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PubMed1989

Primary pulmonary hypertension. Vascular structure, morphometry, and responsiveness to vasodilator agents.

The use of pharmacologic agents in the treatment of pulmonary hypertension has not proved to be uniformly successful or predictable. One possible reason for the vagaries in response is that the pulmonary vascular lesions are not consistent. We examined the relation between the structure of the pulmonary resistance vessels in unexplained (primary) pulmonary hypertension and the response to pulmonary vasodilators. Our study involved 19 patients with clinically unexplained pulmonary hypertension (mean pressure, 59 +/- 14 mm Hg). After characterizing them clinically and performing control hemodynamic measurements, we determined the acute effects of a series of vasodilator agents that have different mechanisms of action. In 16 patients, lung biopsy material was related to the hemodynamic studies; in nine patients, including six who had undergone open lung biopsy, the hemodynamic studies were related to the pathologic changes found at autopsy. Histologic specimens from all 19 patients were evaluated qualitatively and sorted into three subsets of hypertensive pulmonary arteriopathy: medial hypertrophy (with minimal intimal proliferation), arteriopathy with plexiform lesions (associated predominantly with concentric laminar intimal proliferation and fibrosis), and arteriopathy with microthrombotic lesions (associated predominantly with eccentric intimal proliferation and fibrosis). The 16 lung biopsies were also quantitated by morphometric techniques. Using a decrease in calculated pulmonary vascular resistance of more than 30% accompanied by a decrease in mean pulmonary arterial pressure of at least 10% to define vasodilation, only four patients were responders. The patients varied considerably in their responses to different vasodilator agents. Patients with similar clinical and hemodynamic profiles differed considerably with respect to the nature of their pulmonary vascular obstructive lesions and their responses to vasodilator agents. Qualitative histologic examination of lung tissue did not provide a basis for predicting how individual patients would respond to vasodilator agents. However, quantitative morphologic analysis of the initial open lung biopsy specimens did prove helpful in predicting acute responsiveness to vasodilator agents and the subsequent clinical course of these patients with unexplained (primary) pulmonary hypertension. An intimal area of more than 18% of the vascular cross-sectional area had an 85% predictive value for identifying the patients who did poorly during the first 36 months of follow-up.

Adolescent↗
PubMed1981

Effect of reserpine pretreatment on in vivo femoral arterial responses to vasodilator agents.

This study determined the effects of reserpine pretreatment (1 mg/kg i.m., 24 hr before) on in vivo femoral arterial responses in the dog to the vasodilator agents acetylcholine, isoproterenol, dibutyryl cyclic AMP, adenosine, nitroglycerin and hydralazine. Femoral blood flow was monitored from the right femoral artery into which i.a. injections of the vasodilator agents were given just distal to the flow probe. Femoral vascular resistance was calculated as the ratio of mean systemic blood pressure to femoral blood flow. The response to each dose of vasodilator agent was evaluated by the magnitude of the slope of the regression line relating the resultant decrease in resistance to the resistance before the injection. Reserpine pretreatment increased slopes of these regression lines for adenosine, nitroglycerin, acetylcholine and isoproterenol, suggesting a general enhancement of vasodilator responses by reserpine. Both hydralazine pretreatment (1 mg/kg i.v., 1 hr before testing) and partial aortic occlusion during testing decreased femoral perfusion pressure without increasing vasodilator responses of the femoral arterial bed to adenosine, nitroglycerin, acetylcholine or isoproterenol. Therefore, the enhancement of vasodilator responses by reserpine was apparently not a result of decreased femoral perfusion pressure due to reserpine.

Acetylcholine↗
PubMedDate not supplied

Effect of vasodilating agents on cochlear blood flow under loud sound exposure.

Loud sound has been proved by means of laser Doppler flowmetry to decline cochlear blood flow. The purpose of this study was to investigate the effect of a vasodilating agent on cochlear blood flow under loud sound exposure, i.e. whether the drug can impede blood flow decrease or not. As a vasodilating agent, dilazep dihydrochloride in a dose of 5 mg/kg was used. This drug caused a stable and significant increase of cochlear blood flow when intravenously injected into guinea pigs. When guinea pigs were exposed to loud sound (120 dB SPL at 10 kHz) for 10 min, cochlear blood flow promptly declined at the onset of sound stimulation and promptly recovered at its cessation. Then, dilazep dihydrochloride 5 mg/kg was injected intravenously into the same animal and loud sound (120 dB SPL at 10 kHz) was exposed for 10 min. Dilazep did not fully block a prompt decline of cochlear blood flow. However, the blood flow level was kept much higher than at pre-injection level. This study shows that a vasodilating agent which normally enhances blood flow probably does not completely block the sound-induced drop response in cochlear blood flow.

Animals↗
PubMed1990

Using inotropic and vasodilating agents in pediatric patients with cardiac disease.

Inotropic and vasodilating agents are traditionally used with diuretics to manage heart failure in children with congenital heart disease. This article reviews the developmental aspects of cardiovascular physiology and the rational use of therapeutic agents for acutely ill surgical and medical pediatric patients with cardiac disease. By understanding the actions and indications for inotropic support and afterload reduction, the critical care nurse can intelligently administer these agents and evaluate their effects.

Cardiotonic Agents↗
PubMed1988

[First-line treatment of cardiac insufficiency: digitalis glycosides, diuretics, vasodilator agents or new cardiotonic agents?].

The advent of vasodilator therapy and new cardiotonic agents has modified the medical treatment of heart failure. First-line treatment is no longer standard; its choice must take into account a number of individual factors such as patient's age, causative cardiopathy, severity of the disease, response to treatment, contra-indications and side-effects of drugs. The aim is to obtain an improvement not only in the patient's comfort but also in long-term prognosis. The prescription of digitalis compounds to heart failure patients with sinus rhythm has been questioned. Alternatives to the conventional therapeutic approach based on cardiac glycosides and diuretics are now available. They include the use at an early stage of vasodilator therapy, and notably angiotensin-converting enzyme inhibitors, in the hope of avoiding gradual reduction of cardiac performance.

Cardiotonic Agents↗
PubMed1986

Alterations with age of the response to vasodilator agents in isolated mesenteric arteries of the beagle.

Responses to vasodilator agents were compared in helical strips of mesenteric beagles of different ages (30 days, 3 months, 2 years and 12 years old), precontracted with prostaglandin F2 alpha (PGF2 alpha). Relaxations induced by isoprenaline and adenosine were related inversely to age, whereas those induced by PGI2 and K+ (5 mM) did not alter with age. Acetylcholine-induced relaxations were less in the arteries from the aged (12 year old) beagles than in those from the younger beagles. Histamine-induced relaxations related directly to age between 30 days and 2 years. Acetylcholine-induced relaxation was reversed to a contraction in infant (30 day old) beagle arteries by removal of the endothelium, and significantly attenuated in the older beagle arteries. In adult (2 year old) and aged beagle arteries, removal of the endothelium attenuated the histamine-induced relaxation. Treatment with indomethacin reversed the histamine-induced relaxation to a marked contraction in aged beagle arteries. It may be concluded that responses mediated by beta-adrenoceptors and P1-purinoceptors are less in aged mesenteric arteries than in those from the younger beagles, whereas responses mediated by PGI2 receptors and the electrogenic Na+ pump do not alter with age. The release of endothelium-derived relaxing factor(s) by acetylcholine appears to be inversely related to age. However, the release of PGI2 possibly caused by histamine may be less in infant beagle mesenteric arteries than in those from the older beagles.

Acetylcholine↗
PubMed1975

Effects of vasodilating agents on the microcirculation in marginal parts of the skeletal muscle.

The present investigation was performed to gain information on the changes in the microcirculation of the skeletal muscle during the application of vasodilating agents. The flow velocity in various microvessels was measured cinematographically in isolated and non-isolated muscles of the hindlimb in cats and rats. During the intra-arterial infusion of acetylcholine (1 mug/kg times min), bradykinin (2 mug/kg times min) and isoprenaline (1 mug/kg times min) a decrease in the flow velocity up to a complete stasis was found in most of the microvessels in the marginal parts of the muscles examined. These reactions set in when the femoral flow increased and disappeared when the femoral blood flow returned to the baseline level. The experiments demonstrate that the increase in total blood flow induced by the intra-arterial infusion of vasodilating agents may be associated with a reduced perfusion of certain parts of the striated muscles.

Animals↗
PubMed1981

The influence of postoperative pharmacological vasodilator agents on the pattern of necrosis in a standardised rat skin flap.

An experimental dorsal rat skin flap which produces a consistent pattern of necrosis is described. As judged by the area of necrosis in this flap, short post-operative courses and several vasodilator agents failed to increase flap survival. However it is not possible to conclude from this that those agents did not influence small vessel blood flow. Necrotic flaps in rats may not be the most appropriate models in which to test the effect of vasodilator agents.

Animals↗
PubMed1979

Choroidal blood flow. IV. effect of vasodilating agents.

The effect of vasodilators on choroidal blood flow (CBF) was studied by the krypton clathrate Kr 85 desaturation technique in anesthetized cats. Niacin, papaverine hydrochloride, phentolamine mesylate, and tolazoline hydrochloride were injected via the lateral long posterior ciliary artery (LLPCA) and the femoral artery. The systemic administration of these drugs via the femoral artery, in the doses used, had no significant effect on mean arterial pressure, choroidal vascular resistance (CVR), or CBF. Local administration of the same agents via the LLPCA caused a decrease in CVR with a corresponding increase in CBF.

Animals↗
PubMed1984

Flow and pressure responses of coronary arteries and veins to vasodilating agents.

The response to a bolus injection of nitroglycerine, adenosine, nifedipine, and dipyridamole of the canine systemic as well as coronary artery and venous circulations was observed and contrasted. Particular attention was paid to the time of change of pressures and flows and to changes in oxygen extraction by the myocardium induced by the pharmacological agents. The dosages of vasodilators used were selected so that no significant change in aortic blood flow occurred. Nitroglycerine and adenosine caused a rapid and similar vasodilation in the coronary circulation. Oxygen extraction was not altered by nitroglycerine, but was decreased by adenosine. The onset time of the vasodilation produced by either nifedipine or dipyridamole was similar, but the time to peak action was much slower for dipyridamole. As well, the effect of dipyridamole on intramyocardial and left intraventricular pressures was more delayed than that following the injection of the other agents. Oxygen extraction was reduced by nifedipine and dipyridamole. These results indicate that pharmacological vasodilating agents can affect coronary arteries, coronary veins, and myocardial oxygen extraction differently.

Adenosine↗
PubMed1992

A multicenter, randomized, double-blind, placebo-controlled trial of pimobendan, a new cardiotonic and vasodilator agent, in patients with severe congestive heart failure.

Pimobendan, a new oral cardiotonic and vasodilator agent, increases myocardial contractile force through specific inhibition of phosphodiesterase type III and increased calcium sensitivity of the myocardial contractile elements. The effects of pimobendan on left ventricular performance and maximal exercise capacity were studied in a multicenter, randomized, double-blind, placebo-controlled trial involving 52 patients with severe congestive heart failure despite diuretics, digoxin, and angiotensin-converting enzyme inhibitors. The acute hemodynamic evaluation included three single doses of 2.5, 5.0, and 10.0 mg of oral pimobendan, which was subsequently administered at a daily dose of 5 or 10 mg for 4 weeks. Acute administration of pimobendan significantly increased the resting cardiac index and lowered pulmonary capillary wedge pressure in a dose-dependent manner, whereas heart rate and systemic arterial pressure were not substantially altered. Patients receiving pimobendan, 5 and 10 mg daily, had a significantly greater increase in maximal exercise duration than those receiving placebo, that is, 144 +/- 30 and 124 +/- 33 seconds versus 58 +/- 25 seconds (p = 0.05). Peak oxygen uptake increased by 1.7 +/- 0.8 and 2.2 +/- 1.3 ml/kg/min in patients receiving pimobendan at a daily dose of 5 and 10 mg, respectively, whereas it decreased by 0.1 +/- 0.6 ml/kg/min in patients receiving placebo (p = 0.06). Thus pimobendan acutely improves resting left ventricular performance and chronically increases exercise duration and peak oxygen uptake in patients with severe congestive heart failure concomitantly treated with digoxin, diuretics, and angiotensin-converting enzyme inhibitors.

Cardiotonic Agents↗
PubMed1981

Effects of vasodilator agents on smooth muscle cells of the coronary artery of the pig.

1 Effects of the vasodilator agents, papaverine, diltiazem, and sodium nitroprusside (SNP) on the electrical and mechanical activities of the smooth muscles of the coronary artery of the pig were compared.2 At a concentration of 10(-5) M, papaverine hyperpolarized and increased the ionic conductance of the membrane, SNP slightly hyperpolarized but diltiazem had no effect on the membrane potential and membrane ionic conductance.3 At a concentration of 10(-5) M, diltiazem abolished the spike evoked by outward current pulses in the presence of tetraethylammonium (TEA) 10 mM, while papaverine and SNP slightly reduced spike amplitude.4 The K-induced contraction produced by any given concentration of [K](o) over 20.2 mM was suppressed by diltiazem and SNP dose-dependently in concentrations greater than 10(-6) M; higher concentrations of papaverine were required to suppress contraction.5 The acetylcholine (ACh)-induced contraction was suppressed by diltiazem and SNP at concentrations greater than 10(-6) M and by papaverine in concentrations over 10(-5) M.6 In saponin-treated skinned muscles, papaverine, diltiazem and SNP had no effect on the pCa-tension relationship, i.e. these agents had no effect on the Ca receptor of contractile proteins. Furthermore, the caffeine-induced contraction in skinned muscles (after Ca loading) was not affected by these agents, i.e. the mechanism of Ca release by caffeine in skinned muscles was not affected.7 Chlorpromazine, an agent interacting with calmodulin, antagonized the contractile effect of calcium on skinned muscle fibres.8 The results obtained are discussed in relation to spike and contraction generating mechanisms, i.e. the effects of these agents on Ca influx and Ca release from stored sites. The results indicated that at equimolar concentrations diltiazem suppressed the mechanical response in the coronary artery of the pig more than SNP or papaverine.

Acetylcholine↗
PubMed1985

The absorption, distribution and excretion of a new antithrombotic and vasodilating agent, cilostazol, in rat, rabbit, dog and man.

The absorption, distribution and excretion of a new antithrombotic and vasodilating agent, cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl)butoxy]-3,4-dihydro-2(1H)- qui nolinone, OPC-13013) was studied after the oral administration of cilostazol or 14C-cilostazol in rats, rabbits, dogs and man. After the oral administration of 14C-cilostazol at a dose of 10 mg/kg in male and female rats and rabbits, and at a dose of 3 mg/kg in dogs, the Tmax, Cmax and T1/2 of the radioactivity were 2 h, 710.5 ng eq X ml-1 and 2.5 h in male rats, 4 h, 11 002.8 ng eq X ml-1 and 3.7 h in female rats, 8 h, 358.1 ng eq X ml-1 and 6.9 h in rabbits, and 3 h, 559.4 ng eq X ml-1 and 1.6 h in dogs, respectively. After the oral administration of 14C-cilostazol at a dose of 10 mg/kg in rats, tissue concentrations of radioactivity in female rats were about 3 to 5 times as high as those in male rats. The blood and tissue concentrations of radioactivity in male and female rats showed a marked sex difference. However, the concentrations in the blood in both male and female rats declined rapidly. There was no evidence of the accumulation of radioactivity in the tissues due to repeated oral administrations of 14C-cilostazol at a dose of 3 mg/kg once a day for 21 days in male rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1981

Immediate central and peripheral haemodynamic effects of a new vasodilating agent Pinacidil (P1134) in hypertensive man.

The purpose of this study was to evaluate the immediate central and peripheral haemodynamic effects of a new vasodilating agent P 1134, in hypertensive man. After oral administration of 25 mg P 1134, the maximal haemodynamic changes were (mean +/- 1 SEM): mean blood pressure fell from 121.8 +/- 6.5 to 80.5 +/- 7.8 mmHg, heart rate increased 24.2 +/- 4.5 beats/min, cardiac output rose 2.9 +/- 0.3 1/min and forearm blood flow increased 1.0 +/- 0.1 ml/100 ml tissue/min. Stroke volume increased 17.0 +/- 2.1 ml and the inotropic state of the heart as judged from systolic time intervals increased. Total peripheral resistance and forearm vascular resistance were both reduced by approx. 50%. Linear correlations were found between the serum concentration of P 1134 and the change in mean blood pressure and total peripheral resistance. Changes in the other parameters mentioned above occurred progressively with changes in mean blood pressure and total peripheral resistance. It can be concluded that P 1134 is a very potent hypotensive agent with a haemodynamic profile identical to that seen with vasodilators with preferably act on precapillary resistance vessels. Potency and maximal efficacy exceeds that of hydralazine and seems like that of minoxidil. P 1134 is remarkably free from side-effects apart from causing water retention as all other vasodilators. It can be administered orally as well as intravenously. This makes P 1134 a very interesting compound in the treatment of moderate to severe hypertension, and further studies are well-founded.

Adult↗
PubMed1997

Study of the in vivo and in vitro cardiovascular effects of a hydralazine-like vasodilator agent (HPS-10) in normotensive rats.

1. In this work, the cardiovascular effects of HPS-10, a new vasodilator agent, were studied in rats. 2. In conscious normotensive rats, oral administration of HPS-10 (4-9 mg kg-1) produced a dose-related and long-lasting fall in systolic arterial blood pressure (ED30 of 5.32 mg kg-1), accompanied by an increase in heart rate (ED30 of 8.43 mg kg-1). This tachycardia was totally inhibited by pretreatment with (+/-)-propranolol (10 mg kg-1, p.o.). 3. In anaesthetized normotensive rats, HPS-10 (0.3-0.6 mg kg-1, i.v.) produced a gradual, dose-dependent and sustained decrease in systolic, diastolic and mean arterial pressure (MAP) (ED30 for MAP of 0.41 mg kg-1, i.v.), accompanied by a significant bradycardia at high doses (> 0.4 mg kg-1; ED20 of 0.61 mg kg-1, i.v.). HPS-10 (0.5 mg kg-1, i.v.) did not modify the positive chronotropic effects induced by intravenous administration of noradrenaline (NA; 5 micrograms kg-1), angiotensin II (AII; 0.2 microgram kg-1) and nicotine (200 micrograms kg-1) but markedly inhibited the hypertensive response produced by these agents. 4. In rat isolated rubbed aorta, HPS-10 (0.1-1 mM) non-competitively and with almost equal effectiveness antagonized the contractions induced by NA, AII (in normal Krebs solution) and Ca2+ (in depolarizing Ca(2+)-free high-K+ 50 mM solution). In the experiments in Ca(2+)-free medium, HPS-10 (1 mM) considerably inhibited the contractions induced by NA, AII and caffeine in rat aorta. 5. Furthermore, in the studies with radioactive Ca2+, HPS-10 (1 mM) did not modify the basal uptake of 45Ca2+ but strongly decreased the influx of 45Ca2+ induced by NA, AII and K+ in rat aortic rings. 6. In rat isolated atria, HPS-10 (1 mM) produced a positive inotropic/negative chronotropic effect. 7. HPS-10 (0.3 mM) significantly inhibited the sustained and transient Ba2+ inward current (IBa) recorded in whole-cell clamped rat aortic myocytes. 8. These results indicate that the non-selective vasorelaxant effects of HPS-10 in rat aortic rings can be attributed to transmembrane Ca(2+)-antagonist activity and an intracellular action on smooth muscle cells. The direct vasodilator action of HPS-10 observed in rat isolated aorta may be responsible for the HPS-10 hypotensive activity in anaesthetized normotensive rats.

Angiotensin II↗