of resting vascular tone in animals and humans. However, the degree to which NO is involved in exercise-induced vasodilation in the skeletal muscle remains unclear. We studied the effect of N-monomethyl-L-arginine (L-NMMA) in a randomized, double-blind, placebo controlled cross over study in 16 young, healthy volunteers ( 8 male, 8 female) at rest and during bicycle exercise stress test. L-NMMA was given as a bolus of 3 mg/kg over 5 minutes followed by a continuous i.v. infusion of 50 microg/kg/min over 75 minutes. Subjects underwent a symptom-limited graded bicycle stress test with a 25 Watt increase in workload every 5 minutes. Skin and muscle blood flow were measured by laser Doppler flowmetry. L-NMMA slightly increased mean arterial blood pressure and decreased NO exhalation, but had no effect on pulse rate, oxygen consumption (VO2), skin or muscle blood flow at rest. Moreover, L-NMMA exerted no effect on exercise-induced changes in hemodynamics. Our results suggest that submaximal inhibition of NO-synthase with L-NMMA at doses that induce moderate hemodynamic changes does not affect exercise induced vasodilation.

Adult↗
PubMed1998

Systemic and renal effects of an ET(A) receptor subtype-specific antagonist in healthy subjects.

1. Endothelins (ETs) might play a pathophysiological role in a variety of vascular diseases. The aim of the present study was to characterize the effects of BQ-123, a specific ET(A) receptor antagonist on systemic and renal haemodynamics in healthy subjects. This was done at baseline and during infusion of exogenous ET-1. 2. The study was performed in a balanced, randomized, placebo-controlled, double blind 4 way cross-over design in 10 healthy male subjects. Subjects received co-infusions of ET-1 (2.5 ng kg(-1) min(-1) for 120 min) or placebo and BQ-123 (15 microg min(-1) for 60 min and subsequently 60 microg min(-1) for 60 min) or placebo. Renal plasma flow (RPF) and glomerular filtration rate (GFR) were assessed by the para-aminohippurate (PAH) and the inulin plasma clearance method, respectively. 3. BQ-123 alone had no renal or systemic haemodynamic effect. ET-1 significantly reduced RPF (-24%, P<0.001) and GFR (-12%, P=0.034). These effects were abolished by co-infusion of either dose of BQ-123 (RPF: P=0.0012; GFR: P=0.020). 4. BQ-123 reversed the renal haemodynamic effects induced by exogenous ET-1 in vivo. This indicates that vasoconstriction in the kidney provoked by ET-1 is predominantly mediated by the ET(A) receptor subtype.

Adult↗
PubMed1998

Exogenous L-arginine does not affect angiotensin II-induced renal vasoconstriction in man.

AIMS: It has been suggested that provision of the substrate of nitric oxide (NO) synthesis, L-arginine, might influence the effects of renal vasoconstrictors. We have therefore studied the effects of pretreatment or concomitant administration of L-arginine on angiotensin II (ANG II)-increased renovascular resistance. METHODS: The study was conducted in a double-blind, randomized, cross-over design. Eight healthy subjects were assigned to placebo or a continuous intravenous coinfusion of ANG II (5.0 ng kg[-1] min[-1], infusion period 75 min) with L-arginine (17 mg kg[-1] min[-1], infusion period 30 min). Nine further subjects received a continuous infusion of ANG II with or without pretreatment of L-arginine. Changes in renal plasma flow (RPF) were estimated by the steady state clearance of PAH. RESULTS: L-arginine alone increased RPF to 110 +/- 10% over baseline (P < 0.003). The ANG II-induced decrease in RPF was not affected by pretreatment or coinfusion of L-arginine. CONCLUSIONS: Our results demonstrate that a counterregulatory response of the renal vasculature to high levels of ANG II does not depend on exogenous L-arginine. In healthy subjects, this lack of functional antagonism at the renal vasculature is therefore not a result of NO substrate availability.

Adult↗
PubMed1998

Age dependence of choroidal blood flow.

OBJECTIVE: To investigate the age dependence of choroidal blood flow. DESIGN: A cross-sectional study. SETTING: Department of Clinical Pharmacology, Vienna University. PARTICIPANTS: A total of 130 healthy volunteers between the ages of 19 and 83 years. MEASUREMENTS: Fundus pulsation amplitude (FPA) with a recently developed laser interferometric method, mean arterial pressure (MAP) with an automated oscillometric device, intraocular pressure (IOP) with an applanation tonometer, and ocular perfusion pressure (OPP) as calculated from MAP and IOP. RESULTS: There was a significant correlation of FPA with age r = -0.242 (P = .005). MAP, IOP, and OPP showed a significant positive correlation with age. Multiple regression analysis showed that FPA is associated with age but not with MAP, IOP, or OPP. CONCLUSION: Choroidal blood flow is reduced in older subjects, which argues in favor of an increase in ocular vascular resistance with age. This may be a risk factor in the development of common ocular diseases such as age-related macular degeneration or glaucoma.

Adult↗
PubMed1998

Short-term oral pentoxifylline use increases choroidal blood flow in patients with age-related macular degeneration.

OBJECTIVE: To study the ocular hemodynamic effects of a 3-month oral treatment with pentoxifylline in patients with nonexudative age-related macular degeneration. DESIGN: Double-blind, placebo-controlled, randomized, parallel group study. SETTING: Outpatient clinic of the Department of Ophthalmology, Vienna University, Vienna, Austria, that specializes in age-related macular degeneration. METHODS: Forty patients with age-related macular degeneration received pentoxifylline (400 mg 3 times a day orally, n=20) or placebo (n=20) for 3 months. Retinal blood flow was assessed by scanning laser Doppler flowmetry and pulsatile choroidal blood flow was assessed by laser interferometric measurement of fundus pulsation amplitude. MAIN OUTCOME MEASURES: Changes in retinal blood flow and fundus pulsation amplitude. RESULTS: Four patients receiving pentoxifylline and 3 patients receiving placebo discontinued medication because of nausea. In the remaining subjects, the use of pentoxifylline increased ocular fundus pulsation amplitude (P<.001 vs placebo and baseline). The maximum increase was 28% after 3 months. In contrast, retinal blood flow was not changed by the use of pentoxifylline. CONCLUSIONS: A 3-month course of oral pentoxifylline treatment increases choroidal but not retinal blood flow in patients with age-related macular degeneration. These data strongly support the concept that pentoxifylline might be useful in the treatment of age-related macular degeneration. Long-term clinical outcome trials are now warranted to test this hypothesis.

Administration, Oral↗
PubMed1998

Noninvasive investigations of the normal ocular circulation in humans.

PURPOSE: To compare the reproducibility of laser interferometric measurements of fundus pulsation, pneumatonometric measurement of pulse amplitude (PA) and pulsatile ocular blood flow (POBF), and Doppler ultrasonic measurements of blood flow velocity in the ophthalmic artery (OA) and the posterior ciliary arteries (PCAs) and to investigate the association of the results obtained with these methods and to characterize ocular hemodynamics during Valsalva maneuver and isometric handgrip. METHODS: All studies were performed in healthy subjects. Fundus pulsation (n = 48), POBF (n = 24), and blood flow velocities (n = 24) were measured at baseline and during the Valsalva maneuver and isometric handgrip. Intraclass correlation coefficients were calculated for test/retest variability, for short-term variability, and for interobserver variability. RESULTS: Intraclass correlation coefficients were between 0.95 and 0.98 for fundus pulsation measurements, between 0.54 and 0.76 for pneumatonometric measurements, between 0.44 and 0.88 for Doppler sonographic measurements in the OA and between 0.32 and 0.60 in the PCAs. There was a high degree of association between pneumatonometric parameters and fundus pulsation amplitude. Valsalva maneuver significantly reduced fundus pulsations, PA, and POBF, whereas isometric handgripping did not change these parameters. CONCLUSIONS: The reproducibility of fundus pulsation measurements was excellent. Reproducibility of pneumatonometric parameters and ultrasonographic measurements in the OA was satisfactory. Reproducibility of ultrasonographic measurements in the PCAs was low. Data obtained during the autonomic stimuli experiments argue against the sole use of systems to measure pulsatile blood flow, if no additional data on flow pulsatility are available. At least in cases when changes in blood pressure are likely to occur the ratio of pulsatile to nonpulsatile blood flow might not be constant and POBF might not be an adequate measure of total ocular blood flow.

Adult↗
PubMed1997

The effect of systemic nitric oxide-synthase inhibition on ocular fundus pulsations in man.

There is experimental evidence that endothelium derived nitric oxide is involved in the regulation of ocular vascular tone. The purpose of this study was to investigate the effects of NO-synthase inhibition by N-monomethyl-L-arginine (L-NMMA) on ocular fundus pulsations in young healthy volunteers. Three milligrams per kilograms L-NMMA were administered i.v. over 5 minutes. Protocol 1: Measurements of blood pressure, pulse rate, fundus pulsation amplitude, NO-exhalation, and cardiac output were performed at baseline and 10, 30, 60, 90, 150, and 300 minutes after L-NMMA infusion (n = 8). Fundus pulsation amplitude, which has been shown to estimate the pulsatile component of the choroidal blood flow, was recorded with a recently developed laser interferometer. Protocol 2: Measurements of blood pressure, pulse rate, fundus pulsation amplitude, NO-exhalation, and blood flow velocity in the ophthalmic artery were performed in a randomized, placebo controlled cross over study (n = 10). Ten minutes after L-NMMA administration fundus pulsation amplitude decreased by 23 +/- 2% (protocol 1) and 19 +/- 1% (protocol 2, P < 0.01 each), cardiac output by 12 +/- 2% (P < 0.01), and exhaled NO by 55 +/- 6% (protocol 1) and 41 +/- 6% (protocol 2, P < 0.01 each). All parameters returned to baseline values within the 300 minutes observation period, with a faster recovery of fundus pulsation amplitude than of cardiac output and exhaled NO. Blood pressure, pulse rate, and ophthalmic artery blood flow velocity showed only minor changes during and after administration of L-NMMA. Our results suggest that systemic NO-synthase inhibition reduces pulsatile choroidal and most likely total choroidal blood flow in humans. The recovery of vascular tone in choroidal vessels seems to be different from the cardiovascular response. Our findings indicate that reduced fundus pulsations after L-NMMA are caused by systemic factors as well as by local reactions of the choroidal vasculature.

Adult↗
PubMed1997

Fundus pulsation measurements in diabetic retinopathy.

BACKGROUND: There is experimental evidence that retinal blood flow is impaired in patients with diabetes mellitus. Much less attention has been paid to choroidal blood flow. Hence it was the aim of the present study to investigate choroidal blood flow in diabetic retinopathy. METHODS: A new non-invasive laser interferometric technique was used to measure fundus pulsations in the macula. The fundus pulsation amplitude, which is the maximum distance change between cornea and retina during the cardiac cycle, is a measure of local pulsatile blood flow. The eyes (n = 214) were divided into four groups according to the modified Airlie House classification: (1) no retinopathy (control group), (2) background retinopathy, (3) moderate to severe preproliferative retinopathy, (4) proliferative retinopathy. In 83 eyes of different group fundus pulsation measurements were repeated after 1-6 weeks. RESULTS: Fundus pulsation amplitudes were significantly smaller in group 4 than in the control group (P < 0.027). The reproducibility of the measurements was high and did not differ among the study groups. CONCLUSIONS: Local fundus pulsations in the macula are reduced in proliferative diabetic retinopathy, which is compatible with previous findings of reduced choroidal blood flow in late stages of the disease. Laser interferometric measurement of fundus pulsations is non-contactile, assures optimal comfort for the patient and could be used for the long-term observation of patients with diabetes mellitus.

Adult↗