Action of nicotine on coronary vascular resistance in dogs

1962 ◽  
Vol 203 (4) ◽  
pp. 621-625 ◽  
Author(s):  
Floyd E. Leaders ◽  
J. P. Long
Keyword(s):  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Force Of Contraction ◽  
Parasympathetic Nerve ◽  
Intracoronary Administration ◽  
Chromaffin Tissue

The effect of nicotine, norepinephrine, acetylcholine, and sympathetic and parasympathetic nerve stimulation on perfusion pressure in the left descending coronary artery has been evaluated. Nicotine administered intra-arterially produced an increase in coronary vascular resistance as indicated by an increase in coronary perfusion pressure. It was concluded that this results from sympathetic nervous system activity or release of catecholamines from chromaffin tissue. Ganglia or ganglion-like structures are apparently involved. Other drugs and procedures that were used in attempting to localize the site of nicotine action are discussed. The experimental procedures were also used with preparations that measured myocardial force of contraction. The contractile force of the myocardium, as well as coronary perfusion pressure, was increased with intracoronary administration of nicotine or norepinephrine and sympathetic nerve stimulation. Coronary vascular resistance was increased by these agents and procedures. Vagal nerve stimulation or intracoronary administration of acetylcholine usually decreased the force of contraction and coronary perfusion pressure.

Canine coronary vasodepressor responses to hypoxia are abolished by 8-phenyltheophylline

1989 ◽  
Vol 257 (4) ◽  
pp. H1043-H1048 ◽  
Author(s):  
H. M. Wei ◽  
Y. H. Kang ◽  
G. F. Merrill
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Vasodepressor Response

Anesthetized randomsource mongrel dogs of either sex were instrumented to investigate the effects of 8-phenyltheophylline on changes in coronary perfusion pressure caused by systemic hypoxia under conditions of controlled constant coronary blood flow. In the absence of 8-phenyltheophylline, coronary perfusion pressure decreased from 98 +/- 10 to 69 +/- 4 mmHg (P less than 0.05) at the end of 3 min of systemic hypoxia [arterial partial pressure of oxygen (PO2) = 23 +/- 2 mmHg]. Calculated coronary vascular resistance decreased concomitantly by 30 +/- 5% (P less than 0.05). In the presence of continuously infused 8-phenyltheophylline, equally severe hypoxia increased coronary perfusion pressure from 112 +/- 10 to 129 +/- 13 mmHg (P less than 0.05). Under these conditions, calculated coronary vascular resistance increased 14 +/- 3% (P less than 0.05). Dose-dependent attenuation of the coronary vasodilator response to exogenous adenosine under normoxic conditions was produced by 8-phenyltheophylline. In vehicle-treated dogs, repeat bolus injections of adenosine consistently lowered coronary perfusion pressure by 45 +/- 15%. The vasodepressor response did not vary from one injection to the next. These data demonstrate that under conditions of controlled constant coronary blood flow, treatment with 8-phenytheophylline abolishes coronary vasodilation caused by systemic hypoxia.

Dynamics of myocardial oxygen consumption and coronary vascular resistance

1977 ◽  
Vol 233 (1) ◽  
pp. H34-H43 ◽  
Author(s):  
F. L. Belloni ◽  
H. V. Sparks
Keyword(s):  
Oxygen Consumption ◽  
Vascular Resistance ◽  
Coronary Sinus ◽  
Myocardial Oxygen Consumption ◽  
Time Course ◽  
Coronary Perfusion Pressure ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Constant Flow

Coronary vascular resistance may be regulated in part by substances whose concentrations are determined by or reflect the rate of myocardial oxygen consumption (e.g., adenosine, vessel wall PO2). We tested this hypothesis by comparing the time course of changes in myocardial oxygen consumption and coronary vascular resistance following 20 beat/min changes in heart rate. Main left coronary arteries of in situ dog hearts were perfused with blood at constant flow. Coronary sinus O2 content was monitored continuously with a densitometer and reflected the time course of changes in oxygen consumption and also the effects of vascular transit between tissue and the coronary sinus. These transit effects were estimated from dye transit curves and added to the time course of changes in coronary perfusion pressure which was proportional to coronary vascular resistance at constant flow. Coronary sinus O2 content changes preceded the adjusted time course of vascular resistance. This supports the hypothesis that coronary vascular resistance is regulated in part by factors closely linked to oxidative metabolism.

Effect of cardiac cooling on coronary vascular resistance in normothermic dogs

1960 ◽  
Vol 199 (1) ◽  
pp. 163-166 ◽  
Author(s):  
Robert A. Hardin ◽  
Jerry B. Scott ◽  
Francis J. Haddy
Keyword(s):  
Vascular Resistance ◽  
Control Level ◽  
Coronary Perfusion Pressure ◽  
Effect Of Temperature ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
External Work ◽  
Cold Blood ◽  
Warm Blood ◽  
Arch Of The Aorta

Coronary vascular resistance was observed while the temperature of the heart was lowered to 25°C. The heart was beating but performing no external work. This was accomplished by shunting the blood around the heart and lungs, clamping the arch of the aorta and perfusing cold or warm blood at a constant rate into the ascending aorta. In most instances, coronary perfusion pressure decreased during perfusion with cold blood. The pressure suddenly fell further as perfusion with warm blood was restarted and then gradually returned to the control level. The heart spent an increased proportion of time in systole during perfusion with cold blood. These findings indicate that local cardiac cooling by the method utilized causes active dilatation of the coronary vascular bed of the dog. This dilatation may result from some direct effect of temperature change upon vascular smooth muscle.

The effects of periarterial nerve activation on coronary vessel tone in an isolated and perfused slab of beef ventricle

1979 ◽  
Vol 57 (3) ◽  
pp. 291-297 ◽  
Author(s):  
Stanley Kalsner
Keyword(s):  
Coronary Artery ◽  
Nerve Stimulation ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Coronary Vessel ◽  
Cholinergic Innervation ◽  
Coronary Perfusion ◽  
Direct Effects ◽  
Secondary Complications ◽  
Release Of Noradrenaline

The direct effects of extrinsic nerve stimulation on coronary artery tone are unclear because of the complications arising from alterations in myocardial dynamics which themselves alter flow. An isolated and perfused nonbeating slab of beef ventricle was utilized in the present experiments to eliminate secondary complications and the effects of periarterial nerve activation on coronary perfusion pressure were examined. It was found that stimulation induced vasoconstrictor responses which were enhanced by physostigmine, a cholinesterase inhibitor, and blocked by atropine. These responses were duplicated by exogenous acetylcholine both in the perfused preparation and in isolated strips of coronary artery. Although added noradrenaline gave vasodilatation, no response attributable to the release of noradrenaline from nerves was obtained. It is concluded that the coronary vasculature of the beef receives a cholinergic innervation and that its activation, especially under conditions of reduced transmitter degradation, may induce considerable coronary vessel constriction.

Influence of arterial oxygen tension on coronary vasodilator action of nitroglycerine

1969 ◽  
Vol 47 (1) ◽  
pp. 93-98 ◽  
Author(s):  
R. F. P. Cronin ◽  
A. Kovacs
Keyword(s):  
Vascular Resistance ◽  
Venous Blood ◽  
Arterial Oxygen Tension ◽  
Coronary Perfusion Pressure ◽  
Arterial Oxygen ◽  
Myocardial Segment ◽  
Coronary Perfusion ◽  
Coronary Vascular Resistance ◽  
Arterial Blood ◽  
Vasodilator Action

In 11 anesthetized open-chest dogs, controlled perfusion of the left circumflex coronary artery was accomplished by shunting blood from the femoral artery and vein via a peristaltic pump. The pO2 of the perfusing blood was altered by changing the proportion of arterial and venous blood reaching the inflow side of the pump. Coronary perfusion pressure (CPP) was measured during stepwise reduction in the left circumflex coronary flow (LCF) over the range 120–10 cc/min. Resistance to coronary blood flowin the perfused myocardial segment was calculated as the ratio CPP/LCF and plotted against flow. Resistance-flow curves for the perfused coronary segments were obtained at pO2 values ranging between 95 and 25 mm Hg. Lowering the pO2 of the perfusing blood caused a reduction in coronary vascular resistance (CVR) in the perfused segment. When nitroglycerine was infused in a dosage of 3–6 μg/kg per minute, arterial blood pressure and heart rate were unaltered but CVR was reduced. The reduction in CVR was inversely proportional to the pO2 of the perfusing blood, the maximal vasodilator effect being observed at pO2 > 60 mm Hg. Nitroglycerine caused no significant change in coronary vascular resistance at pO2 < 39 mm Hg and did not prevent or delay the appearance of excess lactate in the coronary venous blood.

Contribution of extravascular compression to reduction of maximal coronary blood flow

1992 ◽  
Vol 262 (1) ◽  
pp. H68-H77
Author(s):  
F. L. Abel ◽  
R. R. Zhao ◽  
R. F. Bond
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Perfusion Pressure ◽  
Left Ventricular Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Coronary Perfusion ◽  
Storage Site

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

scholarly journals Cardiac arrest complicating cardiogenic shock: from pathophysiological insights to Impella-assisted cardiopulmonary resuscitation in a pheochromocytoma-induced Takotsubo cardiomyopathy—a case report

2021 ◽  
Vol 5 (3) ◽  
Author(s):  
Filippo Zilio ◽  
Simone Muraglia ◽  
Roberto Bonmassari
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Left Ventricle ◽  
Cardiogenic Shock ◽  
Takotsubo Cardiomyopathy ◽  
Perfusion Pressure ◽  
Coronary Perfusion Pressure ◽  
Left Ventricular ◽  
Coronary Perfusion ◽  
Refractory Cardiac Arrest

Abstract Background A ‘catecholamine storm’ in a case of pheochromocytoma can lead to a transient left ventricular dysfunction similar to Takotsubo cardiomyopathy. A cardiogenic shock can thus develop, with high left ventricular end-diastolic pressure and a reduction in coronary perfusion pressure. This scenario can ultimately lead to a cardiac arrest, in which unloading the left ventricle with a peripheral left ventricular assist device (Impella®) could help in achieving the return of spontaneous circulation (ROSC). Case summary A patient affected by Takotsubo cardiomyopathy caused by a pheochromocytoma presented with cardiogenic shock that finally evolved into refractory cardiac arrest. Cardiopulmonary resuscitation was performed but ROSC was achieved only after Impella® placement. Discussion In the clinical scenario of Takotsubo cardiomyopathy due to pheochromocytoma, when cardiogenic shock develops treatment is difficult because exogenous catecholamines, required to maintain organ perfusion, could exacerbate hypertension and deteriorate the cardiomyopathy. Moreover, as the coronary perfusion pressure is critically reduced, refractory cardiac arrest could develop. Although veno-arterial extra-corporeal membrane oxygenation (va-ECMO) has been advocated as the treatment of choice for in-hospital refractory cardiac arrest, in the presence of left ventricular overload a device like Impella®, which carries fewer complications as compared to ECMO, could be effective in obtaining the ROSC by unloading the left ventricle.

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