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PubMed1991

Left ventricular geometry, myocardial function and energetics of the dilated left ventricle. Influence of vasodilators and positive inotropic substances.

Vasodilators have been shown to improve hemodynamics of the failing heart as a short-term effect and to decrease mortality as a long-term result. We therefore studied the effect of different vasodilators on myocardial mechanics and energetics in patients with idiopathic dilated cardiomyopathy (IDC) NYHA II to III. In these patients undergoing routine heart catheterization myocardial oxygen consumption was measured using the argon method, and left ventricular pressure and geometry were obtained from left ventricular angiography using a Millar tip microcatheter. All data were analyzed for one single heart beat. The best correlation was found between MVO2/beat and the systolic stress-time integral which considers left ventricular pressure, wall thickness, and geometry. The relation between MVO2/beat and peak systolic wall stress was less relevant. No correlation was found between MVO2/beat and pressure-volume work, dP/dtmax, and mean velocity of circumferential fiber shortening. The intravenous application of nitroprusside and the ACE-inhibitor benazepril decreased both the systolic stress-time integral and the myocardial oxygen consumption in proportion to each other indicating unchanged economy of myocardial contraction. In contrast to other vasodilators, beta 1-agonists and phosphodiesterase inhibitors increase myocardial oxygen consumption independently of changes in the stress-time integral. In conclusion, vasodilators decrease left ventricular pressure and chamber size and thereby proportionally reduce MVO2/beat. The reduction of energy needed for myocardial contraction may partially explain the long-term effects of the ACE-inhibitors and combinations of vasodilators. Pure positive inotropic substances, especially beta 1-agonists, increase myocardial oxygen consumption with minor changes of systolic stress-time integral.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Volume↗
PubMed1987

Effects of vasodilator antihypertensive agents on renal function.

The effects of calcium antagonist and noncalcium antagonist vasodilator antihypertensive agents were examined using renal clearance, hemodynamic, and micropuncture techniques in anesthetized normotensive dogs, rats, and conscious spontaneously hypertensive rats. At doses that either failed to affect mean arterial pressure or lowered it equally, the calcium antagonist vasodilator agents nifedipine and felodipine produced a natriuresis and renal vasodilatation whereas the noncalcium antagonist vasodilator agents hydralazine and minoxidil produced an antinatriuresis and renal vasoconstriction. These findings support the view that the development of tolerance to the antihypertensive effect of noncalcium antagonist vasodilators, which is usually reversed by concomitant diuretic administration, is dependent on renal sodium and water retention. In addition, the capacity of calcium antagonist vasodilators to directly inhibit renal tubular sodium reabsorption explains their natriuretic action and the absence of antinatriuresis may contribute to lesser development of tolerance.

Animals↗
PubMed1987

Nitrendipine and the pressure-dependent vasodilation of vessels in the hydronephrotic kidney.

The influence of renal perfusion pressure on the vasodilation of the kidney caused by a calcium antagonist, nitrendipine, was studied. The diameter of several preglomerular and postglomerular vessels in the split hydronephrotic kidney of Inactin-anesthetized rats were measured by in vivo television microscopy. A reduction in the renal perfusion pressure to 80 mm Hg (femoral artery pressure) was achieved by clamping of the aorta above the renal arteries. The pressure reduction induced vasodilation of the arcuate arteries (proximal and distal), interlobular arteries (proximal and distal), and the afferent arterioles near the interlobular arteries. The afferent arterioles at sites near the glomerulus showed no pressure-dependent vasodilation. Topically applied nitrendipine led to a dose-dependent preglomerular vasodilation that did not further increase during perfusion pressure reduction. From these experiments, it is concluded that nitrendipine-induced renal vasodilation is independent of the renal perfusion pressure and primarily caused by its direct effect on preglomerular vessels.

Acetylcholine↗
PubMed1986

[Therapy of chronic heart failure with vasodilators].

The chronic heart insufficiency is essentially characterized by a disturbed regulative function of the peripheral circulation. These processes taking place within efforts for compensation close the chain of the vicious circle. The vasodilators with their different principles of effect affect in various places of the vegetative nervous system up to the smooth musculature of the vessels and modulate the peripheral part of the cardiovascular system. Via a changed behaviour of the impedance also with the arterial vasodilation the ejection behaviour of the insufficed hearts changes. With the increase of the ejection fraction the filling pressure can decrease, also when only the arterial branch of the periphery of the vessels is influenced. In case of an additional vasodilation of the capacity vessels greater influences of the preload are present. As a rule after the full use of the conventional therapy with digitalis and saluretics is resorted to the adjuvant therapy with vasodilators. Good experiences in the therapy of chronic heart insufficiency are present above all for hydralazine and prazosin as well as increasingly also for captopril, when vasodilating and at the same time positively inotropic medicaments are disregarded. In future, depending upon haemodynamic and neurohumoral (PNA, PRAA) findings in problematic cases and aimed additional adjuvant therapy will be aspired to.

Adrenergic beta-Agonists↗
PubMed1988

The effects of indomethacin on the systemic and regional vasodilator responses to minoxidil in the conscious dog.

To define the role of endogenous prostaglandin (PG) synthesis in the vasodilator response to minoxidil (MNX), whole body and regional hemodynamics were measured in conscious, MNX-pretreated dogs before and after the administration of the cyclooxygenase inhibitor indomethacin (INDO). Twenty minutes after an i.v. dose of 2.0 mg/kg, INDO did not affect the reductions in mean arterial pressure and total peripheral resistance achieved with 1.0 mg/kg of MNX i.v. INDO appeared to selectively reverse MNX's vasodilation in the skin and stomach, as vascular resistance in these two tissues increased to pre-MNX levels. Since INDO also exerts a selective vasoconstriction in the skin and stomach of conscious, nonpretreated dogs (Humphrey and Zins, 1983), the fact that skin and stomach resistances were near baseline with this drug combination implies that MNX continues to exert a net vasodilation in these vascular beds. In contrast to INDO's negligible hemodynamic interactions, MNX's vasodilation was nearly completely reversed by continuous i.v. infusions of the direct vasoconstrictor arginine vasopressin (ADH) administered at a mean dose of 35 mU/kg/min. MNX's reversal by ADH was not matched by maximally effective i.v. infusions of the alpha-adrenergic agonist norepinephrine at a mean dose of 0.4 micrograms/kg/min. These results indicate that the sustained peripheral vasodilation seen with MNX in the conscious dog is not dependent upon the synthesis of endogenous, PG-like dilator substances, as defined by concomitant INDO administration.

Animals↗
PubMedDate not supplied

Vasodilator responses in perfused rabbit kidney: the role of endothelium.

The responses to vasodilator agents of renal vasculature were studied in perfused rabbit kidney. Acetylcholine (ACh) and calcium-ionophore (A23187), as endothelium-dependent relaxing agents, and prostacyclin (PGI2), an endothelium-independent vasodilator, induced a rapid and reversible fall in perfusion pressure of the noradrenaline (NA) constricted renal vasculature. The vasodilator responses of the preparations were not lost after perfusing the kidney with hypotonic Krebs-solution or 10 mumol/l mepacrine. Collagenase treatment significantly reduced the vasodilator responses, not only to ACh and A23187, but also to PGI2. Perfusion of the renal vascular bed with dexamethason did not influence the vasodilator responses. Exposure of the renal vasculature to p-bromophenacylbromide (PBPB), which is a known inhibitor of phospholipases, markedly reduced the ACh- and A23187-induced vasodilatation. The responses to PGI2, however, were also moderately depressed in the presence of PBPB. The lipoxygenase-inhibitor nordihydroguaiaretic acid (NDGA), inhibited the responses to ACh and A23187, but did not reduce the responses to PGI2. Some commonly used methods and chemicals, that have been successful in destroying the endothelium of large vessels, were not effective in renal vasculature. We failed to demonstrate that the inhibitory actions of these treatments were specific for the endothelium-dependent responses. Our results provide indirect evidence for the involvement of lipoxygenase products in the vasodilatation responses of the rabbit kidney and for a possible role of endothelium in the reactivity of renal vasculature.

Animals↗
PubMed1979

[Vasodilators in the treatment of cardiac insufficiency (author's transl)].

The use of vasodilators represents a new approach to the treatment of cardiac insufficiency, either chronic or acute. Their field of action is venous, arterial or mixed. Decreasing the pre-load, the "venous" vasodilators lighten the congestive symptoms of cardiac insufficiency. By decreasing the post-load, the "arterial" vasodilation increases the cardiac output. Some vasodilators, venously administered, imply a continuous hemodynamic checking (Sodium Nitroprussiate, Phentolamine, injectable Trinitrine). Others are active orally (Trinitrine, Isosorbide Dinitrate, Hydralazine, etc.). Vasodilating treatment is recommended for acute cardiac insufficiency, particularly during myocardium infarct and some acute valvular insufficiencies. It is also successfully used in acute lung edema. Finally it takes an increasing importance in the treatment of chronic cardiac insufficiency.

Acute Disease↗
PubMed1980

[Long-term use of vasodilators in patients with congestive cardiomyopathy (author's transl)].

Three patients with congestive cardiomyopathy were studied for the acute and chronic hemodynamic effects of vasodilators using right heart catheterization, echocardiography and exercise tolerance test. All of the three were in congestive heart failure and were on digoxin and furosemide. Various vasodilators were used, which included isosorbide dinitrate, hydralazine, phentolamine and prazosin. Favorable acute hemodynamic effects were seen in all three. However, on continued use, all three showed evidence of tolerance to vasodilators by hemodynamic measurements. The first patient died in heart failure, complicated by pulmonary infarction. The second died suddenly after discharge from the hospital, while maintained in good control of the congestive heart failure. The third patient had recurrence of congestive heart failure after discharge, which was controled by the hospitalization and change to different vasodilator agents. Favorable hemodynamic effects were readily seen following vasodilators in patients with confestive cardiomyopathy. However, on chronic use some tolerance to the agents was observed. This needs to be investigated as to the mechanism so these agents can be more effectively utilized in these patients who are usually resistant to the conventional mode of therapy.

Adult↗
PubMed1980

Does histamine influence vasodilation caused by prolonged arterial occlusion or heavy exercise?

Vasodilation induced by prolonged arterial occlusion or fatiguing exercise is thought by some to be due, in part, to histamine. To test this hypothesis, we studied isolated canine gracilis muscles perfused at low, constant flow. Diphenhydramine and cimetidine, H1 and H2 receptor antagonists, respectively, were used in combination. Vasodilation induced by a supramaximal dose of histamine was abolished but vasodilation after occlusions thought capable of inducing ischemic injury was unchanged in magnitude or time course. Vasodilation during moderate or heavy exercise at constant flow was also unaffected. We conclude that reactive hyperemia and exercise vasodilation in skeletal muscle do not depend even in part on histamine.

Animals↗
PubMed1980

[Methodology of hemodynamic study of a vasodilator drug (author's transl)].

The mechanism of action of a vasodilator drug is complex and depends on its predominant site of action: arterial or venous system. it leads to a) complex alteration of ventricular load that changes cardiac output, b) alteration of myocardial energetic metabolism. To classify a vasodilator drug, it is useful to study: a) its mechanism of action on the peripheral vascular system, b) the left ventricular function, and c) the coronary blood flow and the myocardial metabolism. The peripheral action of the drug is assessed by simultaneous measurement of peripheral blood flow, arterial pressure and venous pressure. From these data, arterial resistance (AR) and venous tone (VT) are calculated. A change of AR and for VT permits to classify a vasodilator drug as arterial, venous or both arterial and venous. Changes of factors of ventricular load are appreciated by measurement of aortic pressure, left ventricular pressure and ventricular volumes. If no change of heart rate occures, modification of stroke volume and cardiac output is due to a reduction of end diastolic volume (venous vasodilator drug) or of end systolic volume (arterial vasodilator drug).

Cardiac Output↗
PubMedDate not supplied

The position of NO among endogenous vasodilators.

Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.

Acetylcholine↗
PubMed1994

Vasodilator responses to calcitonin gene-related peptide (CGRP) and amylin in the rat isolated perfused kidney are mediated via CGRP1 receptors.

This study was designed to characterize the calcitonin gene-related peptide (CGRP) receptors mediating vasodilation in the rat isolated perfused kidney and to address the question as to whether amylin, a 37 amino acid peptide having about 50% overall sequence homology with CGRP, interacts with common CGRP receptors or acts via distinct amylin receptors. Human alpha-CGRP (h alpha CGRP) and human beta-CGRP, rat alpha-CGRP and rat amylin amide produced dose-related vasodilation of the perfused renal vascular bed with pD2 estimates of rat alpha-CGRP (10.8 +/- 0.2), h alpha CGRP (10.5 +/- 0.2), human beta-CGRP (10.5 +/- 0.2) and rat amylin amide (9.4 +/- 0.3). In contrast, the CGRP2 receptor-selective agonist [acetamidomethyl-cysteine2.7]h alpha CGRP (0.1 mumol) was inactive. The CGRP1-receptor antagonist, h alpha CGRP8-37 reversibly antagonized the vasodilator response induced by h alpha CGRP with an apparent pK1 of 8.03 +/- 0.21. The analog h alpha CGRP8-37 (1 microM) also reversibly inhibited submaximal responses to rat amylin amide. In contrast, rat amylin8-37 (1 microM) had no significant inhibitory effect either on rat amylin amide- or on h alpha CGRP-induced vasodilation (P > .05), showing that rat amylin8-37 does not have affinity for the CGRP1 receptor in this preparation. These data suggest that the predominant CGRP receptors in the rat renal vascular bed are of the CGRP1 type, and that the vasodilation induced by rat amylin amide is due to CGRP1 receptor activation.

Amyloid↗
PubMed1994

A potential mechanism of vasodilation after warm heart surgery. The temperature-dependent release of cytokines.

Peripheral vasodilation is a common feature of warm heart surgery and creates clinical concerns when pressor agents become necessary because of the potential for some of these drugs to adversely affect flow through newly engrafted arterial and venous bypass conduits. The possible role of a temperature-dependent production of cytokines in the pathogenesis of this vasodilation was investigated in a two-part study. In part I, lipopolysaccharide-activated peritoneal rabbit macrophages (5 x 10(6)/ml) were incubated at 30 degrees or 37 degrees C up to 9 hours and the concentration of tumor necrosis factor released in the supernatant was serially measured by a bioassay. Tumor necrosis factor production was found to increase over time for each of the two temperatures of incubation but was significantly higher throughout the observation period in normothermic experiments than in those done at 30 degrees C. Part II was a prospective clinical study involving 30 patients who underwent either cold (core temperature 28 degrees to 30 degrees C, n = 15) or warm (37 degrees C, n = 15) cardiopulmonary bypass and in whom serum levels of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were measured by enzyme-linked immunosorbent assays at 2, 4, 10, and 24 hours after bypass. Cytokine levels were found to be consistently higher in patients having normothermic bypass. Differences between the two groups were significant 2 hours after bypass for tumor necrosis factor alpha and interleukin-6 (p < 0.02 and p = 0.0001, respectively) and 4 and 10 hours after bypass for interleukin-1 beta (p < 0.01 and p < 0.04, respectively). The incidence of vasodilation necessitating vasopressor support was twofold higher in the normothermic group (six patients versus three in the hypothermic group). Taken as a whole, patients supported by pressor agents had significantly higher cytokine levels after bypass than those who did not require pressor therapy. Our results suggest that vasodilation occurring with warm heart operation is, at least partly, mediated by a temperature-dependent release of cytokines. Vasodilation might therefore be mitigated by simply allowing the core temperature to drift during bypass. Our recent clinical experience suggests that this "tepid" heart surgery (32 degrees to 34 degrees C) effectively blunts most of the vasodilatory response to strictly normothermic bypass without compromising maintenance of myocardial aerobiosis during arrest.

Animals↗
PubMed1993

Antagonism of acetylcholine and adenosine rat cremaster arteriolar vasodilation by combination of NO antagonists.

It has become evident that complete elimination of the vasodilator response to agonists that require the release of nitric oxide (NO) is necessary for certain studies of the microcirculation. The A2 and A3 arterioles of the rat cremaster muscle microcirculation were studied by video-microscopy. At control, arterioles at rest or constricted by arginine vasopressin (AVP) were dilated by intra-arterially injected acetylcholine (ACh), intra-arterially injected adenosine (ADO) and topical adenosine. The NO antagonists, Nw-nitro-L-arginine methyl ester (L-NAME) and hydroquinone (HQ), which acts as an antagonist by generating free radicals, in maximal doses, individually partially blocked the vasodilator actions of intra-arterial ACh and intra-arterial ADO. Combining L-NAME and HQ eliminated the vasodilation by intra-arterial ACh and intra-arterial ADO. Sodium nitroprusside dilated the arterioles to the resting level or above at control and in the presence of the antagonists either individually or when combined. However, the NO antagonists did not block the arteriolar vasodilator responses to topical ADO. The reduction of the production of NO and enhancement of its destruction by superoxide radicals results in the total absence of the vasodilator response due to intra-arterially injected acetylcholine and adenosine. The data suggest that luminal ADO receptors cause arteriolar dilation by endothelial-dependent mechanisms and abluminal receptors cause dilation by another mechanism.

Acetylcholine↗
PubMed1993

Microinjection of L-lactate in the preretinal vitreous induces segmental vasodilation in the inner retina of miniature pigs.

PURPOSE: The authors investigated the hypothesis that the retinal vasomotor effect of acute hypoxia is mediated by lactate. METHODS: Retinal vasomotor arteriolar response was measured in the intact eyes of miniature pigs after systemic administration and after local preretinal juxta-arteriolar microinjection of lactate. RESULTS: Injection of L-lactate (physiologically produced lactate) into the systemic circulation decreased the arterial blood pH but did not dilate the retinal arterioles. By contrast, microinjections of L-lactate (0.5 mol/l, pH 2) into the juxta-arteriolar vitreous induced a reversible segmental vasodilation of 32 +/- 4% (standard deviation). This vasodilation did not depend on periarteriolar pH lowering because microinjections of a 0.5 mol/l L-lactate at neutral pH also dilated segmentally the retinal arterioles (37 +/- 5.5%). The effect of lactate was stereospecific because microinjections of the isomer D-lactate (0.5 mol/l, pH 2) did not affect the arteriolar caliber (P = 0.63). Perfusion of the eye with the cyclo-oxygenase inhibitor indomethacin, through cannulization of the sublingual artery, caused a generalized reversible arteriolar vasoconstriction of 51 +/- 9.8% but did not inhibit the segmental vasodilator effect of locally microinjected L-lactate. CONCLUSIONS: It is known that acute hypoxia in the isolated retina causes an increase in lactate production. In the intact eye, there is a retinal vasodilation, which is not inhibited by indomethacin. Hence, it was concluded that retinal, but not blood, lactate is a possible mediator of the acute hypoxia-induced vasodilation.

Animals↗
PubMed1996

Inhibition of cerebral neurogenic vasodilation by L-glutamine and nitric oxide synthase inhibitors and its reversal by L-citrulline.

The possibility that L-citrulline is able to reverse inhibition of neurogenic vasodilation in isolated porcine cerebral arteries produced by nitric oxide synthase (NOS) inhibitors and Gln was examined by using in vitro tissue bath techniques. The results indicated that transmural nerve stimulation elicited a frequency-dependent and tetrodotoxin-sensitive vasodilation in isolated ring segments of arteries with or without endothelial cells. The dilation was abolished by L-N-omega-nitro-L-Arg and L-N-omega-L-Arg methyl ester and was completely reversed by L-citrulline, but not by D-citrulline. In parallel studies, the transmural nerve stimulation-induced relaxation was blocked in part by Gln. The blockade was completely reversed by L-citrulline and L-Arg, but not by their D-enantiomers. The time courses of relaxation after L-citrulline reversal of inhibition of vasodilation produced by Gln and NOS inhibitors were identical to that of relaxation in the control. The residual relaxation after L-citrulline reversal was abolished by L-NNA and L-N-omega-nitro-L-Arg. At 1 mM, L-glutamate, tau-aminobutyric acid or NH4Cl did not block transmural nerve stimulation-induced relaxation, nor did Gln inhibit sodium nitroprusside-induced relaxation or neuronal NOS activity. These results provide pharmacological evidence that cerebral perivascular nerves can recycle L-citrulline to L-Arg for synthesizing nitric oxide to induce neurogenic vasodilation. Although the exact mechanism of action of Gln in inhibiting nitric oxidergic neurovascular transmission remains undetermined, Gln does not seem to act by releasing ammonium ions, inhibiting NOS or modifying the nitric oxide-cyclic GMP pathway. Cerebral metabolism of Gln may play an important role in regulating nitric oxidergic neurogenic vasodilation.

Animals↗
PubMed1998

The A2A adenosine receptor mediates coronary vasodilation.

The coronary vasodilation caused by adenosine is due to activation of A2 adenosine receptors (A2AdoRs), but the subtype or subtypes of A2AdoR (A2A and/or A2B) that mediate this action are uncertain. The purpose of this study was to test the hypothesis that A2AAdoRs mediate coronary vasodilation caused by exogenous or endogenous adenosine in the guinea pig isolated perfused heart. The newly described A2AAdoR antagonist SCH58261 was used to selectively block A2AAdoRs. Attenuations by SCH58261 of increases in coronary conductance (A2 response) and of atrioventricular nodal conduction time (A1 response) caused by exogenous and endogenous adenosine and by agonists with relative selectivity for A2A and A1AdoRs were measured. The CGS21680-induced increase of coronary conductance was antagonized by SCH58261 in a concentration-dependent and competitive manner with a KB value of 5.01 nm. Also reversed by SCH58261 (60 nmol/L) were the increases in coronary conductance caused by the relatively selective A1AdoR agonists CCPA (70 nM), and (R)-(-)N(b)-(2-phenyl-isopropyl)adenosine (60 nM) but not those caused by sodium nitroprusside (1.2 microM) and diltiazem (0.4 microM). SCH58261 (< or = 100 nM) did not attenuate the A1AdoR-mediated prolongations of S-H interval caused by either adenosine or CCPA. SCH58261 attenuated the coronary vasodilation caused by 50 nM adenosine with an IC50 value of 6.8 +/- 0.6 nM. The coronary vasodilations caused by the nucleoside uptake inhibitor draflazine and the adenosine kinase inhibitor iodotubercidin were completely reversed by 60 nM SCH58261 or adenosine deaminase (7 U/ml). Thus, the A2AAdoR plays a major role as mediator of coronary vasodilation caused by exogenous and endogenous adenosine and by AdoR agonists.

Adenosine↗
PubMed1998

Peripheral vasodilators and the management of peripheral vascular disease and Raynaud's syndrome in general practice.

There is no convincing evidence that peripheral vasodilators produce any significant improvement in exercise tolerance in patients with peripheral vascular disease, and these drugs may do more harm than good. In the treatment of severe Raynaud's syndrome, however, thymoxamine, prazosin or nifedipine is recommended. A descriptive study was carried out, firstly, to determine why these drugs are prescribed in general practice, and secondly, to describe the drug choices in the treatment of both Raynaud's syndrome and peripheral vascular disease in a representative sample of 22 practices in Northern Ireland. Of those patients prescribed peripheral vasodilators 69.6% were diagnosed as peripheral vascular disease, claudication or atherosclerosis. Over three-quarters of peripheral vasodilators prescribed were repeat prescriptions. Of those with Raynaud's syndrome only half were treated appropriately, and certainty of diagnosis did not guarantee appropriate treatment. Peripheral vasodilators accounted for the majority (51.5%) of items prescribed for peripheral vascular disease. A minority of patients with peripheral vascular disease (20.3%) were prescribed aspirin, and a smaller minority (4.4%) had undergone amputation. Peripheral vasodilators were prescribed unnecessarily and inappropriately. Measures to promote evidence-based treatment of both Raynaud's syndrome and peripheral vascular disease in general practice need to be taken.

Journal Article↗