scholarly journals Inhibition of prostaglandin synthesis does not alter the decrease in pre-capillary resistance in the human calf in response to small cumulative increases in venous congestion

2005 ◽  
Vol 109 (3) ◽  
pp. 303-309
Author(s):  
Stephen I. Anderson ◽  
Margaret D. Brown
Keyword(s):  
Blood Flow ◽  
Prostaglandin Synthesis ◽  
Venous Congestion ◽  
Local Flow ◽  
Calf Blood Flow ◽  
Arterial Inflow ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Capillary Resistance ◽  
Human Calf ◽  
Filtration Capacity

The decrease in pre-capillary resistance in the human calf during gradual cumulative increases in venous congestion pressure has been proposed to represent vasodilator signalling between the venous and arterial microcirculations. The present study investigated whether prostaglandins are involved in this local flow regulation by measuring calf blood flow and microvascular filtration capacity using strain gauge plethysmography in young male subjects before (baseline) and after taking either ibuprofen, an inhibitor of prostaglandin synthesis (1600 mg over 2 days), or placebo. At baseline, inflation of a thigh cuff to 50 mmHg in steps of 10 mmHg, each held for 5 min, did not decrease arterial inflow, confirming a reduction of pre-capillary resistance. Ibuprofen reduced resting calf blood flow by 35% (P<0.001), but flow at a Pcuff (cuff pressure) of 50 mmHg was 97% of this value, i.e. pre-capillary resistance had decreased to the same extent as before inhibition of prostaglandin synthesis. Ibuprofen also reduced microvascular filtration capacity (2.98±1.20 compared with 3.71±0.89 ml·min−1·100 ml−1·mmHg−1×10−3; P<0.05), probably due to a combination of reduced arterial inflow and lower venous pressure (8.5±5.2 compared with 12.6±2.8 mmHg; P<0.05) that moderated capillary hydrostatic pressure to override direct effects of inhibition of prostaglandin synthesis on permeability. Placebo was without effect on any measurement. It is unlikely therefore that prostaglandin-mediated vasodilator signals, which have been demonstrated between paired veins and arteries, are important in local vasodilation in response to venous congestion.

The Effect of Inhibition of Prostaglandin Synthesis on Microvascular Haemostatic Plug Formation in the Rabbit

1975 ◽  
Author(s):  
D. Bergqvist ◽  
E. Svensjö ◽  
K.-E. Arfors
Keyword(s):  
Blood Flow ◽  
Mesenteric Artery ◽  
Prostaglandin Synthesis ◽  
Formation Time ◽  
Initial Formation ◽  
Platelet Aggregability ◽  
Inhibition Of Prostaglandin Synthesis ◽  
The Difference ◽  
The Stability ◽  
Plug Formation

Bleeding induced by microvascular transection in the rabbit mesentery stops by the formation of a haemostatic plug. Normal platelets as well as the normal coagulation and fibrinolytic systems are essential for haemostatic plug formation, the initial formation being mainly ADP-dependent and the stability mainly an effect of fibrin formation. The difference in haemostasis between arterioles and venules was abolished by aspirin (Arfors et al. Scand. J. Haematol. 9, 322, 1972). In this study we have investigated the effect of indomethacin. As with aspirin, venular haemostatic plug formation time was shortened and plug stability increased. Local infusion of PGE1 into the cranial mesenteric artery significantly prolonged arteriolar and venular haemostatic plug formation time. Measuring blood flow velocity, vessel contraction and haemostatic plug volume makes it possible to determine the proportion of platelets participating in the formation of an effective plug in individual vessels. Platelet aggregability is significantly higher in plugs formed at injuries on the arteriolar side of the microcirculation than on the venular, but this difference is totally abolished after indomethacin. In conclusion the difference in haemostasis between arterioles and venules in this model can be explained by prostaglandin being formed in the mesenteric preparation.

Changes in microvascular fluid filtration capacity during 120 days of 6° head-down tilt

2001 ◽  
Vol 91 (6) ◽  
pp. 2517-2522 ◽  
Author(s):  
F. Christ ◽  
J. Gamble ◽  
V. Baranov ◽  
A. Kotov ◽  
A. Chouker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Water Permeability ◽  
Strain Gauge ◽  
Venous Pressure ◽  
Venous Congestion ◽  
Edema Formation ◽  
Fluid Filtration ◽  
Fluid Homeostasis ◽  
Strain Gauge Plethysmography ◽  
Filtration Capacity

We used venous congestion strain gauge plethysmography (VCP) to measure the changes in fluid filtration capacity ( K f), isovolumetric venous pressure (Pvi), and blood flow in six volunteers before, on the 118th day (D118) of head-down tilt (HDT), and 2 days after remobilization (Post). We hypothesized that 120 days of HDT cause significant micro- and macrovascular changes. We observed a significant increase in K f from 3.6 ± 0.4 × 10−3 to 5.7 ± 0.9 × 10−3ml · min−1 · 100 ml−1 · mmHg−1 (+51.4%; P < 0.003), which returned to pretilt values (4.0 + 0.4 × 10−3ml · min−1 · 100 ml−1 · mmHg−1) after remobilization. Similarly, Pvi increased from 13.4 ± 2.1 mmHg to 28.9 ± 2.8 mmHg (+105.8%; P < 0.001) at D118 and was not significantly different at Post (12.4 ± 2.6 mmHg). Blood flow decreased significantly from 2.3 ± 0.3 to 1.3 ± 0.2 ml · min−1 · 100 ml tissue−1 at D118 and was found elevated to 3.4 ± 0.7 ml · min−1 · 100 ml tissue−1at Post. We believe that the increased K f is caused by a higher microvascular water permeability. Because this may result in edema formation, it could contribute to the alterations in fluid homeostasis after exposure to microgravity.

Hyperventilation and human calf blood flow

1966 ◽  
Vol 211 (5) ◽  
pp. 1255-1260 ◽  
Author(s):  
JD Coffman ◽  
P Kelly
Keyword(s):  
Blood Flow ◽  
Calf Blood Flow ◽  
Human Calf

Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog

1979 ◽  
Vol 237 (3) ◽  
pp. F182-F187
Author(s):  
M. C. Blasingham ◽  
A. Nasjletti
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin Synthetase ◽  
Renal Functions ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.

Exaggerated renal vascular reactivity to angiotensin and thromboxane in young genetically hypertensive rats

1990 ◽  
Vol 259 (2) ◽  
pp. F372-F382 ◽  
Author(s):  
C. Chatziantoniou ◽  
F. H. Daniels ◽  
W. J. Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Receptor Agonist ◽  
Vascular Reactivity ◽  
Prostaglandin Synthesis ◽  
Genetic Hypertension ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Renal Vascular

The objective of this study was to test the hypothesis that angiotensin II and thromboxane A2 (TxA2) contribute to the elevated renal vascular resistance observed during the development of genetic hypertension. In 6-wk-old anesthetized spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats, renal blood flow (electromagnetic flowmetry) and carotid arterial pressure were measured during bolus injections of different doses of angiotensin II and U46619 (stable receptor agonist of TxA2) into the renal artery before and during inhibition of prostaglandin synthesis by indomethacin. In all cases, arterial pressure remained unchanged at the pre-injection levels. Under control conditions, angiotensin II reduced renal blood flow in SHR almost twice as much as in WKY. This strain difference was abolished by inhibition of prostaglandin synthesis, suggesting that a deficiency in the action of endogenous vasodilator prostaglandins is responsible for the enhanced response to angiotensin II in SHR. Under control conditions, the TxA2-receptor agonist produced similar reductions of renal blood flow in SHR and WKY. However, after indomethacin, the agonist-induced vasoconstriction was twice as large in SHR as in WKY, suggesting that SHR kidneys have an increased vascular reactivity to TxA2, which is unmasked when indomethacin reduces elevated levels of endogenous TxA2. These findings indicate important strain differences between young SHR and WKY in the renal vascular response to angiotensin II and TxA2 that may contribute to the renal vasoconstriction observed during the development of genetic hypertension.

Impaired retrograde transmission of vasodilatory signals via the endothelium in pre-eclampsia: a cause of reduced tissue blood flow?

2004 ◽  
Vol 106 (1) ◽  
pp. 19-25 ◽  
Author(s):  
N. ANIM-NYAME ◽  
S. R. SOORANNA ◽  
M. R. JOHNSON ◽  
M. H. SULLIVAN ◽  
J. GAMBLE ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cell Adhesion ◽  
Adhesion Molecule ◽  
Cell Adhesion Molecule ◽  
Cell Activation ◽  
Venous Congestion ◽  
The Other ◽  
Tissue Blood Flow ◽  
Calf Blood Flow ◽  
Cell Adhesion Molecule 1

There is evidence that tissue blood flow is regulated by retrograde transmission of signals initiated at capillary and post-capillary sites, and transmitted via the endothelium to modulate pre-capillary resistance. We have used pre-eclampsia as a model to test the hypothesis that normal endothelium is required to enable adjustment of blood flow to match tissue requirements. Integrity of the endothelial pathway was assessed by measuring calf blood flow at increasing venous pressures, using an established small cumulative-step venous-congestion plethysmography protocol in ten women with pre-eclampsia, 17 normal pregnant controls and ten non-pregnant women. Endothelial cell activation was assessed by measuring plasma levels of the cell adhesion molecules, intercellular cell-adhesion molecule-1 (ICAM-1), vascular cell-adhesion molecule-1 (VCAM-1) and E-selectin. Baseline calf blood flow was significantly lower in pre-eclampsia than in the other two groups (P<0.0001; ANOVA). In the pre-eclampsia group, there was a fall in blood flow as venous congestion pressure was raised (P<0.0001; ANOVA). No such change was observed in the other two groups. A significant inverse correlation was observed between the reduction in blood flow in pre-eclampsia and the levels of E-selectin (r=-0.92, P=0.0002), VCAM-1 (r=-0.93, P=0.0008) and ICAM-1 (r=-0.86, P=0.001). The differences between the pre-eclamptic women and the other two groups support the notion that the failure to sustain blood flow during a cumulative pressure step protocol in the pre-eclamptic group might be influenced by interference with the retrograde transmission of signals via the endothelium in these patients.

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