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PubMed1994

The role of ATP in non-adrenergic sympathetic vascular control of the nasal mucosa in anaesthetized cats and dogs.

1. In anaesthetized cats and dogs, local intra-arterial injection of noradrenaline and alpha, beta-methylene adenosine 5'-triphosphate (mATP) reduced both nasal arterial blood flow and nasal mucosal volume (a measure of capacitance vessel function). The responses to mATP were not modified by pretreatment with the adrenoceptor antagonists phentolamine and propranolol or the purinoceptor antagonist suramin. The vascular effects of noradrenaline were not altered by suramin, but were virtually abolished by adrenoceptor antagonists. 2. After adrenoceptor blockade, frequency-dependent reductions in nasal arterial blood flow with sympathetic nerve stimulation were reduced by 25 and 39% in cats and dogs, respectively; whereas the volume response was reduced by 56% in cats and 54% in dogs. The remaining non-adrenergic sympathetic nerve-evoked vascular responses were not influenced by suramin. 3. During desensitization to mATP induced by local intra-arterial infusion for 5 min, the remaining non-adrenergic nasal blood flow and volume responses to sympathetic nerve stimulation were reduced in the dog but not in the cat. 4. It is suggested that both adrenergic and non-adrenergic mechanisms are involved in the sympathetic control of the nasal mucosa vascular bed of both species. Since desensitization to mATP markedly reduces the remaining non-adrenergic nasal vasoconstriction evoked by sympathetic nerve stimulation in the dog, ATP is a possible sympathetic mediator in the nasal vascular bed in this species.

Adenosine Triphosphate↗
PubMed1996

Different alpha-adrenoceptor subtypes mediate constriction of arterioles and venules.

Recent studies indicate that rat vascular smooth muscle can express mRNAs for the alpha 1A-(alpha 1c-), alpha 1B-, alpha 1D-, alpha 2B-, and alpha 2D-adrenoceptors (ARs). The present study sought to determine which subtypes mediate constriction of resistance and capacitance vessels in rat cremaster skeletal muscle using videomicroscopy. Arterioles (125 microns internal diameter) were isolated, cannulated, and pressurized in a tissue bath. Vascularly "isolated" first-order venules (211 microns) were studied in situ in the cremaster muscle maintained in a tissue bath. Concentration-response curves for stimulation of alpha 1-ARs (norepinephrine plus 1 microM rauwolscine) and alpha 2-ARs (UK-14,304 plus 10 microM 5-methyl-urapidil) were obtained in the presence or absence of alpha-AR subtype-selective antagonists. Chloroethylclonidine (35 and 70 microM), which is most potent against alpha 1B-ARs, had no effect on alpha 1-constriction of arterioles but decreased venule alpha 1-sensitivity (50% effective concentration) by 13-fold (P < 0.01). The alpha 1A- and alpha 1D-selective AR antagonists WB-4101 (50 nM) and 5-MU (350 nM) had no effect on venule alpha 1-sensitivity but reduced arteriole alpha 1-AR sensitivity by 35-fold (P < 0.001) and 6-fold (P < 0.01), respectively. The alpha 1D-antagonist BMY-7378 (350 nM) decreased arteriole sensitivity by fourfold (P < 0.01) but had no effect on venule sensitivity. The alpha 2D-antagonist BRL-44408 (1 microM) caused a ninefold (P < 0.01) decrease in arteriole sensitivity to UK-14,304, whereas the alpha 2B-antagonist ARC-239 (1 microM) had no effect. BRL-44408 also caused a fourfold decrease (P < 0.01) in arteriole sensitivity to oxymetazoline, an agonist selective for alpha 2D- over alpha 2B-ARs. Venule sensitivity to UK-14,304 was reduced fivefold by BRL-44408 (P < 0.05), whereas ARC-239 had no effect. alpha 2 Subtype-selective antagonists inhibited UK-14,304 constriction of venules, with 50% inhibitory concentration values for BRL-44408 (alpha 2D-selective) of 6.04 +/- 0.07, and for the alpha 2B-selective antagonists ARC-239 of 4.79 +/- 0.20, spiroxatrine of 4.91 +/- 0.07, and SK&F-104856 of 5.06 +/- 0.10. These results suggest that constriction of rat skeletal muscle arterioles is mediated predominantly by an alpha 1D-like receptor and the alpha 2D-AR, whereas constriction of venules is dominated by the alpha 1B- and alpha 2D-adrenergic receptor subtypes.

Adrenergic alpha-Antagonists↗
PubMed1988

Splanchnic circulation following coeliac plexus block.

Both the capacitance vessels and the resistance vessels of the splanchnic area are innervated by the sympathetic nerve fibers. We investigated the effect of abdominal visceral sympathectomy on splanchnic circulation, and the effect of altered splanchnic circulation on systemic circulation in ten mongrel dogs. Abdominal visceral sympathectomy was induced by coeliac plexus block with 1 ml/kg (body weight) of 1% lidocaine infiltrated around the coeliac artery. Comparison was made with infiltration of physiologic saline of the same volume. The saline infiltration caused no significant changes in the hemodynamic parameters of systemic and splanchnic circulation. Mean arterial pressure decreased significantly from 18.2 +/- 2.0 to 14.4 +/- 1.9 kPa following the coeliac plexus block, with a concomitant decrease in the cardiac index from 2.63 +/- 0.46 to 2.30 +/- 0.54 l X min-1 X m-2, while systemic vascular resistance was unchanged. Portal vein blood flow, hepatic artery blood flow and, therefore, splanchnic blood flow decreased by 8 to 17%. Portal vascular and hepatic artery resistances were not affected by abdominal sympathectomy. It was concluded that the capacitance vessels in splanchnic circulation are dilated during abdominal sympathetic denervation, causing a blood shift from systemic to splanchnic circulation. On the other hand, the resistance vessels in splanchnic circulation are affected little by abdominal visceral sympathectomy.

Animals↗
PubMed1985

Improvement of coronary blood flow by augmentation of coronary vascular compliance.

Coronary blood flow occurs predominantly during the diastolic period of the cardiac cycle. This study investigated the effects of increasing the diastolic coronary perfusion pressure by artificially increasing the epicardial coronary capacitance function, using a buffer chamber. The left anterior descending (LAD) coronary artery was cannulated in six dogs and perfused by tubing via the carotid artery. A significant stenosis was produced with a screw clamp, resulting in a distal coronary pressure of about 35 mm Hg. A buffer chamber was placed on the perfusion line distal to the stenosis to buffer the distal coronary perfusion pressure. Myocardial blood flow as measured by microspheres showed a 39.6% increase in blood flow during buffered perfusion as compared to nonbuffered perfusion: 0.415 +/- 0.279 versus 0.316 +/- 0.238 ml/min/g. The calculated diastolic pressure time index (DPTI) increased 54.1% during buffered perfusion. Flow increased significantly in the endocardial and mid-wall layers but not in the epicardium. It is concluded that coronary blood flow can be augmented by increasing the coronary capacitance function in this model.

Animals↗
PubMed1989

The effect of topical nasal anaesthesia on allergen-induced symptoms, obstruction and blood flow.

The effect of topical anaesthesia on the nasal mucosa before and after allergen challenge was evaluated in 12 subjects with strictly seasonal allergic rhinitis. A single-blind randomized placebo-controlled design was used. The nasal challenge was carried out after pre-treatment of the nasal cavity with 52 mg of lidocaine/nasal cavity, or placebo applied topically in spray form. The number of sneezes was counted. The amount of nasal secretion was estimated by weighing used paper handkerchiefs. The capacitance and resistance vessel reactions were monitored by determining nasal peak flow and 133Xe wash-out respectively. After placebo pre-treatment the two doses of allergen induced moderate symptoms and vascular changes. Pre-treatment with local anaesthesia did not affect any of the symptoms nor did it affect the decrease in the tone of the capacitance vessels. It was found that topically applied lidocaine per se did not have any effect on nasal mucosal blood flow as measured using the 133Xe wash-out technique. However, the local anaesthesia did block the allergen-induced increase in the tone of the resistance vessels. In conclusion, a redundancy of systems appears to be involved in nasal allergic reactions. Although a reflex-induced mechanism may well play a significant role in the induction of the signs and symptoms of nasal allergic reactions, the redundancy of systems involved may well override any reduction in one single system, as appears to be the case in the present study. Lidocaine per se did not influence the nasal mucosal blood flow.

Administration, Topical↗
PubMed1986

[Resistance, capacitance and exchange functions of the vessels of the small intestines and skeletal muscles during exposure of the body to intense heat].

Rise of body temperature to 41.0-41.2 degrees C led to an increase of the integral, pre- and postcapillary resistance in the vascular bed of the cat small intestine and skeletal muscles. The increase of the resistance function in veins led to an increase of the mean capillary hydrostatic pressure. The above shifts enhanced with increasing of the hyperthermia. The latter was found to reduce distensibility of veins and the capillary filtration coefficient (CFC) in the small intestine vascular bed but to increase the CFC in skeletal muscles. The role of the small intestine and skeletal muscles venous vessels in the shifts of the filtration-absorption ration and the capacitance function in hyperthermia is discussed.

Adaptation, Physiological↗
PubMed1981

Effects of papaveroline-monosulphate on the systemic and regional circulation in the dog.

The effects of papaveroline 6'-sulphonic of N-methylglucamine (UTEN), administered by intravenous injection in doses ranging from 10 to 20 mg/kg, on cardiac dynamics and peripheral blood flow distribution were studied in conscious and anesthetized dogs, using electromagnetic flowmeters implanted around the ascending aorta, pulmonary artery, left coronary artery, superior mesenteric artery, and renal and external iliac arteries. In the conscious dogs, blood pressure after the injection of the drug showed an initial fall and returned to normal control values after a transitory increase. The changes in aortic pressure were accompanied by an increase in heart rate, cardiac output, stroke volume and cardiac work. The administration of UTEN was also associated with an increase in the peripheral blood flow and a decrease in their calculated resistances and in total peripheral resistances. Similar variations were observed in the anesthetized dogs. The effects of UTEN were compared with those of other vasodilator drugs (papaverine, isoxsuprine and D.E.D.). From the results obtained it is possible to conclude that UTEN produces a vasodilation in all investigated vessels, whereas other vasodilator agents only act in some particular vascular beds; moreover, the effect of UTEN is longer-lasting. There is also a probable constriction in the capacitance vessels, as shown by haemodynamic changes in the pulmonary circulation.

Animals↗
PubMed1991

Cardiovascular effects of cromakalim (BRL 34915) in healthy volunteers.

1. The effect of oral doses of cromakalim 0.5, 1.0, 1.5 and 2.0 mg on several cardiovascular parameters was studied in healthy male volunteers. 2. In the first study, no dose of cromakalim reduced systolic or diastolic blood pressure in the supine or standing position. Reductions of diastolic blood pressure after exercise (P less than 0.01) were observed 4 h after administration of 2.0 mg. 3. There was a trend towards increased heart rate after 2.0 mg at all time intervals, and significant changes were observed in supine and standing heart rate at 2 and 4 h (P less than 0.01). No significant change was observed in exercise heart rate. 4. In the second study small increases in forearm blood flow were observed from 3 h to 5 h after oral administration of 1.0 and 2.0 mg of cromakalim. Forearm vascular resistance was significantly reduced after 2.0 mg (P less than 0.025) when compared with placebo. No change was observed in forearm venous capacitance after either dose of cromakalim, or placebo. Supine heart rate was significantly increased 4 h after 2.0 mg of cromakalim (P less than 0.025). 5. These results show that oral administration of cromakalim decreases diastolic blood pressure and forearm vascular resistance. A hypotensive effect is probably attenuated by reflex tachycardia.

Administration, Oral↗
PubMedDate not supplied

Hemodynamic mechanisms of neurogenic pulmonary edema.

Acute lung injury has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. Early studies in our laboratory demonstrated that pulmonary hemorrhagic edema (PHE) of acute and fulminating type occurred accompanying severe hypertension and bradycardia (Cushing responses) in animals following cerebral compression (CC) or intracranial hypertension (ICH). The lung pathology was prevented by spinal transection and sympathoadrenergic blocking agents, but was not affected by decerebration, adrenalectomy, vagotomy and atropine. The effects of central sympathetic activation due to ICH on the systemic and pulmonary resistance and capacitance vessels were studied in dogs with a total heart bypass preparation. ICH caused an increase in vascular resistance with a reduction in the vascular capacity of the systemic and pulmonary circulation. The relative importance of hemodynamic changes was further analyzed with the measurement of aortic and pulmonary flows and the use of right and left heart bypass. The overall pattern of imbalance in the right and left cardiac output was characterized by an immediate fall in aortic flow accompanying a slower decline in pulmonary arterial flow. In rats with a right heart bypass, ICH produced severe pulmonary venous hypertension and PHE. In the left heart-bypassed rats, ICH induced systemic hypertension, whereas no significant changes occurred in the lungs. Our studies reveal that: (1) ICH elicits vasoconstriction of the systemic and pulmonary resistance and capacitance vessels and (2) the major cause of volume and pressure loading in the pulmonary circulation is acute left ventricular failure resulting in a dramatic decrease in aortic flow.

Animals↗
PubMed2000

Carotid and aortic baroreflexes of the rat: I. Open-loop steady-state properties and blood pressure variability.

To characterize the baroreflex in central nervous system-intact neuromuscular-blocked rats, we measured the vascular and cardiac responses and compared direct stimulation of the aortic depressor nerve (ADN) with a capacitance electrode (differentially activating either A or A + C fibers) to carotid sinus pressure with a micro-balloon (SINUS). One-thousand-two-hundred-ninety-seven open-loop measurements of systolic blood pressure (SBP), heart rate, venous pressure (VBP), and mesenteric (msBF), femoral (fmBF), and skin (skBF) blood flow were completed; the linear range of the effects was determined for each response and stimulus mode. The rats were sinoaortic denervated (SAD). The open-loop stimulation effect was very stable; e.g., the mean effect of 790 ADN stimulations during >7 days was -9.8 mmHg, with an average drift of +0.001 mmHg/h. In contrast, there was large variability of the SBP baseline (e.g., SD = +/-10.9), which was due to SAD (+/-6.3 to +/-16.3 mmHg, t = -13. 9, df = 4, P < 0.0002) and was reversed by ganglionic block (+/-10.8 to +/- 2.9 mmHg, t = -12.9, df = 3, P < 0.001). The ADN stimuli produced larger depressor responses than sinus stimuli (-66 vs. -45 mmHg); all component responses paralleled the magnitude of the SBP effect, except interbeat interval (IBI), for which the ADN DeltaIBI was approximately 10 times that of SINUS. For all stimuli, fmBF increased and msBF did not. Mesenteric and femoral vascular conductance both increased, whereas VBP decreased and skBF followed SBP. We found that for all baroreflex response components, with the exception of SINUS-elicited DeltaIBI, there was an orderly, substantially linear, relationship between stimulus strength and response magnitude.

Animals↗
PubMed1986

Bier's spots reconsidered: a tale of two spots, with speculation on a humerus vein.

It is a widely accepted opinion that some of the spots produced on the forearm and hand by external compression of the brachial artery are the visible evidence of an intraosseous shunt in the humerus. These spots were first evaluated systematically by Bier in 1898. Additional studies were conducted by Rehberg and Carrier in 1922 and by Wolf in 1924, the latter's conclusions providing the currently accepted view. We examined these spots with laser Doppler velocimetry and found no differences in cutaneous perfusion among spots of different coloration. Further, there was no difference between any of the spots produced by occluding the brachial artery and values obtained from the forearm of postmortem subjects. It appears that the differences in coloration are not due to an intraosseous vascular shunt at the level of the mid humerus but, instead, are due to a capacitance phenomenon with venodilation in the dark areas and venoconstriction in the pale areas.

Brachial Artery↗
PubMed2001

Activation of the novel prothrombinase, fg12, as a basis for the pregnancy complications spontaneous abortion and pre-eclampsia.

PROBLEM: Impaired trophoblast invasion during the first trimester of pregnancy is linked to spontaneous abortion, and defective invasion in the second trimester to hypertension + proteinuria (pre-eclampsia). Hypertension developing during the third trimester of human pregnancy represents, in part, a corrective response in the mother to provide adequate placental perfusion for fetal growth when trophoblast has not to invaded and converted the myometrial porprtion of maternal spiral arteries into to low resistance-high capacitance conduits. Deportation of vesicles from hypoxemic trophoblast is thought to cause hypertension plus proteinuria, vascular damage and a systemic coagulopathy. Trophoblast invasion may be inhibited by local cytokines, such as TGF-betas but Thl-type cytokines associated with pre-eclapmsia and spontaneous abortions (e.g., IL-1, TNF-alpha, IFN-gamma) are not known to inhibit migration at in situ concentrations. Trophoblast invasion is also inhibited by the binding of surface integrins to fibronectin and fibrin, and fibrin production is stimulated by these Th1 cytokines via up-regulation of prothrombinases(s) such as fg12 which directly and via TNF-alpha-facilitated inflamation compromise trophoblast cell integrity. We, therefore, asked if fg12 expression and TNF-alpha are increased in first trimester human miscarriage and in third trimester pre-eclampsia. METHODS: fg12 mRNA was detected using in situ hybridization and fg12 protein by immunohistochemistry. TNF-alpha mRNA and protein were similarly tested. The techniques were validated using uterine sections from day 8.5 of CBA x DBA/2 pregnancies, and then were applied to sections of placentae from normal and pre-eclamptic pregnancies with and without intrauterine fetal growth restriction (IUGR). Fibrin was detectectd by immunohistochemistry. RESULTS: Expression of fg12 protein correlated with fg12 mRNA expression in mouse uteri and in placentae from normal human pregnancies. Increased expression of fg12 and TNF-alpha mRNA and protein, and increased fibrin deposition was detected in placental trophoblast. CONCLUSIONS: Activation of fg12 prothrombinase by Th1-type cytokines in pregnancy may lead to spontaneous abortion, or in ongoing pregnancy, to pre-eclampsia and/or IUGR.

Abortion, Spontaneous↗
PubMed1992

Calcium channels and nifedipine inhibition of serotonin-induced [3H]thymidine incorporation in cultured cerebral smooth muscle cells.

Cultures of smooth muscle cells were prepared from the basilar artery of adult guinea pigs. Passaged cultures (10-30 passages) that expressed serotonin receptors were studied using [3H]thymidine incorporation. When tested in quiescent medium, serotonin potently stimulated [3H]thymidine incorporation (EC50 of 31 nM) by as much as 400% at 24 h. The number of cells was not significantly increased at 24 or 48 h. At concentrations of 10(-8)-10(-5) M 5-HT, [3H]thymidine uptake was reduced 40-50% by the dihydropyridine Ca2+ channel blocker, nifedipine (1 microM). To demonstrate a possible mechanism for the sensitivity to nifedipine, Ca2+ currents were measured using the whole cell patch clamp technique. The cells expressed dihydropyridine-sensitive L-type Ca2+ channels, but not other subtypes of Ca2+ channels, as indicated by the kinetic and voltage-dependent characteristics of the current and by the stimulatory effect of Bay K 8644. The magnitude of the Ca2+ currents was related exponentially to the membrane surface area, measured as cell capacitance. These data support the association of dihydropyridine-sensitive Ca2+ channels with mitogenesis in vascular smooth muscle, and suggest an alternate mechanism of action for the beneficial effect of dihydropyridines in prophylaxis of cerebral vasospasm.

Animals↗
PubMed1995

Region of epidural blockade determines sympathetic and mesenteric capacitance effects in rabbits.

BACKGROUND: The mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. The role of capacitance changes in the splanchnic venous bed can be clarified by comparing blocks of differing segmental distributions. Specifically, we speculated that blocks that include the innervation to the mesenteric circulation alter hemodynamics, sympathetic activity, and venous capacitance to a greater extent than blocks without blockade of sympathetic nerves to this critical vascular bed. METHODS: Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric vein diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Responses were compared after administration of epidural lidocaine using a dose and catheter level that limited anesthetic to lumbar levels (lumbar group) or thoracic levels (thoracic group). In addition, hemodynamic responses were recorded after thoracolumbar block in animals receiving alpha-chloralose but breathing spontaneously (spontaneous ventilation group) and in awake animals (awake group). RESULTS: Mean arterial pressure decreased 38.3 +/- 5.8% in the thoracic group but only 16.5 +/- 2.8 in the lumbar group. Sympathetic efferent nerve activity decreased in the thoracic group but increased in the lumbar group. An increase in vein diameter followed thoracic epidural anesthesia, but venoconstriction was observed after lumbar epidural block. The addition of intravenous sedation with alpha-chloralose did not increase the hypotensive effect of epidural anesthesia in this model. CONCLUSIONS: Block of sympathetic fibers to the splanchnic circulation with thoracic epidural lidocaine produces mesenteric venodilatation that contributes to hypotension in rabbits. A lesser decrease in blood pressure follows blocks limited to lower segments, because baroreceptor stimulation produces increased splanchnic sympathetic activity and mesenteric venoconstriction. Responses in this model are comparable with and without general anesthesia and mechanical ventilation. To minimize hemodynamic consequences, epidural blockade should ideally be confined to the fewest necessary segments, avoiding splanchnic innervation if possible.

Anesthesia, Epidural↗
PubMed1975

Effect of dihydroergotamine on perpheral circulation during epidural anaesthesia in man.

The effect of intravenous administration of dihydroergotamine (DHE) on regional blood flow in the forearm and calf after pharmacological nerve blockade of the lower body induced by epidural anaesthesia has been studied in 13 subjects. After anaesthesia, DHE induced a significant increase in blood flow in the forearm with intact innervation and a significant decrease in blood flow in the nerve-blocked calf. On the average, the arterial blood pressure increased slightly. The calculated local vascular resistance increased in the nerve-blocked calf, probably due to a direct myogenic constrictive effect of DHE. In the intact forearm, local vascular resistance decreased. The results indicate that DHE exerts a complex effect on resistance vessels in addition to its well-known effect on the capacitance vessels.

Anesthesia, Epidural↗
PubMed1992

Nitrates.

Nitrates have been used for the last 130 years to treat and control the symptoms of angina pectoris. Within the last 15 years, nitrates also have been shown to limit infarct size and to be beneficial in the treatment of patients with severe intractable heart failure, cardiogenic shock, severe mitral and aortic regurgitation, hypertensive episodes, and portal hypertension. The adequate use of nitrates to treat these disorders requires the ability to document a hemodynamic response and to closely monitor the adverse consequences of this therapy. Nitrates work by directly relaxing smooth muscle in resistance and capacitance vessels, thereby causing generalized dilation. Nitrates reduce preload and, at higher doses, reduce systemic vascular resistance and afterload. This chapter reviews the physiologic mechanisms that underlie nitrate therapy, the appropriate indications for nitrate use, the usefulness of specific agents, and their appropriate nursing implications.

Cardiovascular Diseases↗
PubMed1987

[Efficacy of regulation of the vascular tone of the lungs].

Vasomotor responses to activation of sympathetic and parasympathetic lung nerves were studied in the minor circulation, as well as the effect of some vasoactive substances upon vessels and changes in the alveolar air composition. The efficacy of neurohumoral and physical stimuli influence upon the lung resistance function seems to be more obvious at the local level rather than at organic one. This is reflected in actualization of the lung vasomotor control mainly through regional redistribution of the lung blood flow at minimal shifts of the integral vascular resistance. Active changes of the tone of the minor circulation vessels may participate in formation of the lung blood volume shifts in transitory states of the circulation system. Physiological significance of changes in the resistance and capacitance functions of the lung vessels, is discussed.

Animals↗
PubMed1986

Role of reflex sympathetic withdrawal in the hemodynamic response to an increased inotropic state in patients with severe heart failure.

Newer positive inotropic agents used in the treatment of severe heart failure not only increase cardiac contractility, but also cause peripheral vasodilation. It is not known to what extent this vasodilation is due to a direct peripheral action of the drug, as opposed to reflex withdrawal of sympathetic tone secondary to an augmented inotropic state. In 16 patients with severe heart failure, a 48 hour intravenous infusion of milrinone, a positive inotropic vasodilator drug, resulted in an increase in stroke volume index from 26 +/- 2 to 34 +/- 3 ml/m2 (p less than 0.001), a reduction in forearm vascular resistance measured by venous plethysmography from 43 +/- 5 to 27 +/- 3 U (p less than 0.003) and an increase in forearm venous capacitance from 2.1 +/- 0.2 to 2.9 +/- 0.2 ml/100 ml (p less than 0.001). To determine whether a withdrawal of sympathetic tone contributed to this vasodilation, milrinone was infused directly into the left main coronary artery in eight of the patients, thereby eliminating any direct vascular effects of the drug. Intracoronary milrinone (50 micrograms/min) caused an increase in peak positive first derivative of pressure (658 +/- 49 to 784 +/- 68 mm Hg/s; p less than 0.01) and stroke volume index (20 +/- 2 to 25 +/- 3 ml/m2; p less than 0.0001), which was associated with a reduction in plasma norepinephrine from 540 +/- 101 to 423 +/- 90 pg/ml (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Drug Administration Schedule↗