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PubMed1994

Splanchnic haemodynamics and vasoactive agents in experimental cirrhosis.

It is well known that portal hypertension is associated with a hyperdynamic systemic circulatory state. This study measures systemic and splanchnic haemodynamics in an experimental rat model of hepatic cirrhosis. It also investigates the association between haemodynamic changes in cirrhotic animals and circulating levels of the vasoactive hormones glucagon and vasoactive intestinal polypeptide (VIP). Splanchnic blood flow was significantly increased in the cirrhotic group (13.2 +/- 1.3 vs. 9.2 +/- 1.6 ml/min, P < 0.05). Circulating levels of glucagon and VIP were two and five fold increased respectively in cirrhotic animals compared to controls. There was a strong correlation between portal pressure and glucagon levels in the cirrhotic group (r = 0.85). Raised splanchnic blood flow is partly responsible for elevated portal pressure in this model and this rise may be humorally mediated.

Animals↗
PubMed1984

Effects of nifedipine on renal vascular responses to vasoactive agents in rabbits.

The present study was designed to investigate the effects of the Ca-antagonist, nifedipine, on receptor-mediated renal vascular responses to vasoconstrictors (angiotensin II, norepinephrine and vasopressin) and vasodilators (bradykinin and prostaglandin E2). Renal blood flow was estimated by noncannulating electromagnetic flowmetry in anesthetized rabbits. Vasoactive substances were infused directly into the renal artery. After the intravenous administration of nifedipine (50 micrograms/kg), decreases in renal blood flow in response to angiotensin II infused at rates of 2.5, 5 and 10 ng/kg/min were attenuated by 64% (p less than 0.01), 45% (p less than 0.05) and 42% (p less than 0.05), respectively. Decreases in renal blood flow in response to vasopressin infused at rates of 10, 20 and 50 mU/kg/min were also attenuated by nifedipine, 50% (p less than 0.05), 57% (p less than 0.05) and 38% (p less than 0.05), respectively. However, renal vasoconstrictor responses to norepinephrine (25, 50 and 100 ng/kg/min) did not change significantly after the administration of nifedipine. Increases in renal blood flow induced by the intrarenal infusion of bradykinin (2.5, 5 and 10 ng/kg/min) and prostaglandin E2 (20, 50 and 100 ng/kg/min) were not affected by nifedipine. These results suggest that receptor-mediated vasoconstrictor responses of the renal vascular bed to angiotensin II and vasopressin are produced mainly by Ca++ influx but that of norepinephrine is not. Furthermore, it is confirmed that the renal vasodilator effect of bradykinin and prostaglandin E2 is not altered by nifedipine in anesthetized rabbits.

Angiotensin II↗
PubMed1981

Vascular response of the chicken hindlimb to vasoactive agents, asphyxia, and exercise.

Previous studies in live chickens have measured heart rate, blood pressure, and cardiac output during drug administration or asphyxia and made assumptions concerning the peripheral vasculature. The present study employs a constant-flow, isolated hindlimb perfusion technique to measure directly changes in skeletal muscle vascular resistance induced either by local intra-arterial (i.a.) bolus, or continuous i.a. infusion, of various vasoactive substances. Prostaglandin E1 (0.5 microgram, bolus) produced arteriolar vasodilation lasting 10 min, as indicated by a fall ian perfusion pressure. Bolus injection of histamine (10 microgram diphosphate) or adenosine (5 and 10 microgram) produced vasodilation of less than 2-min duration. Theophylline infusion (5 microM infused at 1 mL/min, i.a.) blocked the effect of adenosine. Norepinephrine (1 microgram) produced vasoconstriction which was reduced 60% by systemic alpha-adrenergic blockade with phenoxybenzamine (7.5-10 mg/kg). Tracheal occlusion produced intense vasoconstriction which was reduced 70% by alpha-adrenergic blockade. Electrical stimulation of the peripheral end of the cut sciatic nerve (6 Hz) produced an immediate vasodilation lasting several minutes.

Acetylcholine↗
PubMed1990

Responses of isolated cerebral arteries to vasoactive agents.

One hypothesis of cerebral vasospasm contends that the slow onset and eventual disappearance of the spasm of subarachnoid hemorrhage is caused by the finite production of spasmogens. These are generated and accumulate in the basal cisterns as the result of chemical reactions between blood elements, arterial wall, leptomeninges, and brain. The spasmogens may spread in the general direction of bulk CSF flow to affect arteries more distally. Pharmacodynamic studies performed on isolated cerebral arteries show that a vast array of naturally occurring substances are vasoactive. Among these, derivatives of arachidonate (eicosanoids) are strong candidates as spasmogens because they produce strong, prolonged contractions in human arteries and because the CSF levels of some eicosanoids are preferentially elevated in subarachnoid hemorrhage patients who experience severe spasm. The spasm may be largely refractory to treatment because the intravasation of blood elements and the coagulum serve as barriers to therapeutic agents and because cerebral arteries are devoid of vasa vasorum; however, in animal models of chronic subarachnoid hemorrhage, calcium antagonists given intrathecally will reverse the spasm. Other therapeutic strategems are being tried experimentally and clinically, including compounds like prostacyclin that relax cerebral arteries and inhibit platelets. In vitro studies indicate further that some plasma proteins (e.g., haptoglobin, antithrombin III) and several products of endothelial synthesis (PGI2, EDRF) may naturally provide protection against the genesis of vasospasm. The in vitro responses to bloody CSF are capricious but are not due to many pharmacologically defined substances, including hemoglobin. Hemoglobin and its derivatives, however, may be critical to the enhanced lipid peroxidation and free-radical production that occur in subarachnoid hemorrhage.

Animals↗
PubMed2005

Skeletal muscle blood flow in anaesthetized horses. Part II: effects of anaesthetics and vasoactive agents.

OBJECTIVE: This review aims at evaluating studies investigating the effects of anaesthesia on skeletal muscle blood flow and associated cardiovascular function in anaesthetized horses and discusses how the results of these studies contribute to our understanding of the pathogenesis and prevention of post-anaesthetic myopathy. DATABASE USED: Pubmed & personal files. CONCLUSION: There is little published information on the effects of anaesthesia on skeletal muscle blood flow in horses. Available reports predominantly refer to halothane and isoflurane. The effects of vasoactive drugs have mainly been studied in halothane-anaesthetized horses. The results of these studies support the importance of cardiac output in the maintenance of adequate arterial blood pressure, perfusion pressure and muscle blood flow. Adequate perfusion pressure appears to be important for overcoming the detrimental effects of high intra-compartmental pressure in dependent muscles and hydrostatic pressure in nondependent muscles.

Anesthesia, Inhalation↗
PubMed1986

The effect of vasoactive agents on the left ventricular end-systolic pressure-volume relation in closed-chest dogs.

The left ventricular end-systolic pressure-volume relation has received intense interest as a relatively load-insensitive measure of cardiac performance. In clinical studies, pharmacologic manipulation of blood pressure has been used to determine this relation. Since previous studies have shown that acute changes in the resistance and impedance of the arterial circulation influence the left ventricular end-systolic pressure-volume relation, the use of vasoactive drugs in its determination may affect the results achieved. This study was undertaken to determine whether clinically used vasoactive drugs influence the left ventricular end-systolic pressure-volume relation. Sixteen dogs were previously instrumented with micromanometer pressure transducers and three sets of piezoelectric crystals to permit determination of left ventricular pressure and volume. The dogs were studied after autonomic blockade and sedation. End-systolic pressure-volume relations were generated by caval occlusion at control levels of blood pressure, after infusion of a vasopressor (methoxamine, n = 6; angiotensin II, n = 10), and then after infusion of nitroprusside. A composite end-systolic pressure-volume relation was also constructed with the use of control, vasopressor, and vasodilator points in each dog. Angiotensin II resulted in a leftward shift in the relation (Vo decreased from 14.32 +/- 7.3 to 8.04 +/- 10.4 ml, p less than .05) with no significant effect on slope. Methoxamine shifted the relation to the left (Vo decreased from 13.98 +/- 8.74 to -0.47 +/- 12.06 ml, p less than .05) and also reduced the slope (5.41 +/- 3.09 vs 8.28 +/- 3.94 mm Hg/ml, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1994

Central-to-peripheral arterial pressure gradient during cardiopulmonary bypass: relation to pre- and intra-operative data and effects of vasoactive agents.

A significant central-to-peripheral arterial pressure gradient may exist during and after cardiopulmonary bypass (CPB). The etiology and mechanisms of this phenomenon remain controversial. We studied the pressure gradient between aorta, brachial artery and radial artery in 68 patients, scheduled for elective coronary artery bypass surgery. We evaluated whether choice of cardioprotection during CPB (use of cold cardioplegic solution or use of intermittent crossclamping under protection with lidoflazine), and choice of pulsatile or nonpulsatile flow during the course of CPB, affected the magnitude and duration of the systolic pressure gradient. We also studied whether central-to-peripheral pressure gradient was influenced by administration on CPB of different vasoactive drugs with different mode of action: sodium nitroprusside (direct action on the vessels), droperidol (alpha-adrenergic blocking action), ketanserin (5-hydroxytryptamine antagonist) and phenylephrine (selective alpha 1-agonist). It appeared that central-to-peripheral gradient occurred early during CPB and remained constant throughout the course of CPB. The gradient disappeared within 60 min after weaning from CPB. We found the main pressure gradient to occur between the brachial and the radial artery. There was no relation between magnitude of the gradient and sex, weight, length or age of the patient. There was also no relation between magnitude of the pressure gradient and type of cardioprotection, choice of pulsatile vs nonpulsatile flow on CPB and duration of CPB. We also found no relation between pressure gradients and changes in temperature, haematocrit and systemic vascular resistance. The pressure gradient was not affected by any of the vasoactive drugs.

Aged↗
PubMed2006

Effect of the molecular adsorbent recirculating system and Prometheus devices on systemic haemodynamics and vasoactive agents in patients with acute-on-chronic alcoholic liver failure.

INTRODUCTION: Patients with acute-on-chronic liver failure show an aggravated hyperdynamic circulation. We evaluated, in a controlled manner, potential changes in systemic haemodynamics induced by the molecular adsorbent recirculating system (MARS) and the Prometheus system liver detoxification devices in a group of patients with acute-on-chronic liver failure. METHODS: Eighteen patients (51.2 +/- 2.3 years old; Child-Pugh score, 12.5 +/- 0.2; Maddrey score, 63.1 +/- 5.0; hepatic venous pressure gradient, 17.6 +/- 0.9 mmHg) with biopsy-proven alcoholic cirrhosis and superimposed alcoholic hepatitis were either treated with standard medical therapy (SMT) combined with MARS (n = 6) or Prometheus (n = 6) or were treated with SMT alone (n = 6) on three consecutive days (6 hours/session). Liver tests, systemic haemodynamics and vasoactive substances were determined before and after each session. RESULTS: Groups were comparable for baseline haemodynamics and levels of vasoactive substances. Both MARS and Prometheus decreased serum bilirubin levels (P < 0.005 versus SMT), the Prometheus device being more effective than MARS (P = 0.002). Only MARS showed significant improvement in the mean arterial pressure (Deltachange, +9 +/- 2.4 mmHg versus -0.3 +/- 2.4 mmHg with Prometheus and -5.2 +/- 2.1 mmHg with SMT, P < 0.05) and in the systemic vascular resistance index (Deltachange, +131.5 +/- 46.2 dyne x s/cm5/m2 versus -92.8 +/- 85.2 dyne x s/cm5/m2 with Prometheus and -30.7 +/- 32.5 dyne x s/cm5/m2 with SMT; P < 0.05), while the cardiac index and central filling remained constant. This circulatory improvement in the MARS group was paralleled by a decrease in plasma renin activity (P < 0.05), aldosterone (P < 0.03), norepinephrine (P < 0.05), vasopressin (P = 0.005) and nitrate/nitrite levels (P < 0.02). CONCLUSION: The MARS device, and not the Prometheus device, significantly attenuates the hyperdynamic circulation in acute-on-chronic liver failure, presumably by a difference in removal rate of certain vasoactive substances. These findings suggest conspicuous conceptual differences among the albumin dialysis devices.

Adult↗
PubMed1992

Effects of aortic pressure and vasoactive agents on the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

1. We have developed a new preparation for continuously measuring changes in vascular resistance of the vasa vasorum of the canine isolated thoracic aorta perfused at a constant flow rate with Krebs-bicarbonate solution. 2. An increase of more than 150 mmHg in aortic pressure caused a significant increase in the vascular resistance of the vasa vasorum. 3. 5-Hydroxytryptamine (5-HT), noradrenaline (NA), adrenaline and dopamine caused dose-dependent increases in the vascular resistance of the vasa vasorum. The decreasing order of potency in the vasoconstrictor responses was as follows: 5-HT >> NA = adrenaline >> dopamine. The 5-HT- and adrenaline-induced vasoconstrictor responses were inhibited by methysergide and by phentolamine plus propranolol, respectively. 4. Acetylcholine (ACh), isoprenaline (ISP), histamine (His), ATP, ADP and adenosine produced dose-related decreases in the vascular resistance of aortic vasa vasorum perfused with the Krebs solution containing 10(-5) M-NA. The decreasing order of potency in the response was as follows: ACh = ISP > His >> adenosine = ATP = ADP. The ACh-, ISP- and His-induced vasodilator responses were antagonized by atropine, propranolol and famotidine, respectively. 5. The results suggest that the preparation described is useful for studying the regulation of vascular resistance of aortic vasa vasorum and that aortic pressure and vasoactive compounds may directly regulate the vascular resistance of the vasa vasorum in canine isolated thoracic aorta.

Animals↗
PubMed2001

Responsiveness of human varicose saphenous veins to vasoactive agents.

AIMS: To test in vitro the constrictor and relaxation responsiveness of variously diseased segments of human saphenous vein from patients with varicose vein disease. METHODS: The vein segments were derived (i) from the inguinal saphenous vein (valvularly incompetent and slightly dilated; tissue A); (ii) from the distal end of the lower leg just above the medial ankle (competent; tissue B); (iii) from a tributary to the long saphenous vein just below the knee (dilated, incompetent and overtly varicose; tissue C). The contractile responses were tested with phenylephrine (an alpha-adrenergic receptor agonist) and aescin, a clinically used phlebotonic drug derived from horse chestnut extract. Relaxant responses were tested with acetylcholine and sodium nitroprusside. RESULTS: Both contractile agents contracted vein segments from the inguinal and ankle area with similar potency and efficacy, but were virtually without effect in the overtly varicose segments from the calf. EC50 values (molar concentration of the agonist that produces 50% of the maximum effect) in tissues A and B were 2.9 +/- 0.3 and 2.5 +/- 0.5 micromol l(-1) (phenylephrine) and 9.4 +/- 1.0 and 15.9 +/- 2.5 micromol l(-1) (aescin); the corresponding maximum effects (maximum effect, percent of KCl-induced contraction) were 76 +/- 3 and 70 +/- 4% (phenylephrine) and 70 +/- 2 and 71 +/- 3% (aescin) (P = NS in both cases for A vs B). In tissue C, the maximum effects were 5 +/- 5% (phenylephrine) and 10 +/- 7% (aescin) of KCl-induced contraction (not significantly different from zero). Acetylcholine-induced relaxation was similar for vein segments from locations A and B, whereas sodium nitroprusside was more effective in tissue B than A. CONCLUSIONS: These findings support the notion that abnormalities within the venous wall affect venous smooth muscle contractility. Since competent and incompetent clinically normal vessels show normal contractile responses, whereas varicose vessels are not responsive to vasoactive drugs, it is likely that pharmacological treatment regimens are effective in early, but not in late stages of the disease.

Acetylcholine↗
PubMed2003

Validation of laser Doppler flowmetry coupled with intra-dermal injection for investigating effects of vasoactive agents on the skin microcirculation in man.

OBJECTIVE: To determine the reproducibility of laser Doppler flowmetry coupled with intra-dermal saline delivery. METHODS: Delivery of saline was judged visually by two operators ( n=100), using a graduated syringe (Becton-Dickinson), by expelling saline onto a weighing boat. Volume was assessed by weight. Skin blood flow following intra-dermal injection of saline was assessed in 18 healthy volunteers; 10 attended twice to assess between-day reproducibility, and 8 attended once to assess between-site reproducibility. Results are expressed as mean value+/-SEM and 95% confidence interval for mean differences. RESULTS: There was no difference between operators in mean injection weight, both weights being 10.3+/-0.1 mg (mean difference 0.08, 95% confidence interval, CI -0.23 to 0.39 mg; n=100, P=0.9). Intra-dermal saline caused a nine-fold increase in blood flow (0.03+/-0.003 to 0.27+/-0.02 perfusion units, PU; n=18, P<0.001). This response had a rapid onset, with the maximal effect seen at 4 min and a duration of greater than 30 min. There was no difference in the magnitude of the response between the dominant and non-dominant arms, AUC was 2.9+/-0.4 and 2.9+/-0.4, respectively (mean difference -0.05, 95% CI -0.8 to 0.73 PU; n=18, P=0.93). However, there was a trend towards differences between study visits 1 and 2: AUC was 3.2+/-0.6 and 2.0+/-0.5, respectively (mean difference 1.2, 95% CI -0.03 to 2.43 PU; n=10, P=0.7). There was no difference in the magnitude of responses between different sites on the forearm ( n=64, P=0.6). CONCLUSIONS: These studies demonstrate that the technique of laser Doppler flowmetry coupled with intra-dermal injection is a safe, well-tolerated technique with good reproducibility. A trend towards reduced between-day reproducibility emphasizes the importance of vehicle control sites when investigating the effects of vasoactive compounds. This technique provides a reliable method for the intra-dermal delivery of drugs, despite the direct effect of injection of saline on blood flow.

Adult↗
PubMedDate not supplied

Sonographic investigation of flow patterns in the perfused human placenta and their modulation by vasoactive agents with enhanced visualization by the ultrasound contrast agent Albunex.

PURPOSE: Our objective was to demonstrate sonographically the flow distribution in the circulation of human placentae as well as the sensitivity of the human fetal capillary bed to vasoconstriction and dilatation. METHODS: Five human full-term placental lobules were maintained in vitro with fetal and maternal flow. Commercial ultrasound scanners were used for imaging. Albunex (1 ml bolus) was administered to the fetal "artery" to monitor patterns of flow. U46619 (1 ml, 10(-6) M; a thromboxane agonist and potent vasoconstrictor) and/or nitroglycerin (a potent vasodilator) were added to the fetal artery. RESULTS: Following the addition of U46619, mean "fetal pressures" rapidly rose from 23.2 +/- 0.8 to 118 +/- 2. 9 mm Hg (mean +/- standard error of mean; p < 0.001); venous flow rates decreased. As demonstrated by color Doppler imaging, flow markedly changed from a pattern of general distribution throughout the lobule to flow only near the chorionic plate. Color persistence was 94.4 +/- 6.5 seconds with Albunex after nitroglycerin and 39.8 +/- 3.4 seconds with Albunex after injection of U46619 (p < 0.001). Nitroglycerin had no effect when injected by itself but returned "constricted" flow to a "normal" pattern when injected after U46619. CONCLUSIONS: The contrast medium Albunex improved visualization of the fetal circulation throughout the lobule. Flow in the human placental capillary bed can be regionally manipulated throughout the placental lobule by vasomodulators and monitored by Albunex-enhanced sonographic examination.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1976

The effects of acetylcholine, biogenic amines and other vasoactive agents on the cardiovascular functions of the Eel, Anguilla japonica.

The blood pressure in the cardinal vein, cardiac chambers and ventral and dorsal aortae have been recorded from conscious eels in water. At low doses, acetylcholine reduced the heart rate but increased the transbranchial differential blood pressure. The effects were abolished by atropine but not by tubocurarine. At doses in excess of 0.1 mug/kg, a secondary rise in arterial blood pressure was observed which could be abolished by bretylium, phentolamine or phenoxybenzamine. Catecholamines did not affect the heart rate although a transient bradycardia due to reflex inhibition could be observed with adrenaline and noradrenaline. Catecholamines increased the cardiac contractile force through an alpha-adrenergic mechanism which was blocked by phentolamine but not by propranolol. The relative potency was noradrenaline greater than adrenaline greater than isoprenaline. A beta-adrenergic receptor located in the branchial circulation led to vasodilation and decrease in transbranchial differential pressure. Both alpha-(vasoconstriction) and beta-(vasodilation) adrenergic receptors were present in the systemic circulation. Dopamine, 5-HT, GABA and bradykinin caused bradycardia abolishable by vagotomy or atropine treatment. Angiotensin II was hypertensive but did not affect the heart rate nor the transbranchial differential pressure. Tyramine caused release of endogenous catecholamines. With repeated doses, tachyphylaxis to the drug was observed. Histamine was without any obvious cardiovascular effects in the eel.

Acetylcholine↗
PubMed1992

Spatial heterogeneity of the metabolic response of RIF-1 tumors to a vasoactive agent evaluated in vivo by one-dimensional 31P chemical-shift imaging.

Localized 31P NMR spectroscopy was used to evaluate the spatial heterogeneity of the metabolic response of RIF-1 tumors to hydralazine. Volume localized 31P spectra were obtained from subcutaneous RIF-1 tumors using one-dimensional chemical-shift imaging, before and 20 min after treatment with 5 mg/kg hydralazine, administered intravenously. Following treatment all of the tumors showed an overall decrease in the ratio of nucleoside triphosphate (NTP) to inorganic phosphate (Pi) and a decrease in pH. However, spatial localization revealed that the reduction in NTP/Pi was not uniform within some tumors. This was partly due to regional differences in the levels of metabolites existing before treatment. Normal tissue adjacent to the tumor did not show a significant decrease in high-energy metabolites or pH.

Animals↗
PubMed1984

Scanning electron microscopy of nasal arterioles effected by vasoactive agents.

Morphological changes in nasal blood vessels induced by alpha- and beta-adrenergic and cholinergic agonists were studied under a scanning electron microscope after removal of extracellular connective tissue and the basal lamina. Arterioles were constricted and dilatated following topical application of alpha-adrenergic and cholinergic agonists. Distinctive morphological changes were observed on their smooth muscle cells. Smooth muscle cells of constricted arterioles had a rugged surface with numerous fine invaginations. However, in dilatated arterioles the cells had a smooth surface and intercellular spaces were clearly revealed. No remarkable changes were produced in smooth muscle cells by the beta-adrenergic agonist. It is concluded that nasal arterioles are sensitive to alpha-adrenergic and cholinergic stimulation but not to beta-adrenergic stimulation.

Animals↗
PubMed1978

Modifications by stretches of the mechanical response of isolated cerebral and extracerebral arteries to vasoactive agents.

Length-tension relationship was compared in helically cut strips of canine cerebral, coronary, mesenteric, renal, and femoral arteries. Tension developed progressively by increasing the stretch; with the same strain, a greater passive tension developed in cerebral than in extracerebral arteries. The peak active tension developed by serotonin (cerebral, coronary), norepinephrine (mesenteric, renal and femoral) or K+ (coronary) was obtained at a resting tension of 1.5 g (other than coronary) or 2.0 g (coronary). Papaverine (10(-4) M) caused a relaxation in cerebral arterial strips contracted with serotonin to a level lower than that prior to the addition of serotonin, the relaxation from the initial level of tension being related directly to the stretch applied. The relaxing effect of adenosine was related directly to stretches of cerebral arterial strips. It seems likely that a rise of intra-arterial pressure effects a greater increase in the wall stiffness in cerebral than in extracerebral arteries. The responsiveness to vasoconstricting and vasodilating agents of both cerebral and extracerebral arteries appears to increase when the arteries are distended.

Adenosine↗