PubMed Health⌕ Search

Biomedical subjects

A Deussen

Publications and source records attributed to A Deussen.

65 records · Page 4Linked to original sources
PubMed1986

Adenosine, dipyridamole and isosorbide dinitrate are ineffective to prevent the sympathetic initiation of poststenotic myocardial ischemia.

An activation of cardiac sympathetic nerves increases coronary vascular resistance distal to severe stenoses and induces ischemia of the dependent myocardium. The selective alpha 2-adrenoceptor antagonist rauwolscine and the calcium antagonist nifedipine prevent both poststenotic vasoconstriction and ischemia. To exclude the possibility that the beneficial action of nifedipine is based on unspecific coronary dilation rather than a functional antagonism against alpha 2-adrenoceptor mediated poststenotic vasoconstriction we now tested coronary dilatory drugs with a different underlying mechanism. The left ventrolateral cervical cardiac sympathetic nerve was stimulated in 12 anesthetized, vagotomized dogs. A severe stenosis of left circumflex coronary artery was defined by the absence of a postocclusive reactive hyperemia. Sympathetic stimulation increased end-diastolic poststenotic resistance from 0.45 +/- 0.10 to 0.83 +/- 0.18 mmHg X min X 100 g/ml and induced a net lactate production of the poststenotic myocardium. Adenosine (50 micrograms/kg X min i.c., n = 5), dipyridamole (0.2 mg/kg i.v., n = 3) and isosorbide-dinitrate (1 mg i.c., n = 4) did not prevent the increase in resistance and the net lactate production. Thus the effectiveness to prevent alpha 2-adrenergic poststenotic coronary constriction appears to be specific for alpha 2-antagonists and calcium antagonists.

Action Potentials↗
PubMed1985

Alpha 2-adrenoceptor-mediated coronary vasoconstriction persists after exhaustion of coronary dilator reserve.

The effect of intracoronary administration of the selective alpha 2-adrenoceptor agonist B-HT 920 on coronary resistance was tested in 14 open-chest dogs before and after exhaustion of coronary dilator reserve. Under both conditions B-HT 920 increased coronary resistance to the same extent: 27 +/- 4% before and 32 +/- 3% after. Administration of B-HT 920 did not affect cardiovascular haemodynamics significantly, although after exhaustion of coronary dilator reserve left ventricular dP/dtmax decreased slightly by 12 +/- 5%. While efferent cardiac sympathetic discharge remained constant during control conditions it increased by 27 +/- 7% when B-HT 920 was administered into a stenotic coronary artery. We conclude that, in contrast to observations made on alpha 1-adrenoceptors, activation of coronary alpha 2-adrenoceptors may have deleterious effects after exhaustion of coronary dilator reserve because these receptors mediate a comparable constriction in well- and under-perfused coronary vessels. Thus they are unlikely to favour a redistribution of coronary blood flow into under-perfused myocardial regions. In addition, this unfavourable effect of B-HT 920 on coronary perfusion after coronary dilator reserve has been exhausted may be further exacerbated by an increase in efferent sympathetic discharge.

Adrenergic alpha-Agonists↗
PubMed1985

Cardiac sympathetic nerve activity and progressive vasoconstriction distal to coronary stenoses: feed-back aggravation of myocardial ischemia.

This study tested the hypothesis that the relative ischemia distal to a severe coronary stenosis increases the activity of cardiac sympathetic nerves which in turn results in poststenotic vasoconstriction and an aggravation of ischemia. An acute severe stenosis which reduced coronary blood flow to 50% of control was produced in 23 anesthetized, vagotomized dogs and maintained for 20 min. The activity of postganglionic cardiac sympathetic nerves increased by 23 +/- 4% within 20 min. In parallel, poststenotic coronary resistance increased from 0.48 +/- 0.03 to 0.61 +/- 0.03 mm Hg X min X 100 g/ml resulting in a net lactate production after 15 min. Pretreatment with aspirin (6 mg/kg i.v.; n = 5) was without any influence on these reactions. The selective alpha 2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.; n = 6) and the calcium antagonist nifedipine (10 micrograms/kg i.v.; n = 6) prevented the progressive increase in poststenotic resistance and lactate production, but still permitted an increase in sympathetic activity. Segmental anesthesia of cardiac sympathetic nerves by epidural infiltration of procaine at segments C7-T6 (n = 6) prevented the sympathetic activation, the progressive increase in poststenotic resistance and the resulting myocardial ischemia. Sympathetic activation and a concomitant increase in poststenotic resistance resulting in myocardial ischemia were also found in 6 dogs with intact vagus nerves. These data support the hypothesis of a vicious cycle between poststenotic coronary vasoconstriction and sympathetic activation resulting in severe myocardial ischemia.

Animals↗
PubMed1985

Role of cardiac sympathetic nerves in the genesis of myocardial ischemia distal to coronary stenoses.

This manuscript summarizes the effects of cardiac sympathetic nerve activation on coronary blood flow and myocardial function, metabolism, and morphology distal to stenoses. Whereas cardiac sympathetic nerve activation induces an increase in myocardial function and metabolism accompanied by metabolic coronary dilation under physiological conditions, this response is different in the presence of coronary stenoses. With decreasing coronary hyperemic reserve, distal to an increasing degree of coronary stenosis, the predominant response to sympathetic stimulation is continuously shifted from metabolic dilation to alpha-adrenergic vasoconstriction. With a severe coronary stenosis, both electrical stimulation of cardiac sympathetic nerves and reflex sympathetic activation by carotid occlusion induce poststenotic vasoconstriction and ischemia of the dependent myocardium. Poststenotic vasoconstriction is mediated by vascular alpha 2-adrenoceptors and is prevented by phentolamine, rauwolscine, and nifedipine. Prolonged sympathetic activation even results in patchy subendocardial necroses. There is a vicious cycle between poststenotic vasoconstriction, myocardial ischemia, and cardiac sympathetic nerve activity that results in a progressive perfusion impairment during 20 min severe coronary stenosis.

Animals↗
PubMed1985

Acetylcholine induces constriction of epicardial coronary arteries in anesthetized dogs after removal of endothelium.

The acetylcholine-induced relaxation of isolated coronary arteries is reversed to contraction in the absence of endothelium. The importance of endothelium for the regulation of coronary blood flow remains unclear. We thus tested the effects of acetylcholine on epicardial arteries and on coronary resistance vessels in situ in 8 anesthetized dogs. The left circumflex coronary artery was perfused at constant pressure. Epicardial vasomotion was evaluated by sonomicrometry, the vasomotion of coronary resistance vessels by calculated end-diastolic resistance. Acetylcholine (1 microgram/kg/min i.c.) decreased epicardial resistance by 8.6 +/- 1.6% and end-diastolic resistance by 65.8 +/- 6.3%. The epicardial coronary segment was perfused with distilled water for 65 +/- 5 s to denude it of endothelium. After removal of epicardial endothelium, the decrease in end-diastolic resistance caused by acetylcholine was unchanged (59.6 +/- 1.2%); however, epicardial resistance was increased by 7.7 +/- 1.7%. Application of glyceryl trinitrate (5 micrograms/kg/min i.c.) induced a similar decrease of epicardial resistance before and after removal of endothelium:7.9 +/- 1.4 and 6.2 +/- 1.9%, respectively. We conclude that acetylcholine-induced dilation of epicardial coronary arteries is endothelium-dependent in vivo. However, the constriction of epicardial coronary arteries in the absence of endothelium is insufficient to reduce blood flow and to induce myocardial ischemia.

Acetylcholine↗
PubMedDate not supplied

Nifedipine prevents sympathetic vasoconstriction distal to severe coronary stenoses.

Cardiac sympathetic nerve stimulation ( CSNS ) can induce vasoconstriction distal to severe coronary stenoses by activation of vascular alpha 2-adrenoceptors. Whether nifedipine can antagonize this CSNS -induced vasoconstriction was tested in 11 anesthetized, vagotomized dogs. CSNS decreased the end-diastolic resistance of intact coronary arteries from 0.76 +/- 0.07 to 0.56 +/- 0.05 mm Hg x min x 100 g/ml (p less than 0.05). In contrast, the resistance distal to severe stenoses, which were defined by a reduction of the postocclusive reactive hyperemia to almost zero, was increased during CSNS from 0.52 +/- 0.06 to 0.87 +/- 0.14 mm Hg x min x 100 g/ml (p less than 0.05). This increase in resistance was associated with severe ischemia, as indicated by a net lactate production of the circumflex-perfused myocardium and a decrease in systolic segment shortening from 8.4 +/- 0.7 to 7.0 +/- 0.7% (p less than 0.05). Both intracoronary (10 micrograms) and intravenous (10 micrograms/kg) administration of nifedipine did not change the poststenotic resistance at rest, but did prevent the CSNS -induced increase in resistance, the decrease in regional contraction, and the net lactate production. We conclude that nifedipine can prevent the deleterious role of alpha-adrenoceptor-mediated vasoconstriction in the genesis of myocardial ischemia.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo.

The role of alpha-adrenoceptor subtypes mediating vasoconstriction of large epicardial and small resistive coronary arteries was investigated in 26 open-chest dogs. The left circumflex coronary artery was perfused at a constant pressure. Large vessel vasomotion was determined by measurement of circumflex coronary arterial diameter (ultrasonic transit-time technique); the vasomotion of the small resistive coronary arteries was determined from calculated end-diastolic circumflex artery resistance. beta-Receptors were blocked by propranolol (2 mg/kg i.v.) and both vagal nerves were cut. In eight dogs, the intracoronary administration of the alpha 1-adrenoceptor agonist methoxamine (500 micrograms) increased calculated large vessel resistance by 18.8 +/- 5.7% and end-diastolic resistance by 9.5 +/- 0.3%. Intracoronary administration of the alpha 2-adrenoceptor agonist BHT 920 (500 micrograms) did not affect large vessel resistance, but increased end-diastolic resistance by 37.5 +/- 5.6%. In an additional 18 dogs, left cardiac sympathetic nerve stimulation induced an increase in large vessel resistance by 11.1 +/- 0.9% and in end-diastolic resistance by 31.8 +/- 3.0%. The increase in large vessel resistance was prevented by the alpha 1-adrenoceptor antagonist prazosin (1.2 mg/kg i.v.), which still permitted an increase in end-diastolic resistance by 23.0 +/- 3.2%. The increase in end-diastolic resistance was prevented by the alpha 2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.), which still permitted an increase in large vessel resistance by 11.9 +/- 2.4%. The calcium antagonist nifedipine (20 micrograms/kg i.v.) prevented both the increase in large vessel resistance and end-diastolic resistance during sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗