Effect of histamine and cimetidine on retinal and choroidal blood flow in humans

2005 ◽  
Vol 289 (5) ◽  
pp. R1387-R1391 ◽  
Author(s):  
Hemma Resch ◽  
Claudia Zawinka ◽  
Solveig Lung ◽  
Günther Weigert ◽  
Leopold Schmetterer ◽  
...  

Intravenous administration of histamine causes an increase in choroidal blood flow and retinal vessel diameter in healthy subjects. The mechanism underlying this effect remains to be elucidated. In the present study, we hypothesized that H2 receptor blockade alters hemodynamic effects of histamine in the choroid and retina. Eighteen healthy male nonsmoking volunteers were included in this randomized, double-masked, placebo-controlled two-way crossover study. Histamine (0.32 μg·kg−1·min−1 over 30 min) was infused intravenously in the absence (NaCl as placebo) or presence of the H2 blocker cimetidine (2.3 mg/min over 50 min). Ocular hemodynamic parameters, blood pressure, and intraocular pressure were measured before drug administration, after infusion of cimetidine or placebo, and after coinfusion of histamine. Subfoveal choroidal blood flow and fundus pulsation amplitude were measured with laser-Doppler flowmetry and laser interferometry, respectively. Retinal arterial and venous diameters were measured with a retinal vessel analyzer. Retinal blood velocity was assessed with bidirectional laser-Doppler velocimetry. Histamine increased subfoveal choroidal blood flow (+14 ± 15%, P < 0.001), fundus pulsation amplitude (+11 ± 5%, P < 0.001), retinal venous diameter (+3.0 ± 3.6%, P = 0.002), and retinal arterial diameter (+2.8 ± 4.2%, P < 0.01) but did not change retinal blood velocity. The H2 antagonist cimetidine had no significant effect on ocular hemodynamic parameters. In addition, cimetidine did not modify effects of histamine on choroidal blood flow, fundus pulsation amplitude, retinal venous diameter, and retinal arterial diameter compared with placebo. The present data confirm that histamine increases choroidal blood flow and retinal vessel diameters in healthy subjects. This ocular vasodilator effect of histamine is, however, not altered by administration of an H2 blocker. Whether the increase in blood flow is mediated via H1 receptors or other hitherto unidentified mechanisms remains to be elucidated.

1998 ◽  
Vol 76 (4) ◽  
pp. 418-427 ◽  
Author(s):  
J K Shoemaker ◽  
M E Tschakovsky ◽  
R L Hughson

The hypothesis that the rapid increases in blood flow at the exercise onsetare exclusively due to the mechanical effects of the muscle pump was tested in six volunteersduring dynamic handgrip exercise. While supine, each subject completed a series of eightdifferent exercise tests in which brachial artery blood pressure (BP) was altered by25–30 mmHg (1 mmHg = 133.3 Pa) by positioning the arm above or below the heart.Two different weights, corresponding to 4.9 and 9.7% of maximal voluntary isometriccontraction, were raised and lowered at two different contraction rate schedules (1s:1s and 2s:2swork–rest) each with a 50% duty cycle. Beat-by-beat measures of mean blood velocity (MBV)(pulsed Doppler) were obtained at rest and for 5 min following step increases in work ratewith emphasis on the first 24 s. MBV was increased 50–100% above rest following the firstcontraction in both arm positions (p < 0.05). The increase in MBV from rest was greaterin the below position compared with above, and this effect was observed following the first andsubsequent contractions (p < 0.05). However, the positional effect on the increase inMBV could not be explained entirely by the ~40% greater BP in this position. Also, the greaterworkload resulted in greater increases in MBV as early as the first contraction, compared withthe light workload (p < 0.05) despite similar reductions in forearm volume followingsingle contractions. MBV was greater with faster contraction rate tests by 8 s of exercise. Itwas concluded that microvascular vasodilation must act in concert with a reduction in venouspressure to increase forearm blood flow within the initial 2–4 s of exercise.Key words: Doppler, mean blood velocity, arterial diameter,handgrip exercise, perfusion pressure.


1995 ◽  
Author(s):  
Charles E. Riva ◽  
Benno L. Petrig ◽  
Mark J. Mendel ◽  
Stephen D. Cranstoun

2011 ◽  
Vol 92 (6) ◽  
pp. 545-551 ◽  
Author(s):  
C. Strohmaier ◽  
R.M. Werkmeister ◽  
B. Bogner ◽  
C. Runge ◽  
F. Schroedl ◽  
...  

2020 ◽  
Author(s):  
Lawrence Labrecque ◽  
Jonathan Smirl ◽  
Patrice Brassard

Hysteresis in the cerebral pressure-flow relationship describes the superior ability of the cerebrovasculature to buffer cerebral blood flow changes when mean arterial pressure (MAP) acutely increases compared to when it decreases. This phenomenon can be evaluated by comparing the relative change in middle cerebral artery mean blood velocity (MCAv) per relative change in MAP (%ΔMCAv/%ΔMAP) during either acute increases or decreases in MAP induced by repeated squat-stands (RSS). However, no real baseline can be employed for this particular protocol as there is no true stable reference point. Herein, we characterized the %ΔMCAv/%ΔMAP metric using the greatest MAP oscillations induced by RSS without using an independent baseline value. We also examined whether %ΔMCAv/%ΔMAP during each RSS transition were comparable between each other over the 5-min period. %ΔMCAv/%ΔMAP was calculated using the minimum to maximum MCAv and MAP for each RSS performed at 0.05 Hz and 0.10 Hz. We compared averaged %ΔMCAv/%ΔMAP during MAP increases and decreases in 74 healthy subjects [9 women; 32 ± 13 years]. %ΔMCAv/%ΔMAP was lower for MAP increases than MAP decreases (0.05 Hz: 1.25 ± 0.22 vs. 1.35 ± 0.27 %/%, p<0.0001; 0.10Hz: 1.31 ± 0.24 vs. 1.60 ± 0.50 %/%, p<0.0001). For both frequency and MAP direction, time during RSS had no effect on %ΔMCAv/%ΔMAP. This novel analytical method supports the use of the RSS model to evaluate the directional behavior of the pressure-flow relationship. These results contribute to the importance of considering the direction of MAP changes when evaluating dynamic cerebral autoregulation.


2012 ◽  
Vol 38 (1) ◽  
pp. 158-167 ◽  
Author(s):  
Simon Hétu ◽  
Mylène Pouliot ◽  
Ghassan Cordahi ◽  
Réjean Couture ◽  
Elvire Vaucher

2001 ◽  
Vol 91 (5) ◽  
pp. 2359-2365 ◽  
Author(s):  
Amit Anand ◽  
Stacia Remsburg-Sailor ◽  
Sandrine H. Launois ◽  
J. Woodrow Weiss

The mechanisms by which obstructive apneas produce intermittent surges in arterial pressure remain poorly defined. To determine whether termination of obstructive apneas produce peripheral vasoconstriction, we assessed forearm blood flow during and after obstructive events in sleeping patients experiencing spontaneous upper airway obstructions. In all subjects, heart rate was monitored with an electrocardiogram and blood pressure was monitored continuously with digital plethysmography. In 10 patients ( protocol 1), we used forearm plethysmography to assess forearm blood flow, from which we calculated forearm vascular resistance by performing venous occlusions during and after obstructive episodes. In an additional four subjects, we used simultaneous Doppler and B-mode images of the brachial artery to measure blood velocity and arterial diameter, from which we calculated brachial flow continuously during spontaneous apneas ( protocol 2). In protocol 1, forearm vascular resistance increased 71% after apnea termination (29.3 ± 15.4 to 49.8 ± 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In protocol 2, brachial resistance increased at apnea termination in all subjects (219.8 ± 22.2 to 358.3 ± 46.1 mmHg · l−1 · min; P = 0.01). We conclude that termination of obstructive apneas is associated with peripheral vasoconstriction.


PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e60424 ◽  
Author(s):  
Reinhard Told ◽  
Stefan Palkovits ◽  
Helmuth Haslacher ◽  
Sophie Frantal ◽  
Doreen Schmidl ◽  
...  

1996 ◽  
Vol 13 (4) ◽  
pp. 655-669 ◽  
Author(s):  
Malinda E. C. Fitzgerald ◽  
Paul D. R. Gamlin ◽  
Yuri Zagvazdin ◽  
Anton Reiner

AbstractElectrical stimulation in pigeons of the input from the medial subdivision of the nucleus of Edinger-Westphal (EWM) to the choroidal neurons of the ipsilateral ciliary ganglion, which themselves have input to the choroidal blood vessels of the ipsilateral eye, increases choroidal blood flow (ChBF). Since the EWM receives input from the contralateral suprachiasmatic nucleus (SCN), which in turn receives contralateral retinal input, the present study sought to determine if activation of the SCN by microstimulation or by retinal illumination of the contralateral eye would also yield increases in ChBF in that same eye. Using laser Doppler flowmetry (LDF) to measure ChBF, we found that electrical activation of the contralateral SCN by 100-Hz anodal pulse trains yielded increases in ChBF that were stimulus related and proportional to the stimulating current. These increases in ChBF elicited by the SCN stimulation were accompanied by increases in choroidal volume (vasodilation), but not by increases in systemic blood pressure. Furthermore, the increases could be blocked reversibly by lidocaine injection into the EWM. These results suggest that the increases in ChBF in the eye contralateral to the SCN stimulation were specifically mediated by the SCN-EWM pathway. Retinal illumination with a fiber optic light source was also found to increase ChBF in the illuminated eye, and these effects too could be blocked reversibly with lidocaine injection into the EWM or permanently by the EWM lesion. Control studies confirmed that the light-elicited increases were mediated by increases in choroidal volume (i.e. vasodilation), were not accompanied by systemic blood pressure increases, and were not artifactually generated by transocular illumination of the LDF probe. Thus, the SCN-EWM circuit may be involved in regulating ChBF in response to the level of retinal illumination and/or the visual patterns falling on the retina.


2019 ◽  
Vol 10 (10) ◽  
pp. 4942 ◽  
Author(s):  
Léo Puyo ◽  
Michel Paques ◽  
Mathias Fink ◽  
José-Alain Sahel ◽  
Michael Atlan

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