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At least 199 records · Page 11Linked to original sources
PubMed1999

Progressive treatment of erectile dysfunction with intracorporeal injections of different combinations of vasoactive agents.

To account for severity of disease in patients with erectile dysfunction, we introduced a progressive treatment technique using four protocols of drug injections. The study group consisted of 452 men aged 26-85 gamma with erectile dysfunction. Protocol I. All patients began with a combination of papaverine and Regitine in doses adjusted to the estimated severity of dysfunction and to age, up to a maximum dose of 25 mg papaverine and 1.5 mg of Regitine. Protocol II. Patients who could not achieve sufficient rigidity on protocol I were switched to prostin VR, to a maximum of 25 mcg. Protocol III. Patients who failed protocol II received papaverine, Regitine and prostin VR. Protocol IV. Patients who failed protocol III received atropine sulfate (0.02-0.06 mg) in addition to papaverine, Regitine and prostin. Sufficient rigidity was achieved as follows: Protocol I=305 (67.4%) of the original cohort; Protocol II= 61 of the 147 failures with Protocol I (41.5%); Protocol III = 55 of the 86 failures with Protocol 11 (63.9%); Protocol IV = 20 of the remaining 31 patients (64.5%). Overall, sustained rigidity was achieved in 441 of the 452 patients (97.5%). Eleven patients (2.5%) failed all four protocols and were offered a penile prosthesis. Therefore, using our progressive method, by starting with the most available and inexpensive drugs, patients with erectile dysfunction can be given optimal treatment according to the severity of their disease. The success rate is high while costs are kept to a minimum.

Adult↗
PubMed2006

Changing the pathophysiology of solid tumours: the potential of TNF and other vasoactive agents.

Solid tumour therapy with chemotherapeutic drugs is hampered by a number of factors resulting in poor results and failure of initially promising drugs. From the application of Tumour Necrosis Factor alpha in the melphalan-based Isolated Limb perfusion some lessons could be learned. Most importantly, combination of treatment approaches, certainly when multiple targets are involved, increases the effectiveness of the therapy. Clinical outcome may improve dramatically when the tumour pathophysiology is changed in such a way that co-administered chemotherapeutics are more active or are capable of reaching the tumour cells better. Here some of the methodologies and drug combinations which improve solid tumour therapy through acting on the tumour pathophysiology are discussed.

Antineoplastic Agents↗
PubMed1995

Regulation of U-937 monocyte adhesion to cultured human mesangial cells by cytokines and vasoactive agents.

Leukocyte adhesion to kidney cells is an early event in renal inflammation, such as glomerulonephritis. We developed an experimental model of monocyte adhesion to cultured human mesangial cells. U-937 myelomonocytic leukaemia cells, similar to peripheral blood human monocytes, irreversibly bound to mesangial cell monolayers upon 30-180 min coincubations (to a max. of 13,600 +/- 1100/cm2 monolayer), as assessed by cell counting, U-937 labelling with 3H-thymidine, and colorimetry of nuclear staining with crystal violet. Adhesion was enhanced in mesangial cells proliferating in response to 17% fetal bovine serum, indicating expression of a proinflammatory phenotype. E. coli lipopolysaccharide (LPS), tumour necrosis factor-alpha (TNF-alpha) and protein kinase C activation with phorbol myristate acetate (PMA) potentiated monocyte binding during either coincubation or 24-h pretreatment (0.1 microM PMA, +200 +/- 21%). Binding was also promoted by pretreatment with vasoconstrictors, such as the thromboxane A2 mimetic, U-46619 (10 nM-1 microM, max. +35 +/- 3%), or 1 microM angiotensin II (+64 +/- 4%). To elucidate the mechanisms of monocyte adhesion, we analysed the adhesion molecules expressed by human mesangial cells, employing reverse transcription/polymerase chain reaction to detect ICAM-1, VCAM-1 and E-selectin gene expression. Proliferating cells express VCAM-1 and ICAM-1, confirmed by immunocytochemical staining and 79 +/- 3% inhibition of stimulated adhesion by pretreatment of mesangial cells with an anti-ICAM-1 monoclonal Ab. E-selectin transcription was not detectable.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Chemical compatibility of inotropic and vasoactive agents delivered via a multiple line infusion system.

OBJECTIVES: To determine the chemical compatibility of three different triple drug admixtures diluted with either 5% dextrose in water or 0.9% NaCl solution when administered via a multiple line infusion system (Omni-Flow 4000, Abbott Laboratories, Abbott Park, IL). The triple drug admixtures were: a) dobutamine, dopamine, and norepinephrine; b) nitroglycerin, sodium nitroprusside, and dobutamine; and c) nitroglycerin, dopamine, and dobutamine. DESIGN: Two phase in vitro compatibility study. SETTING: Pharmaceutical laboratory. SUBJECTS: None. INTERVENTIONS: Phase I assessed chemical stability when the triple drug admixture was placed in a single container. In phase II, individual drug components of the admixtures were infused via the multiple line infusion system. Samples were collected at time 0, 1 hr, 2 hrs, 4 hrs, 12 hrs, and 24 hrs. All samples were frozen and stored at -70 degrees C until assayed. MEASUREMENTS AND MAIN RESULTS: Samples were assayed using stability-indicating high performance liquid chromatography. The triple drug admixtures were considered to be chemically stable if there was < or = 10% loss of stated potency over 24 hrs. In phase I, chemical stability was observed for all triple drug admixtures at 24 hrs. In phase II, dobutamine, dopamine, norepinephrine, and sodium nitroprusside showed chemical stability at 24 hrs. Nitroglycerin showed a two-fold increase in concentration at 24 hrs compared with the initial concentration through the test infusion system; however, this amount was still one third lower than originally anticipated. CONCLUSIONS: All triple drug admixtures were chemically stable when placed in single containers. Dobutamine, norepinephrine, and sodium nitroprusside showed chemical stability when delivered via a multiple line infusion system. The reduced recovery of nitroglycerin from the test infusion system may result from adsorption of the nitroglycerin to the polyvinyl chloride plastic cassette and tubing during infusion.

Chromatography, High Pressure Liquid↗
PubMed1993

Mechanisms of endothelium-dependent responses to vasoactive agents in isolated porcine coronary arteries.

In isolated porcine coronary arteries, acetylcholine elicited contractions that were potentiated by endothelium denudation. In endothelium-intact strips, the contraction deteriorated by repeated trials and was reversed to a relaxation. NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor, abolished the relaxation or reversed it to a contraction. Endothelium-dependent relaxations caused by serotonin were also reversed to a contraction by treatment with L-NA. Relaxations caused by substance P were dependent on the endothelium and were abolished by oxyhemoglobin; however, L-NA did not completely abolish the relaxation. It may be concluded that porcine coronary arteries respond to acetylcholine with contractions by a direct action on smooth muscle that are minimized by stimulated release of NO from the endothelium. It appears that the relaxation caused by serotonin is due to NO released from the endothelium, whereas the substance P-induced relaxation is associated mainly with endothelium-derived NO produced by NO synthase sensitive to L-NA and also with NO produced via a L-NA-resistant process or via a pathway distinct from that through NO synthase.

Acetylcholine↗
PubMed1998

Effects of boron neutron capture therapy using borocaptate sodium in combination with a tumor-selective vasoactive agent in mice.

Boron neutron capture therapy (BNCT) destroys tumor cells by means of alpha particles and recoil protons emitted by 10B(n, alpha)7Li reaction. For BNCT to be effective, the tumor/normal tissue concentration ratio of 10B must be larger than 1.0, because neutron distribution is not selective. We examined the combination of 10B-enriched borocaptate sodium (BSH) with flavone acetic acid (FAA) as a model compound which causes vascular collapse in squamous cell carcinoma in mice (SCCVII tumors) and would increase the tumor/normal tissue concentration ratio of 10B. FAA (200 mg/kg, i.p.) was injected, and 5 min later BSH (75 mg/kg, i.v.) was administered, followed 15 to 180 min later by irradiation with thermal neutrons. The 10B concentrations were measured by prompt gamma ray spectrometry. Without FAA, tumor 10B concentrations were less than or equal to normal tissue concentrations at all time intervals, except that the concentrations were 1.7- to 2.7-fold greater in tumor than muscle at 15 and 180 min after injection of BSH. With FAA, 10B concentrations 2.1- to 6.9-fold greater in tumor than in muscle were achieved at all intervals tested. For blood and skin, significant differential accumulations were found in tumors at 120 and 180 min. Tumor/liver ratios were less than 1 at all times. Cell survival was determined by in vivo/in vitro colony assay, and increasing radiosensitization correlated with increasing tumor 10B concentrations, whether or not they were achieved with FAA. Tumor control rates, determined at 180 days after BNCT, similarly appeared to depend only on 10B levels at the time of irradiation. Because 10B levels correlate with the radiation response of tissues, a therapeutic gain would be expected whenever the tumor levels exceed normal tissue levels, such as in tumors located in muscle irradiated at 15-180 min after FAA + BSH, or in those in skin irradiated at 120 and 180 min.

Animals↗
PubMedDate not supplied

Cardiovascular responsiveness to vasoactive agents in rats with obstructive jaundice.

1. Pressor responses to tyramine, beta-phenylethylamine and angiotensin II were normal in urethane-anaesthetized rats 7 days after division of the common bile duct. The pressor response to noradrenaline was enhanced at the highest dose level used. 2. The hypotensive response to haemorrhage was exaggerated in bile duct divided rats. 3. The exaggerated haemorrhagic hypotension of bile duct divided rats is unlikely to be the result of impaired vascular response to noradrenaline or angiotensin II, or of accumulation of false neurotransmitters by sympathetic nerves.

Anesthesia↗
PubMed1989

Vascular responses to vasoactive agents in dietary alcohol-treated rats.

1. Young male Sprague-Dawley rats were fed on either solid regular rat chow, control liquid diet or liquid diet containing alcohol for 26 weeks. 2. Phenylephrine (0.5, 1, 2 or 4 micrograms/kg) was injected to monitor the reflexogenic bradycardia and nitroprusside (2, 4, 8 or 16 micrograms/kg) was also used to establish the relationship between drug-induced hypotension and baroreceptor-mediated tachycardia. 3. Multiunit renal nerve activity was determined under pentobarbitone anaesthesia as an index of sympathetic nerve activity during the treatment with phenylephrine or nitroprusside. 4. Alcohol-fed rats showed greater nerve responses to phenylephrine without corresponding decrease in heart rate, which suggests alcohol directly affects arterial wall compliance. This study does not support the contention that dietary alcohol increases blood pressure and it impairs significantly the baroreceptor function.

Animals↗
PubMed1996

Comparison of effects of vasoactive agents on adenylate cyclase activity in endothelial and smooth muscle cells from the same specimen of fetal bovine aorta.

1. Adenylate cyclase activity in vascular endothelial cells (EC) has not been adequately defined. We compared adenylate cyclase activities in EC and smooth muscle cells (SMC) from the same specimen of fetal bovine aorta. 2. The basal adenylate cyclase activities of EC and SMC did not differ significantly (18.9 +/- 0.8 and 21.4 +/- 1.7 pmol/mg protein per min, n = 10, respectively). 3. The adenylate cyclase of EC responded dramatically to catecholamines, with the ED50 value for isoproterenol being 0.036 mu mol/L, and was also more sensitive to calcitonin gene-related peptide than that of SMC. 4. The adenylate cyclase of SMC was more sensitive to prostaglandins (with the ED50 for PGI2 being 0.024 mu mol/L) and glucagon than that of EC, and responded modestly to catecholamines and was almost selectively sensitive to beta1-adrenoceptor agonists. 5. Maximum responses of adenylate cyclase to F-, guanosine 5'-o-(3-thiotriphosphate) and forskolin were greater in SMC than in EC. 6. Based on these findings, it was concluded that EC and SMC differed significantly in adenylate cyclase responsiveness to agonists including hormones, prostaglandins, peptides and substances which may modify the effects of G proteins, although they shared a common developmental origin. Presumably, beta-adrenoceptor agonists in EC and prostaglandins in SMC may appear to play an important role in cellular functions which are mediated by increases in cAMP.

Adenine↗
PubMed2006

Role of the endothelium on vasoactive agents in patients with liver cirrhosis.

BACKGROUND AND AIM: Patients with liver cirrhosis exhibit peripheral vasodilatation and decreased vasoconstrictor responsiveness. We investigated the role of the endothelium in these patients. METHODS: Nine patients with cirrhosis and seven controls were recruited. Responses to acetylcholine, bradykinin and sodium nitroprusside were obtained using forearm plethysmography. Responses to norepinephrine (100 ng/min) were obtained in the absence and combined presence of the cyclo-oxygenase inhibitor, indomethacin, and the nitric oxide (NO) synthase inhibitor, N(G)-monomethyl-L-arginine. RESULTS: Responses to acetylcholine (area under curve: controls vs cirrhotic, 10326 +/- 1400 vs 18490 +/- 2787 units; P = 0.036), but not to bradykinin (15619 +/- 3557 vs 12415 +/- 3823 units) or sodium nitroprusside, were significantly higher in patients with cirrhosis. Responses to norepinephrine were significantly dampened in cirrhotics (percentage increase in forearm blood flow; controls vs cirrhotics, -50.50 +/- 2.69 vs-26.39 +/- 5.44; P = 0.036) but this blunted response was no longer apparent following the administration of both blockers. CONCLUSIONS: We conclude that: (i) there is an increased response to acetylcholine but not to bradykinin; and (ii) that an enhanced production of prostacyclin and/or NO is responsible for the dampened response to norepinephrine.

Acetylcholine↗
PubMed1978

Age-related changes in the response of rabbit isolated aortae to vasoactive agents.

1 In helically-cut strips of aortae from rabbits of different ages (2 to 360 days old), responses to vasoconstrictor and vasodilator agents were compared. 2 The passive tension developed by the same magnitude of stretch was markedly less in aortae from immature rabbits than in aortae from mature rabbits. 3 Contractile responses to noradrenaline and K+ increased with age in the range from 2 to 90 days. High concentrations of noradrenaline (10(-5) and 5 X 10(-5) M) produced relaxation of aortic strips from immature rabbits (2 to 30 days). The response to histamine was not altered with age. Age-dependent reductions (90 to 360 days) in the response to 5-hydroxytryptamine were observed. 4 Relaxations induced by isoprenaline of aortic strips contracted with prostaglandin F2alpha increased with age in the range from 2 to 30 days but decreased with age from 30 to 360 days. Similar age-related alterations in the relaxant response to adenosine were observed. 5 It is concluded that aortae from immature rabbits are more distensible than those from mature rabbits; alpha-adrenoceptors mature during an early postnatal period (2 to 30 days), and 5-hydroxytryptamine receptor mechanisms deteriorate with age (older than 90 days). The beta-receptor mechanism does not seem to alter greatly with age.

Aging↗