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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two types of vasodilators are used for treatment of acute myocardial infarction: Nitrates on the one hand with predominant venodilation and agents like Phentolamie and Nitroprusside on the other hand with venodilation as well as arteriolar vasodilation. Different opinions exist with respect to indication of these vasodilators. They are used for reduction of arterial blood pressure, for reduction of left ventricular filling pressure and for increase of cardiac output. A marked decrease in ejection fraction is the hemodynamic basis of application of vasodilators in the latter indication. By reduction of peripheral vascular resistance emptying of the left ventricle in these patients is enhanced.) As a working hypothesis in clinical situation elevated filling pressure indicates a decreased ejection fraction. The first part of this investigation deals with relation of left ventricular and diastolic pressure to ejection fraction. A good correlation between these two parameters was found in 717 patients with coronary artery disease. However variability was so wide that regression from enddiastolic pressure to ejection fraction in the individual seemed impossible. In 26.6% of patients with ejection fraction over 0.6%, filling pressure was 20 mm Hg or more. On the other hand, in 34.7% of patients with ejection fraction below 0.3% filling pressure was 20 mm Hg or less. As a consequence of practical value, reduced ejection fraction has to be assumed, if a patient presents elevated filling pressure and reduced cardiac output. In the second part, the hemodynamic effects of Phentolamine in 12 patients with acute myocardial infarction and elevated filling pressure (PCV resp. PADP greater than 18 mm Hg) are described. Maximal effects on hemodynamic variables were: reduction of peripheral vascular resistance by 31.4%, of left ventricular filling pressure by 16.2%, and of mean arterial pressure by 17.0%. Cardiac output increased by 25.8% and heart rate rose by 14.8%. At optimal efficacy, stroke volume increased by 23.7%. Further increase of infusion rate with concomitant fall of peripheral vascular resistance resulted in decrease of stroke volume and tachycardia. Most serious side effects consisted in sudden fall of blood pressure. Therefore intraarterial monitoring of blood pressure is demanded. The third part deals with hemodynamic effects of nitrates (Isosorbiddinitrate 10 mg p.o.) in patients with acute myocardial infarction and elevated filling pressure. One hour after application peripheral vascular resistance decrease by 16.5%, filling pressure by 20.8%, and mean arterial pressure by 9.0%. Cardiac output stroke volume and heart rate did not change significantly. No side effects were observed with Isosorbiddinitrate although two cases of nitrate syncope occurred with Nitroglycerin, resulting in bradycardia and hypotension. Indications for vasodilator therapy therefore has to be handled as follows: Nitrates should be given to patients with elevated filling pressure and normal cardiac output...
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PMID:[Hemodynamic guidelines in the treatment of acute myocardial infarction by means of vasodilators]. 16 46

In organ culture of the cervicovaginal epithelium from neonatal mice, the epithelium synthesizes a material with specific antigenic properties (CVA). CVA was studied with immunofluorescence and the amount estimated semiquantitatively. In line with earlier studies, adenosine 3',5'-cyclic monophosphate (dibutyryl derivative (dcAMP), increased the amount of CVA, but adenosine 2',3'-cyclic monophosphate did not. Addition of histamine to the culture medium moderately increased the amount of CVA, whereas the anti-histamine diphenhydramine (H1-antagonist) slightly reduced the strong increase induced by dcAMP and estradiol in combination. No effect was seen under similar conditions using the H2-antagonist metiamide. Taken together with earlier results it is considered possible that the action of histamine and diphenhydramine is related to effects on the cell membranes. Phentolamine had no effect. The dcAMP effect was inhibited by actinomycin D and cycloheximide.
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PMID:Estradiol-17 beta and cAMP: in vitro studies on the cervicovaginal epithelium of neonatal mice. 18 45

Vasodilative treatment of severe heart failure with infusions of phentolamine leads to ventricular unloading and in many cases brings about a dramatic improvement of the patient's condition. Phentolamine is the only one of the vasodilators so far used in the treatment of heart failure that has a positively inotropic effect. In contrast to sodium nitroprusside and nitroglycerin, it also increases stroke volume at normal filling pressures. Although vasodilative therapy has resulted in a notable decline in the mortality from severe heart failure among hospitalized patients, the long-term prognosis after discharge remains poor. One of the chief reasons is that there has hitherto been no effective orally administrable drug suitable for protracted therapy. Initial clinical studies with a newly developed slow-release formulation of phentolamine have shown that the preparation produces remarkably good effects in patients with chronic heart failure: systolic pressure rises, the amplitude of the blood pressure is augmented and there is an increase in urinary excretion accompanied with a corresponding reduction in weight. In practically all cases, there is a distinct decrease in the size of the heart and in pulmonary congestion.
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PMID:[Treatment of heart failure with phentolamine (Regitin)]. 89 48

Ouabain and vanadate are known as potent inhibitors of Na, K-ATPase in various tissues including smooth muscles. Both agents showed contractile action on various smooth muscles in a similar fashion: stronger contractile action on the aortae of rats (WKY and stroke prone spontaneously hypertensive rats, SHRSP) and guinea-pigs, and weaker contractile actions on basilar and mesenteric arteries of the same animals. Time to peak tension, however, was far longer in ouabain-induced contraction. Phentolamine depressed ouabain-induced contractions, while vanadate-induced contractions were not affected. Elevation of K+ concentration to 20 or 30 mM potentiated vanadate-induced contraction markely, while it potentiated ouabain-induced contraction only slightly. DIDS blocked vanadate-induced contraction but showed no effect on ouabain-induced contraction. Removal of Ca abolished ouabain-induced contractions, while vanadate-induced contractions of reduced height could be observed in the absence of Ca. Verapamil depressed both ouabain- and vanadate-induced contractions of WKY and SHRSP aorte aut exhibited no effect on the guinea-pig aorta. Thus, although similarities of the action of ouabain and sodium vanadate were observed, the modes of the actions were revealed to be different in the two agents. Inhibition of Na, K-ATPase might be involved in the case of ouabain-induced contractions, and inhibition of Ca-ATPase of membranous systems might be involved in vanadate-induced contraction.
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PMID:Comparison of contractile effects of sodium vanadate and ouabain in vascular smooth muscles of guinea-pigs and rats. 303 52

1. The swimmeret system can be excited by perfusing the neuropeptide proctolin through the isolated ventral nerve cord of the crayfish. Previously silent preparations begin to generate a characteristic motor pattern, the swimmeret rhythm, in the nerves that innervate the swimmerets. The response to proctolin is dose dependent and reversible. The threshold concentration of proctolin perfused through the ventral artery is approximately 10(-8) M. The EC50 is 1.6 X 10(-6) M. 2. Proctolin-induced motor patterns have periods and phases similar to those of spontaneously generated motor patterns. The durations of the bursts of impulses in power-stroke motor neurons generated in the presence of proctolin are, however, significantly longer than those that occur during spontaneous activity. 3. DL-Octopamine inhibits the swimmeret system, both when the system is spontaneously active and when it has been excited by proctolin. The inhibition by octopamine is dose dependent and reversible. The threshold for inhibition is approximately 10(-6) M, and the EC50 is approximately 5 X 10(-5) M. 4. Octopamine's effect is mimicked by its agonists, synephrine and norepinephrine. Synephrine has a lower threshold concentration than does octopamine, but norepinephrine is much less effective than octopamine. 5. Octopamine's inhibition is partially blocked by an antagonist, phentolamine. 6. Phentolamine also blocks inhibition of the swimmeret system by inhibitory command interneurons. This block is dose dependent and can be partially overcome by stimulating the command interneurons at higher frequencies. 7. Perfusion with 11 other suspected crustacean neurotransmitters and transmitter analogues did not similarly excite or inhibit the swimmeret system, so we suggest that proctolin and octopamine are transmitters used by the neurons that normally control expression of the swimmeret rhythm.
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PMID:Modulation of the crayfish swimmeret rhythm by octopamine and the neuropeptide proctolin. 311 73

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system. 351 28

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was observed in both areas. Administration of Physostigmine, a cholinesterase inhibitor, at a dose of 0.15 mg/Kg by intravenous route, induced an increase of CBF in the ischemic cortex. This change in CBF reached 120% of pre-occlusion level in the periphery and 80% of pre-occlusion value in the center of the area of distribution of the occluded artery. Although Physostigmine induced an increase in arterial blood pressure, the cerebral hyperemia observed both in normal and ischemic cortex could still be demonstrated after blockade of the pressor effect by bleeding or Phentolamine administration.
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PMID:Physostigmine induced reversal of ischemia following acute middle cerebral artery occlusion in the rat. 376 45

The effects of changing intraluminal pressure on contractions induced by 70 mM potassium (K+) and 10(-7), 10(-6), and 10(-5) M serotonin (5-HT) were studied in vitro in bovine middle cerebral arteries. Changes in vessel outside diameter in whole-mounted cylindrical sections of artery were detected with a photoelectric infrared device. High K+-or 5-HT (10(-5)M)-induced contractions peaked at 25 mm Hg and were significantly correlated with increasing intraluminal pressure between 25 and 175 mm Hg. Contractions induced with lower concentrations of 5-HT (10(-6), 10(-7) M), norepinephrine, and histamine peaked at 75 mm Hg but were not significantly correlated with rising pressure. Phentolamine (2 X 10(-6) M) added to the extraluminal bath had negligible influence on pressure's ability to affect K+- and 5-HT-induced contractions differently. Reducing bath temperature to 27 degrees C reduced the K+ response at each pressure, but similar temperature changes had little affect on the 5-HT-induced contractions. The K+ response became less sensitive to increasing pressure at low temperatures. Nifedipine (10(-7) M) almost totally eliminated K+-induced contractions, while significantly reducing the responses to all concentrations of 5-HT. The 5-HT responses appeared more sensitive to increasing intraluminal pressure in the presence of nifedipine. Maximum Ca++-induced contractions in the presence of 10(-5) M 5-HT and high K+ occurred at 25 mm Hg, while Ca++-induced contractions and Ca++-induced contractions in the presence of 10(-7) 5-HT or K+ plus 5-HT were maximum at 75 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence that intraluminal pressure affects high potassium- and serotonin-induced contractions differently in the bovine middle cerebral artery: an in vitro study. 381 Jul 76

The hemodynamic and respiratory effects of phentolamine i.v. (15-30 mg/h) on pulmonary hypertension following chronic obstructive pulmonary disease (COPD) have been studied in 13 patients under stable conditions. Phentolamine produced a significant reduction in mean pulmonary arterial pressure, right and left ventricular filling pressures and right ventricular stroke work index. Cardiac index and oxygen delivery increased significantly. Individual analysis showed that in 7 patients the driving pressure decreased across the pulmonary circulation with concomitant increase in cardiac output, suggesting a direct vasodilating effect of phentolamine on the pulmonary circulation. Pulmonary gas exchange did not change significantly. In conclusion, in patients with pulmonary hypertension following COPD phentolamine given i.v. may have beneficial effects on right ventricular function and peripheral oxygen delivery without detrimental effect on gas exchange.
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PMID:[Hemodynamic and respiratory effects of phentolamine in pulmonary hypertension secondary to chronic obstructive syndrome]. 397 79

Alpha receptor blocking drugs like Phentolamine, Phenoxybenzamine and Prazosin are potent vasodilators for the treatment of severe left ventricular failure refractory to treatment with digitalis and diuretics. 11 patients with congestive heart failure showed significant clinical and haemodynamic improvement after 4-week administration of 9 mg Prazosin/day. The cardiothoracic ratio was reduced significantly. Haemodynamically a marked decrease of peripheral vascular resistance, an increase of cardiac output, stroke volume and stroke work was noted. Heart rate and plasma catecholamines (dopamine, adrenaline, noradrenaline) showed no significant change. It is concluded that Prazosin exerts a beneficial effect in severe congestive heart failure after 4 week treatment without significant counterregulation to the vasodilatation.
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PMID:[Alpha receptor blocking and cardial insufficiency]. 612 99


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