scholarly journals Studies on the Nervous Control of the Coronary Circulation (III) : THE EFFECT OF THE STIMULATION OF THE PERIPHERAL END OF THE VAGAL NERVE UPON THE CORONARY BLOOD FLOW

1958 ◽  
Vol 21 (12) ◽  
pp. 662-668
Author(s):  
KUNITAKE HASHIBA
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Circulation ◽  
Vagal Nerve ◽  
Nervous Control ◽  
Stimulation Of

Coronary vasodilation mediated by T cells expressing choline acetyltransferase

2021 ◽  
Vol 321 (5) ◽  
pp. H933-H939
Author(s):  
Adrian H. Chester ◽  
Ann McCormack ◽  
Edmund J. Miller ◽  
Mohamed N. Ahmed ◽  
Magdi H. Yacoub
Keyword(s):  
T Cells ◽  
Blood Flow ◽  
Blood Vessel ◽  
Coronary Blood Flow ◽  
Choline Acetyltransferase ◽  
Vascular Endothelium ◽  
Coronary Circulation ◽  
Direct Interaction ◽  
Coronary Vasodilation ◽  
Ischemic Events

This study shows ChAT-expressing T cells can induce vasodilation of the blood vessel in the coronary circulation and that this effect relies on a direct interaction between T cells and the coronary vascular endothelium. The study establishes a potential immunomodulatory role for T cells in the coronary circulation. The present findings offer an additional possibility that a deficiency of ChAT-expressing T cells could contribute to reduced coronary blood flow and ischemic events in the myocardium.

THROMBOLYSIS BY TISSUE-PLASMNOCEN ACTIVATOR AND A FIBRIN (OCEN) -DEGRADATION PRODUCT, PEPTIDE 6A, IN A CANINE MDDEL OF ELECTRICALLY-INDUCED CORONARY THROMBOSIS

1987 ◽  
Author(s):  
T Saldeen ◽  
J Mehta ◽  
W Nichols ◽  
D Lew
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Thrombosis ◽  
Canine Model ◽  
Peak Effect ◽  
Endothelial Surface ◽  
Tissue Plasminogen ◽  
Flow Restoration ◽  
Mean Time ◽  
Stimulation Of

Intracoronary thrombus resulting in acute myocardial ischemia can be lysed by thrombolytic agents, such as, streptokinase or t-PA. We examined the potential of a recombitant tissue-plasminogen activator (rt-PA)and a fibrin (ogen)-degradation productpentapeptide 6A, Ala-Arg-Pro-Ala-Lys, corresponding to aminoacids 43-47 in the BB-chain of fibrinogen, which causes marked increase in coronary blood flow and stimulates prostacyclin release, in restoring coronary blood flow in dqgs with experimentally-induced thrombus. An occlusive thrombus was created in the circumflex (Cx) coronary artery in 8 dcgs by electricalstimulation of the endothelial surface. The electrically-induced Cx thrombus consisted primarily of platelets and fibrin. After the occlusive thrcmbus was stable without electrical currant, rt-PA (10ug/kg/minute for 30 minutes intravenously)or peptide 6A (5 unoles/minute for 20 minutes intracorcnary) were randomly administered. Infusion of t-PA restored coronar blood flow (peak 22 ±12 ml/minute, mean ±SD) in five of seven animlas. The time to flow restoration was 12.3 ± 9.1 minutes and the reflow persistedfor20.0 ± 10.9 minutes. Peptide 6A administration also restored coronary blood flow (peak 20 ± 4 ml/ minute) in seven of eight animals with occlusive coronary thrombus. Mean time to blood flow restoration (4.3 ±2.9 minutes) wasshorter(P>0.05) than with rt-PA, but thereflow persisted only for the duration of tine infusion (16.3 ± 10.2 minutes).Peptide 6A adninistration was associatedwith a significant (P±0.05) increase in plasma 6-keto-PGF1α indicating stimulation of prostacyclin release. In addition, plasma t-PA concentrations also increased (F>0.01) at the peak effect of peptide 6A indicating releaseof endogenous t-PA as another potentialmechanism of the thrombolytic effects of peptide 6A. This study demonstrates that peptide 6A exerts coronary thrombolytic effectsccmpa rable to those of t-PA in a canine model of coronary thrombosis.

Chronotropic, inotropic, and coronary artery blood flow responses to stimulation of specific canine sympathetic nerves and ganglia

1984 ◽  
Vol 62 (11) ◽  
pp. 1374-1381 ◽  
Author(s):  
R. D. Janes ◽  
D. E. Johnstone ◽  
J. A. Armour
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Coronary Blood Flow ◽  
Stellate Ganglion ◽  
Sympathetic Nerves ◽  
Neural Stimulation ◽  
Intramyocardial Pressure ◽  
Intact Heart ◽  
Cardiac Nerves ◽  
Stimulation Of

Electrical stimulation of the major sympathetic cardiac nerves and ganglia in chloralose-anesthetized, open-chest dogs elicited specific changes in heart rate, coronary blood flow, regional intramyocardial pressure, or intraventricular pressure. The effects produced by stimulation of a cardiac nerve were similar to, but never greater than those produced by stimulation of the ipsilateral stellate ganglion. Coronary blood flow was increased when neural stimulation increased intramyocardial pressure. In contrast, coronary blood flow was not altered significantly when neural stimulation induced tachycardia without increasing intramyocardial pressure. It is concluded that in the intact heart, electrical stimulation of the sympathetic cardiac nerves or ganglia increases coronary blood flow by augmenting intramyocardial pressure, not chronotropism.

scholarly journals Mechanisms Involving Myocardial Injury in Tropical Stings and Bites

2017 ◽  
Vol 2017 ◽  
pp. 1-3
Author(s):  
Thirunavukarasu Kumanan ◽  
Mahesan Guruparan ◽  
Ratnasamy Vithiya ◽  
Indika Gawarammana
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Myocardial Injury ◽  
Coronary Vasospasm ◽  
Toxic Substances ◽  
Rare Entity ◽  
Acute Myocardial Injury ◽  
Russell’S Viper ◽  
Stimulation Of

It is known that a number of toxic substances produce myocardial injury by several mechanisms involving interruption of coronary blood flow due to stimulation of clotting mechanism and coronary vasospasm. Number of toxic substances may cause direct myocardial toxicity independent of coronary blood flow. Acute myocardial injury due to stings and bites is a rare entity and not well understood. Here we illustrate a case of myocardial injury due to Russell’s viper envenomation.

Estimation of intramyocardial pressure and coronary blood flow distribution

1988 ◽  
Vol 255 (3) ◽  
pp. H664-H672 ◽  
Author(s):  
Y. Sun ◽  
H. Gewirtz
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Coronary Circulation ◽  
Regression Line ◽  
Flow Distribution ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Flow Distribution ◽  
Intramyocardial Pressure ◽  
D Model

To characterize the intramyocardial pressure (IMP) and coronary blood flow distribution in a stenosed coronary circulation, we compared four analog circuits for modeling coronary impedance. The resistor (R)-diode (D) model simulates vascular collapse, and the capacitor (C) simulates compliance effect. Identification of the best model and magnitudes of the endocardial and epicardial IMPs (IMPendo and IMPepi) was done retrospectively using data from studies in 28 anesthetized swine. Performance evaluation was based on comparison of model predicted vs. observed coronary distal pressure (DP) waveforms and endocardial-to-epicardial (endo-epi) flow ratios as determined by radiolabeled microspheres. The R-D-C model gave the best performance at IMPendo = 1.1 times left ventricular pressure (LVP), and IMPepi = 0.1.LVP + 15 mmHg; with good fit to DP (r = 0.98, slope of regression line = 1.0) and estimates of endo-epi flow ratio (r = 0.78, slope = 1.01, P less than 0.02, SEE = 0.21, n = 139). The R-D model gave comparable results even though capacitance was omitted. Although R-C and R models predicted distal coronary pressure well, they failed to predict endo-epi flow ratios (r less than 0.50). The R-D-C and R-D models were applied in seven prospective studies. Both models generated reasonable estimates of endo-epi flow distribution (r = 0.78, n = 50). Thus the R-D-C or R-D models of the stenosed coronary circulation can be used to provide reliable estimates of transmural blood flow distribution.

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