The Effects of Meclofenamate, Captopril and Phentolamine on Organ Blood Flow in the Conscious Rabbit

1981 ◽  
Vol 61 (1) ◽  
pp. 97-105 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Hepatic Artery ◽  
Peripheral Resistance ◽  
Prostaglandin Synthesis ◽  
Organ Blood Flow ◽  
Inhibit Prostaglandin Synthesis ◽  
Conscious Rabbits ◽  
Artery Flow ◽  
Intravenous Sodium

1. Systemic and regional vascular changes were measured in conscious rabbits after intravenous sodium meclofenamate, captopril and phentolamine. These drugs were used respectively to inhibit prostaglandin synthesis and angiotensin-converting enzyme, and to block α-adrenoceptors. 2. Meclofenamate reduced renal and adrenal blood flow by 11 and 28% respectively, and doubled hepatic artery flow. The effect on renal and adrenal flow persisted in the presence of phentolamine. 3. Captopril decreased estimated peripheral resistance and increased cardiac output without changing arterial pressure. Kidney and adrenal flow increased by 70 and 21% respectively. 4. Phentolamine reduced arterial pressure and doubled flow to skeletal muscle and increased hepatic artery flow to the liver. 5. Splenic blood flow was unaffected by meclofenamate, captopril or phentolamine alone. Meclofenamate given after captopril caused a halving of splenic flow and a rise in arterial pressure; these effects were prevented by phentolamine. 6. The results point to a continuing effect of prostaglandin synthesis in maintaining blood flow to the kidney and adrenal gland independent of α-adrenoceptor activation in resting conscious rabbits. An important modulating effect of prostaglandins on sympathetic vascular tone in the spleen is suggested.

Dose-Dependent Effects of Meclofenamate on Peripheral Vasculature of Conscious Rabbits

1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Organ Blood Flow ◽  
Hepatic Circulation ◽  
Peripheral Vasculature ◽  
Conscious Rabbits ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain ◽  
Intravenous Sodium

1. Changes in systemic haemodynamics and organ blood flow were measured in conscious rabbits after various doses of intravenous sodium meclofenamate, an inhibitor of prostaglandin cyclo-oxygenase. 2. Meclofenamate had no effect on arterial pressure or cardiac output but caused a dose-dependent fall in renal blood flow. 3. Meclofenamate also reduced adrenal perfusion but, in contrast, caused a dose-dependent increase in blood flow to the brain, bronchial and hepatic circulation and to the testis. No effect was demonstrated on other organs studied. 4. The effect on the cerebral circulation was observed at the lowest dose of meclofenamate (0.75 mg/kg). Higher total doses were necessary for an effect on the renal and bronchial (3 mg/kg) and testicular and hepatic arteries (6 mg/kg). 5. The results suggest a variety of local vasomotor influences of renal and non-renal prostaglandins in conscious rabbits.

Hyperglucagonemia and hyperkinetic circulation after portocaval shunt in the rat

1987 ◽  
Vol 252 (2) ◽  
pp. G257-G261 ◽  
Author(s):  
D. Kravetz ◽  
M. Arderiu ◽  
J. Bosch ◽  
J. Fuster ◽  
J. Visa ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Hepatic Artery ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Portocaval Shunt ◽  
Plasma Glucagon ◽  
Radioactive Microspheres ◽  
Circulatory Disturbance ◽  
Artery Flow

The study was aimed at investigating whether increased portal venous inflow (PVI) after portocaval shunt (PCS) in the rat is the result of selective splanchnic vasodilatation or whether it is part of a generalized circulatory disturbance. Rats with PCS (n = 9) and sham-operated controls (n = 8) were studied 2 wk after surgery by measuring cardiac output (CO), PVI, and hepatic artery flow (HAF) with radioactive microspheres. Plasma glucagon (GL) was measured by radioimmunoassay. PCS rats had increased CO (46.2 +/- 2.8 vs. 28.2 +/- 1.7 ml X min-1 X 100 g-1, P less than 0.001) and reduced arterial pressure and total peripheral resistance. PVI was markedly increased (7.7 +/- 0.7 vs. 4.3 +/- 0.2 ml X min-1 X 100 g-1, P less than 0.001), but this appeared to be part of a generalized circulatory disturbance, since when PVI is expressed as percent of CO no difference is observed between PCS and sham-operated rats (17.0 +/- 1.5 vs. 15.8 +/- 1.3%, NS), indicating the absence of a preferential splanchnic vasodilatation. GL increased after PCS (548 +/- 130 vs. 156 +/- 23 pg/ml, P less than 0.005), and significant correlations were observed between GL and CO (r = 0.787, P less than 0.001) and between GL and PVI (r = 0.806, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

Contribution of renal nerves to renal blood flow variability during hemorrhage

1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Spectral Power ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Similar Frequency ◽  
Blood Withdrawal ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

Atrial natriuretic peptide increases resistance to venous return in rats

1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Total Peripheral Resistance ◽  
Venous Return ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Atrial Natriuretic

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.

Cutaneous vasoconstriction in conscious rabbits during alerting responses detected by hippocampal theta-rhythm

1997 ◽  
Vol 272 (1) ◽  
pp. R208-R216 ◽  
Author(s):  
Y. H. Yu ◽  
W. W. Blessing
Keyword(s):  
Skeletal Muscle ◽  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Theta Rhythm ◽  
Renal Flow ◽  
Conscious Rabbits ◽  
Hippocampal Theta ◽  
Electroencephalogram Eeg ◽  
Cutaneous Vasoconstriction

We determined whether alerting stimuli cause cutaneous vasoconstriction in conscious rabbits. We compared ear blood flow with renal, mesenteric, and femoral flows at rest and in response to nonnoxious alerting stimuli, which induced theta-rhythm (4-9 Hz) in the simultaneously recorded hippocampal electroencephalogram (EEG). theta-Inducing stimuli (e.g., whistles and fur touches) reduced ear flow by 95 +/- 6%, commencing 1-2 s after the EEG change and lasting 45 s. Renal flow did not significantly change with alerting stimuli, mesenteric and femoral flows slightly decreased, arterial pressure transiently rose (+10 +/- 3 mmHg), and heart rate fell (+43 +/- 9 beats/min). At rest, the coefficient of variation for ear flow (62 +/- 6%) was greater than for other flows (P < 0.01). Phentolamine (1 mg/kg iv) reduced this coefficient to 29 +/- 4% (P < 0.01). Our study demonstrates that alerting responses in conscious rabbits are associated with selective cutaneous vasoconstriction, without increase in flow to skeletal muscle.

scholarly journals Duktus Arteriosus pada Bayi Prematur

2020 ◽  
Vol 1 (2) ◽  
pp. 89-97
Author(s):  
Agus Cahyono
Keyword(s):  
Blood Flow ◽  
Necrotizing Enterocolitis ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Prostaglandin Synthesis ◽  
Treatment Modalities ◽  
Organ Blood Flow ◽  
Descending Aorta ◽  
Drug Adverse Event ◽  
Important Structure

Abstract—Ductus arteriosus (DA) is a connecting vessel between proximal descending aorta and pulmonary artery. This important structure normally close after birth. The opened ductus causes increasing of pulmonary blood flow and decreasing of certain organ blood flow (intestine, skin, muscle, and renal) causing complications such as heart failure, metabolic acidosis, necrotizing enterocolitis, and pulmonary edema/bleeding. Prevalence of DA is 0,2/1000 live birth. In under 1500 g babies the proportion of DA is 25%. Surgery and medicine are the treatment modalities of DA closure. Modalities of medicine are indometacine, ibuprofen, and paracetamol. These three modalities work by inhibiting cyclooxygenase enzime causing blockade of prostaglandin synthesis. Drug adverse event can be minimized by carefull in making treatment choice. Keywords: ductus arteriosus, complication, treatment Abstrak—Duktus arteriosus (DA) merupakan pembuluh darah yang menghubungkan aorta desendens proksimal dan arteri pulmonalis. Struktur yang penting pada janin tersebut secara normal menutup setelah lahir. Duktus yang masih terbuka tersebut mengakibatkan peningkatan aliran darah paru dan penurunan aliran darah ke organ usus, kulit, otot, dan ginjal sehingga menyebabkan komplikasi seperti gagal jantung, asidosis metabolik, necrotizing enterocolitis (NEC), serta edema paru/perdarahan. Prevalensi DA yang masih terbuka adalah 0,2 per 1000 kelahiran hidup. Proporsi bayi yang bergejala dengan DA yang masih terbuka kurang lebih 25% bayi dengan berat badan lahir di bawah 1500g. Pilihan terapi penutupan DA adalah cara bedah dan medis. Cara medis memiliki beberapa pilihan yaitu indometasin, ibuprofen, dan parasetamol. Ketiga modalitas terapi tersebut bekerja melalui penghambatan enzim siklooksigenase sehingga sintesis prostaglandin terhambat. Beberapa hal perlu diperhatikan dalam membuat pilihan terapi sehingga komplikasi yang berhubungan dengan efek samping obat dapat dihindari.. Kata kunci: ductus arteriosus, komplikasi, terapi

Mechanisms for increased blood flow resistance due to leukocytes

1997 ◽  
Vol 273 (6) ◽  
pp. H2884-H2890 ◽  
Author(s):  
Brian P. Helmke ◽  
Shannon N. Bremner ◽  
Benjamin W. Zweifach ◽  
Richard Skalak ◽  
Geert W. Schmid-Schönbein
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Radial Displacement ◽  
Flow Resistance ◽  
Gracilis Muscle ◽  
Hydrodynamic Interactions ◽  
Organ Blood Flow ◽  
Significant Elevation ◽  
Increased Blood Flow ◽  
Isolated Rat

Despite the small number of leukocytes relative to erythrocytes in the circulation, leukocytes contribute significantly to organ blood flow resistance. The present study was designed to investigate whether interactions between leukocytes and erythrocytes affect the pressure-flow relationship in a hemodynamically isolated rat gracilis muscle. At constant arterial flow rate, arterial pressure was increased significantly when relatively few physiological counts of leukocytes were added to a suspension containing erythrocytes at physiological hematocrits. However, the arterial pressure after perfusion of similar numbers of isolated leukocytes without erythrocytes was only slightly increased. An increase in resistance was also observed when leukocytes were replaced with 6-μm microspheres. We propose a new mechanism for increasing the hemodynamic resistance that involves hydrodynamic interactions between leukocytes and erythrocytes. In the presence of larger and less deformable leukocytes, erythrocytes move through capillaries more slowly than without leukocytes. Therefore erythrocytes are displaced from their axial positions. Slowing and radial displacement of erythrocytes serve to increase the relative apparent viscosity attributable to erythrocytes, thereby causing a significant elevation of organ blood flow resistance.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

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