Strain Gauge Plethysmography in the Study of Circulation of the Limbs

Forconi, S; Jageneau, A; Guerrini, M; Pecchi, S.; Cappelli, Roberto

doi:10.1177/000331977903000707

Cited by 21 publications

(9 citation statements)

References 20 publications

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“…After a blood pressure cuff at the right ankle had been inflated to 200 mmHg and had rendered the sole of the foot temporarily ischemic, a thigh blood pressure cuff was inflated additionally to 40 mmHg for 2 min, while the change in lower limb volume was recorded. CVC was defined as volume increase (ml/100 ml) [2,3,12]. CVC was …”

Section: Protocolmentioning

confidence: 99%

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

et al. 2006

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Patients with multiple system atrophy (MSA) often have clinically significant postprandial hypotension (PPH). To elucidate the cause of insufficient cardiac preload augmentation that underlies PPH, we recorded calf venous capacitance (CVC) by strain-gauge plethysmography, in 17 MSA patients and eight healthy controls before and after oral glucose ingestion. Among 17 MSA patients, nine who showed a decrease in systolic blood pressure exceeding 20 mmHg and were diagnosed with PPH. MSA patients without PPH showed a significant decrease in CVC and a significant increase in cardiac output after oral glucose ingestion, as did controls; those with MSA exhibiting PPH showed a significant increase in CVC and no significant change in cardiac output. The change in CVC correlated positively with the decrease in systolic and diastolic blood pressure after glucose ingestion, and also correlated negatively with the increase in cardiac output. Physiologically, PPH is prevented by a decrease in venous capacitance, which increases circulating blood volume and cardiac output. In some MSA patients, failure of venous capacitance to decrease may induce PPH.

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Section: Protocolmentioning

confidence: 99%

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

et al. 2006

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“…Pregnancy and oral contraceptive ther apy produce a significant decrease in venous tone which results in a decrease of the linear velocity of venous blood flow [19], It is doubtful that this was a contributing factor to the differences in our experiments because the venous occlusion period (6 s) was shorter than that required to result in venous conges tion [9], There are several ways in which sex hor mones and oral contraceptives could alter blood flow responses [see refs 17 and 20 for review]: (1) by altering the contraction-relax ation mechanisms of the vascular smooth muscle; (2) by changing the morphology of the vascular wall; (3) by influencing the level and activity of circulating humoral agents, and/or (4) by altering the nervous input to the blood vessels. Since the mechanism of reactive hyperemia probably includes myo genic and metabolic components [2], all of these factors could contribute to the differ ences in blood flow observed between males, untreated females and females receiving oral contraceptive therapy.…”

Section: Discussionmentioning

confidence: 76%

“…This maximum blood flow response corresponded to the first flow recorded after the release of occlusion at all periods of arrest. Since the magnitude of resting forearm blood flow may be an important determinant of the hyperemic response [3], the peak flow was normalized in terms of preocclusion blood flow values [peak flow/rcsting flow quotient (9)]. The duration of the reactive hyperemia was taken as the time at which the reactive hyperemia curve came closest to the preocclusion level of blood flow.…”

Section: Methodsmentioning

confidence: 99%

Influence of Sex Difference and Oral Contraceptives on Forearm Reactive Hyperemia

1981

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Experiments were performed on normal male and female subjects to compare blood flow responses following release of an arterial occlusion (reactive hyperemia). Additionally, the effects of oral contraceptive therapy on the reactive hyperemia reaction were studied in female subjects. Forearm blood flow was measured with a strain-gauge plethysmograph, heart rate with an electrocardiograph, and mean arterial pressure was measured by auscultation. Blood flow was determined before and after circulatory arrest of 1, 3, and 5 min. Blood serum levels of 17β-estradiol, progesterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) were measured by radioimmunoassay. The mean resting forearm blood flow was similar in males and females (∼4 ml/100 ml/min). There were no significant changes in systemic mean arterial pressure or heart rate during the experiments. Following 1 min of arterial occlusion, the peak blood flow responses were similar in males and females. The peak blood flow responses following release of arterial occlusion were lower in males than in untreated females at occlusion intervals of 3 and 5 min. Females receiving oral contraceptives showed reduced peak blood flow responses after circulatory arrest of either 3 or 5 min as compared to untreated females. There were no significant differences in the recovery times of the hyperemic responses between males and females following any of the periods of occlusion. The peak blood flow responses following 3 min of arterial occlusion were significantly correlated with the blood serum levels of 17β-estradiol, LH and FSH, but not with the blood serum levels of progesterone. These results suggest that: (1) sex difference has a marked effect on the blood flow response following arterial occlusion, and (2) hormonal changes influence vascular responsiveness in the female.

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“…Lower limb blood flow at rest was registered at the calf level by venous occlusion strain-gauge plethysmography (Angioflow, Microlab Electronic, Padua, Italy). Flow was expressed as mL of blood perminute per 100 mL of tissue (Whitney 1953;Forconi et al 1979).…”

Section: Studymentioning

confidence: 99%

EVIDENCE OF AN ADENOSINE‐DEPENDENT MECHANISM IN THE HYPOTENSIVE EFFECT OF l‐ARGININE IN MAN

Pasini¹,

Frigerio²,

Blardi³

et al. 1995

Clin Exp Pharma Physio

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1. The hypothesis that endogenous adenosine could play a role in the haemodynamic response to L-arginine is investigated. 2. The study has been divided into two parts. The first part was a single blind, randomized, placebo-controlled study in which L-arginine i.v. infusion (0.07 mmol/kg per min) in five healthy volunteers caused a significant fall in systolic (-14.2%, from 129.0 +/- 8.2 to 110.6 +/- 8.5 mmHg; F = 62.89, P < 0.01), diastolic (-16%, from 80.0 +/- 7.9 to 67.2 +/- 7.0 mmHg; F = 18.97, P < 0.01) and mean (-15.5%, from 96.4 +/- 6.7 to 81.4 +/- 6.5 mmHg; F = 28.78, P < 0.01) arterial blood pressure, with a concomitant increase of plasma adenosine concentration (from 244.0 +/- 32.2 to 637.0 +/- 43.4 nmol/L; F = 79.3 P < 0.01). Maximal effects were obtained at the end of L-arginine infusion: haemodynamic parameters returned to basal values in about 30 min while adenosine concentrations normalized in about 15 min. Saline infusion had no effect on these parameters. 3. In the second study the effect of L-arginine i.v. infusion on arterial blood pressure, lower limb blood flow and plasma adenosine, before and after theophylline treatment (1000 mg/day for 3 days, p.o.) was examined.(ABSTRACT TRUNCATED AT 250 WORDS)

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Strain Gauge Plethysmography in the Study of Circulation of the Limbs

Cited by 21 publications

References 20 publications

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

Altered venous capacitance as a cause of postprandial hypotension in multiple system atrophy

Influence of Sex Difference and Oral Contraceptives on Forearm Reactive Hyperemia

EVIDENCE OF AN ADENOSINE‐DEPENDENT MECHANISM IN THE HYPOTENSIVE EFFECT OF l‐ARGININE IN MAN

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