Effect on apparent liver blood flow of histamine-receptor blockers and inhibition of prostaglandin synthesis

1983 ◽  
Vol 33 (1) ◽  
pp. 91-94 ◽  
Author(s):  
J Feely ◽  
A J J Wood
Keyword(s):  
Blood Flow ◽  
Liver Blood Flow ◽  
Histamine Receptor ◽  
Prostaglandin Synthesis ◽  
Receptor Blockers ◽  
Inhibition Of Prostaglandin Synthesis

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.

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.

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.

Peptic Ulcer Disease in Children

1990 ◽  
Vol 12 (1) ◽  
pp. 15-21
Author(s):  
Joyce D. Gryboski
Keyword(s):  
Blood Flow ◽  
Peptic Ulcer ◽  
Mucosal Blood Flow ◽  
Prostaglandin Synthesis ◽  
Stress Ulceration ◽  
Drug Induced ◽  
Ulcer Disease ◽  
Inhibition Of Prostaglandin Synthesis ◽  
H Pylori ◽  
Gastroduodenal Ulceration

Chronic gastroduodenal ulceration is the end product of an imbalance between acid levels, peptic hostile factors, and mucosal defenses. This condition differs significantly from stress ulceration, in which the primary factor is decreased mucosal blood flow, and from nonsteroidal anti-inflammatory drug-induced injury, in which there is local vascular injury and inhibition of prostaglandin synthesis. The identification of H pylori as a cause of chronic gastritis, duodenitis, and peptic ulcer is required for specific antibacterial therapy.

Effects of indomethacin on cerebral blood flow during hypercapnia in cats

1983 ◽  
Vol 244 (4) ◽  
pp. H519-H524 ◽  
Author(s):  
D. W. Busija ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Cerebral Blood Flow ◽  
Intravenous Administration ◽  
Prostaglandin Synthesis ◽  
Pial Arteries ◽  
Cranial Window ◽  
Window Method ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Cerebral Vasodilatation

To study the contribution of prostaglandins to cerebral vasodilatation during hypercapnia, we inhibited prostaglandin synthesis with indomethacin. We measured cerebral blood flow (CBF) in anesthetized cats with 15-micrometers microspheres during normocapnia (PCO2 approximately 33 Torr), moderate hypercapnia (PCO2 approximately 49 Torr), and severe hypercapnia (PCO2 approximately 65 Torr) before and after intravenous administration of vehicle or indomethacin (3 and 10 mg/kg). Hypercapnia produced graded increments in blood flow to all areas of the brain. Administration of indomethacin did not change control CBF or significantly attenuate increases in CBF during hypercapnia. We examined efficacy and specificity of inhibition of prostaglandin synthesis by indomethacin using the cranial window method. Arachidonic acid (100 and 200 micrograms/ml) and acetylcholine (10(-7) and 10(-6)M or 10(-6) and 10(-5) M), dissolved in artificial cerebrospinal fluid, dilated pial arteries in a dose-dependent fashion. Intravenous administration of indomethacin blocked vasodilatation produced by arachidonic acid but did not affect the response to acetylcholine. Thus indomethacin, at a dose that effectively blocks prostaglandin synthesis, did not alter resting CBF or attenuate the increase in CBF during hypercapnia. This study suggests that steady-state cerebral vasodilatation during hypercapnia is largely preserved after inhibition of prostaglandin synthesis.

Liver Blood Flow as a Major Determinant of the Clearance of Recombinant Human Tissue-Type Plasminogen Activator

1992 ◽  
Vol 67 (01) ◽  
pp. 083-087 ◽  
Author(s):  
A de Boer ◽  
C Kluft ◽  
J M Kroon ◽  
F J Kasper ◽  
H C Schoemaker ◽  
...  
Keyword(s):  
Blood Flow ◽  
Rat Liver ◽  
Healthy Subjects ◽  
Liver Blood Flow ◽  
Major Determinant ◽  
Tissue Type ◽  
Perfused Rat Liver ◽  
Liver Model ◽  
Type Plasminogen Activator ◽  
Proportional Change

SummaryThe influence of changes in liver blood flow on the clearance of rt-PA was studied both in healthy subjects and in a perfused rat liver model. Liver blood flow in healthy subjects was documented indirectly by the clearance of indocyanine green (ICG). Exercise reduced liver blood flow on average by 57% with a 95% confidence interval (95% Cl) ranging from 51% to 62% (n = 5) and increased plasma levels of rt-PA activity (after an i. v. infusion of 18 mg of rt-PA over 120 min) by 119% (95% Cl, 58% - 203%) and rt-PA antigen by 91% (95% Cl, 30% - 140%). In the perfused rat liver model it was shown that halving or doubling of the physiological flow rate of a perfusate, containing rt-PA caused a proportional change in the clearance of rt-PA, while the extraction of rt-PA by the liver remained similar. In conclusion, liver blood flow is a major determinant of the clearance of rt-PA. This may have important implications for dosage of rt-PA in patients with myocardial infarction.

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