Role of the wrist cuff in forearm plethysmography

1991 ◽  
Vol 80 (5) ◽  
pp. 413-417 ◽  
Author(s):  
Jacques Lenders ◽  
Geert-Jan Janssen ◽  
Paul Smits ◽  
Theo Thien
Keyword(s):  
Blood Flow ◽  
Room Temperature ◽  
Forearm Blood Flow ◽  
Large Range ◽  
Cuff Pressure ◽  
Venous Pressure ◽  
Systolic Pressure ◽  
Ambient Temperatures ◽  
The Difference

1. To determine whether a wrist cuff is necessary to measure the forearm blood flow correctly, we studied the effects of wrist cuff inflation to supra-venous and supra-systolic pressure values over a large range of forearm blood flow values: in the basal state, during post-occlusive hyperaemia of the hand, and during heating of the hand with warm air. Eleven healthy men participated, and the study was carried out at two different ambient temperatures of 20 and 25°C. 2. In the basal state, the measured forearm blood flow was lowest with the wrist cuff at supra-systolic pressure. With the wrist cuff at supra-venous pressure the forearm blood flow was also lower than with an uninflated cuff, but only significantly so when the basal forearm blood flow was higher (at a room temperature of 25°C). 3. During post-occlusive hyperaemia, inflating the wrist cuff to supra-systolic pressure produced the lowest forearm blood flow value at both room temperatures. In addition, with the wrist cuff at supra-venous pressure, forearm blood flow values were lower than with the uninflated cuff, but the supra-venous cuff pressure was clearly less efficient in excluding the hand blood flow than the supra-systolic cuff pressure. 4. During heating of the hand, both supra-systolic and supra-venous cuff pressures were effective in excluding the hand blood flow at both room temperatures. The forearm blood flow measured with the wrist cuff at supra-systolic pressure was lower than that measured with the wrist cuff at supra-venous pressure, but the difference was only significant at a room temperature of 20°C. 5. In conclusion, we have demonstrated that a wrist cuff at supra-systolic pressure is most appropriate for the exclusion of the hand circulation in order to measure the forearm blood flow correctly.

The Effect of Caffeine on Digital Haemodynamics

1994 ◽  
Vol 19 (3) ◽  
pp. 301-302 ◽  
Author(s):  
B. BARTON ◽  
J. M. KLEINERT
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Room Temperature ◽  
Systolic Pressure ◽  
Middle Finger ◽  
Distal Phalanx ◽  
Normal Volunteers ◽  
Pulse Volume ◽  
Digital Pressure ◽  
Digital Blood Flow

Caffeine has been shown to increase mean blood pressure, but studies documenting the effect of caffeine on digits are lacking. We evaluated the effect of caffeine on digital blood pressure and pulse volume in normal volunteers. In the first part of the study, 24 subjects were given water containing either 200 mg of caffeine or placebo. Bilateral brachial and middle finger digital pressures were measured at room temperature before ingestion and at 30 and 60 minutes after ingestion. In the second part of the study, pulse volume recordings (PVRs) were obtained in 24 subjects at the level of the distal phalanx of the middle finger of one hand immediately prior to beverage ingestion and at 10 minute intervals for 90 minutes. Differences in mean digital systolic pressure, digital/brachial index, or PVR amplitude between the control and caffeine groups were not statistically significant. The administration of caffeine was found not to alter the haemodynamics of digital blood flow or digital pressure in this population.

Effect of nerve block on response of forearm blood flow to local temperature

1986 ◽  
Vol 61 (1) ◽  
pp. 227-232 ◽  
Author(s):  
C. B. Wenger ◽  
L. A. Stephenson ◽  
M. A. Durkin
Keyword(s):  
Blood Flow ◽  
Nerve Block ◽  
Forearm Blood Flow ◽  
Brachial Plexus Block ◽  
Thermal Sensation ◽  
Strain Gauges ◽  
Forearm Skin ◽  
Plastic Bag ◽  
Plexus Block

To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27–29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.

Abstract 062: Regulation of Nephron Afferent Arteriole Resistance in Obesity: Role of Connecting Tubule Glomerular Feedback

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Sumit R Monu ◽  
Mani Maheshwari ◽  
Hong Wang ◽  
Ed Peterson ◽  
Oscar Carretero
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Tubuloglomerular Feedback ◽  
Afferent Arteriole ◽  
Connecting Tubule ◽  
Single Nephron ◽  
Renal Micropuncture ◽  
The Difference

In obesity, renal damage is caused by increase in renal blood flow (RBF), glomerular capillary pressure (P GC ), and single nephron glomerular filtration rate but the mechanism behind this alteration in renal hemodynamics is unclear. P GC is controlled mainly by the afferent arteriole (Af-Art) resistance. Af-Art resistance is regulated by mechanism similar to that in other arterioles and in addition, it is regulated by two intrinsic feedback mechanisms: 1) tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to an increase in sodium chloride (NaCl) in the macula densa, via sodium–potassium-2-chloride cotransporter-2 (NKCC2) and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation and is mediated by connecting tubule via epithelial sodium channel (ENaC). CTGF is blocked by the ENaC inhibitor benzamil. Attenuation of TGF reduces Af-Art resistance and allows systemic pressure to get transmitted to the glomerulus that causes glomerular barotrauma/damage. In the current study, we tested the hypothesis that TGF is attenuated in obesity and that CTGF contributes to this effect. We used Zucker obese rats (ZOR) while Zucker lean rats (ZLR) served as controls. We performed in-vivo renal micropuncture of individual rat nephrons while measuring stop-flow pressure (P SF ), an index of P GC. TGF response was measured as a decrease in P SF induced by changing the rate of late proximal perfusion from 0 to 40nl/min in stepwise manner.CTGF was calculated as the difference of P SF value between vehicle and benzamil treatment, at each perfusion rate. Maximal TGF response was significantly less in ZOR (6.16 ± 0.52 mmHg) when compared to the ZLR (8.35 ± 1.00mmHg), p<0.05 , indicating TGF resetting in the ZOR. CTGF was significantly higher in ZOR (6.33±1.95 mmHg) when compared to ZLR (1.38±0.89 mmHg), p<0.05 . When CTGF was inhibited with the ENaC blocker Benzamil (1μM), maximum P SF decrease was 12.30±1.72 mmHg in ZOR and 10.60 ± 1.73 mmHg in ZLR, indicating that blockade of CTGF restored TGF response in ZOR. These observations led us to conclude that TGF is reset in ZOR and that enhanced CTGF contributes to this effect. Increase in CTGF may explain higher renal blood flow, increased P GC and higher glomerular damage in obesity.

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

Haemodynamic Effects of Eating: The Role of Meal Composition

1996 ◽  
Vol 90 (4) ◽  
pp. 269-276 ◽  
Author(s):  
U. Høst ◽  
H. Kelbaek ◽  
H. Rasmusen ◽  
M. Court-Payen ◽  
N. Juel Christensen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Forearm Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Gastric Distension ◽  
Left Ventricular Volumes ◽  
Portal Vein Flow

1. The purpose of this study was to investigate the effect of fractional meal stimulation on postprandial haemodynamic changes, the possible correlation between these changes and the potential mediating role of circulating catecholamines and insulin. 2. Healthy young subjects were studied before and after ingestion of isocaloric, isovolumetric high-protein, carbohydrate or fat meals (80–85% of total energy), 60 kJ per kg of body weight. Multigated radionuclide cardiography with autologous 99mTc-labelled erythrocytes was performed for assessment of cardiac output, venous occlusion plethysmography to obtain forearm blood flow and Doppler-ultrasonography for portal vein flow. Plasma levels of catecholamines and insulin were determined by radioimmunoassay. 3. Cardiac output increased considerably after each meal, including the control meal (water) with only minor differences in extent and timing. Left ventricular volumes increased after food intake, most pronounced after carbohydrate and protein. Forearm blood flow increased only after carbohydrate and protein. Portal vein flow increased after all meals, especially after fat, but also after the control meal. There was a significant correlation between the increment in cardiac output and changes in forearm and portal vein flow, but no correlation between either haemodynamic response and plasma catecholamines or insulin. 4. Postprandial cardiovascular changes are not substantially different after various isocaloric and isovolumic meal compositions. Gastric distension seems to play a role in the increase in cardiac output, accomplished by ventricular dilatation. These changes seem to some extent to be linked to changes in muscle and splanchnic flow.

scholarly journals The role of skin and muscle vessels in the response of forearm blood flow to noradrenaline

1964 ◽  
Vol 173 (1) ◽  
pp. 65-73 ◽  
Author(s):  
C. J. Cooper ◽  
J. D. Fewings ◽  
R. L. Hodge ◽  
G. C. Scroop ◽  
R. F. Whelan
Keyword(s):  
Blood Flow ◽  
Forearm Blood Flow

Inhibition of vascular ATP-sensitive K+channels does not affect reactive hyperemia in human forearm

2003 ◽  
Vol 284 (2) ◽  
pp. H711-H718 ◽  
Author(s):  
H. M. Omar Farouque ◽  
Ian T. Meredith
Keyword(s):  
Blood Flow ◽  
Adaptive Response ◽  
Healthy Subjects ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Venous Occlusion ◽  
Channel Inhibition ◽  
Human Forearm ◽  
Hyperemic Response

The extent to which ATP-sensitive K+ channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K+channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced ( n = 9). The contribution of vascular ATP-sensitive K+ channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K+ channel inhibitor ( n = 12). To document ATP-sensitive K+ channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K+ channel opener, was undertaken ( n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K+ channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

Renal effects of prostaglandin inhibition during increases in renal venous pressure

1991 ◽  
Vol 260 (4) ◽  
pp. F525-F529 ◽  
Author(s):  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Changes

The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

Angiotensin in the hemodynamic response to chronic nephron obstruction

1983 ◽  
Vol 245 (1) ◽  
pp. F75-F82
Author(s):  
P. K. Carmines ◽  
G. A. Tanner
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Salt Intake ◽  
Hemodynamic Response ◽  
Local Factor ◽  
High Salt Intake ◽  
The Difference ◽  
Glomerular Hemodynamics ◽  
Captopril Treatment

Microsphere techniques were employed to investigate the role of intrarenal angiotensin generation in producing the arteriolar constriction associated with 24-h tubular obstruction in rats. In each animal, glomerular blood flow (GBF) and nephron vascular resistance were determined for normal and oil-blocked superficial cortical nephrons. In 17 control rats, GBF of normal and blocked nephrons averaged 226 +/- 12 and 130 +/- 9 nl/min, respectively (P less than 0.001). Captopril treatment in five rats (10 mg/kg orally) improved GBF to blocked nephrons to 252 +/- 31 nl/min. Saralasin treatment in six rats (10 micrograms . kg-1 . min-1 i.v.) lessened the difference between GBF of normal and obstructed nephrons. In six rats subjected to a high salt intake and deoxycorticosterone injections, GBF to obstructed nephrons was improved to 181 +/- 21 nl/min. Since both pharmacologic interruption of angiotensin activity and renin suppression were associated with improved GBF of blocked nephrons, these observations support a role for angiotensin as a local factor controlling glomerular hemodynamics of chronically obstructed nephrons.

The mechanism of cardiac shunting in reptiles: a new synthesis.

1996 ◽  
Vol 199 (6) ◽  
pp. 1435-1446 ◽  
Author(s):  
J W Hicks ◽  
A Ishimatsu ◽  
S Molloi ◽  
A Erskin ◽  
N Heisler
Keyword(s):  
Blood Flow ◽  
Digital Subtraction Angiography ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Digital Subtraction ◽  
New Synthesis ◽  
Vagal Nerves ◽  
The Common ◽  
The Difference ◽  
Systemic Arteries

The mechanism of cardiac shunting in reptiles is controversial. Recent evidence suggests that a right-to-left shunt in turtles results primarily from a washout mechanism. The mechanism that accounts for left-to-right (L-R) shunting is unresolved. This study used haemodynamic analysis and digital subtraction angiography to determine the mechanism of L-R cardiac shunting in the turtle Trachemys (Pseudemys) scripta. Animals were instrumented with ultrasonic blood flow probes (Transonic Systems, Inc.) for the measurement of total pulmonary blood flow and total systemic blood flow. In addition, catheters were inserted into the common pulmonary artery (PA), the systemic arteries, the left atrium and right atrium. These catheters were used for the measurement of blood pressure or for the infusion of radio-opaque material. Haemodynamic conditions were altered by electrical stimulation of the afferent (VAF) or efferent vagal nerves or by infusion of vasoactive drugs. Under control conditions, the peak systolic pressure in the systemic arteries was slightly higher than that in the PA (30.6 versus 28.3 mmHg; 4.08 versus 3.77 kPa), whereas diastolic pressure in the PA was significantly less than that in the systemic arteries (9.8 versus 24.4 mmHg; 1.31 versus 3.25 kPa). During VAF stimulation, the peak systolic pressures in the PA and aortae almost doubled. Diastolic pressure in the systemic arteries also doubled, but it increased by only 45% in the PA. Ejection of blood into the PA preceded that into the left aorta by 53 ms under control conditions. This difference increased (by as much as 200 ms) as the difference in the diastolic pressures between the two circulations increased during VAF stimulation. This resulted in the development of a large net L-R shunt. Under these conditions, digital subtraction angiography showed that the L-R shunt resulted from a combination of both washout and pressure mechanisms.

Sign in / Sign up

Export Citation Format

Share Document