Effect of vest cardiopulmonary resuscitation rate on cardiac output and coronary blood flow

1989 ◽  
Vol 17 (8) ◽  
pp. 768-771 ◽  
Author(s):  
SHLOMO A. BEN-HAIM ◽  
RONA SHOFTI ◽  
BILL OSTROW ◽  
URI DINNAR
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cardiopulmonary Resuscitation ◽  
Coronary Blood Flow

Effects of khellin on coronary blood flow and related metabolic functions

1959 ◽  
Vol 196 (2) ◽  
pp. 391-393 ◽  
Author(s):  
Richard L. Farrand ◽  
Steven M. Horvath
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Control Period ◽  
Systemic Arterial Pressure ◽  
Arterial Oxygen ◽  
Arterial Oxygen Content ◽  
Fick Principle ◽  
Metabolic Functions ◽  
Pulmonary Arterial

Khellin, a drug employed as a coronary dilator, was tested to determine its effects on the cardiovascular system of the dog. Ten mongrel dogs were anesthetized with Nembutal and, after control observations were made, given an intravenous administration of 1 mg/kg body weight of khellin. Coronary blood flow and cardiac output samples were drawn during the control period and at 10, 40 and 80 minutes after administration of the drug Cardiac output was calculated by the direct Fick principle and coronary blood flow by the nitrous oxide method. There was a significant (5%) increase in the arterial oxygen content during the 10- and 40-minute intervals, but no change was observed at 80 minutes. An increase in arterial-mixed venous oxygen difference occurred at 40 and 80 minutes. No change in systemic arterial pressure or cardiac output was noted at any time. Coronary blood flow had decreased slightly at 80 minutes. A significant decrease in carbon dioxide content of the arterial, pulmonary arterial and coronary sinus blood was observed, possibly as a consequence of hyperventilation. Khellin appeared to alter the metabolism of the myocardial and splanchnic tissues.

Evaluation of the Effect of Bilateral Internal-Mammary-Artery Ligation on Cardiac Output and Coronary Blood Flow

1959 ◽  
Vol 261 (13) ◽  
pp. 653-655 ◽  
Author(s):  
George G. Rowe ◽  
George M. Maxwell ◽  
Cesar A. Castillo ◽  
C. W. Crumpton ◽  
Richard J. Botham ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Internal Mammary Artery ◽  
Artery Ligation ◽  
Internal Mammary

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Coronary Blood Flow ◽  
Drug Effects ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Energetic Cost ◽  
Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

Analysis of myocardial and total body integral extraction ratios of rubidium-86

1978 ◽  
Vol 235 (6) ◽  
pp. H794-H802
Author(s):  
P. F. McDonagh ◽  
A. F. Salel ◽  
K. A. Krohn ◽  
E. A. Rhode ◽  
D. T. Mason
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Animal Experiments ◽  
Clinical Use ◽  
Right Heart ◽  
Preliminary Study ◽  
Total Body ◽  
Distribution Of Cardiac Output ◽  
Right Heart Bypass

Coronary blood flow (QM) measurement with radiorubidium (Rb) assumes that Rb distributes to the myocardium in proportion to flow. This assumption is correct if the integral myocardial Rb extraction ratio (ERM) equals total body extraction (ERTB). A right-heart-bypass preparation was employed to test the hypothesis that ERM = ERTB and to examine the determinants of Rb extraction. Dogs were anesthetized with pentobarbital, and arterial, coronary venous, and total body venous Rb concentrations were continuously measured for 4 min after injection. We found that ERM (0.56 +/- 0.01) was significantly less than ERTB (0.70 +/- 0.01), P less than 0.01 (n = 29) and concluded that Rb did not distribute in proportion to flow. We do not recommend this method for clinical use. ERM is flow dependent and ERRB is a function of the total cardiac output and the distribution of cardiac output. Before employing Rb in animal experiments, it is recommended that a preliminary study be performed comparing flow measured with Rb to an independent measure of blood flow.

Effects of protoveratrine on coronary blood flow of the renal hypertensive dog

1963 ◽  
Vol 204 (5) ◽  
pp. 895-898 ◽  
Author(s):  
James W. West ◽  
Elwood L. Foltz
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Oxygen Saturation ◽  
Coronary Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Renal Hypertension ◽  
Peripheral Resistance ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Venous Oxygen Saturation

In renal hypertension, protoveratrine decreased coronary blood flow, cardiac oxygen consumption, arterial and venous oxygen saturation, coronary arteriovenous oxygen difference, mean arterial blood pressure, cardiac output, cardiac work, cardiac efficiency, cardiac rate, total peripheral resistance, coronary resistance, respiratory rate, and minute volume. The decrease was significant in all functions except coronary blood flow, coronary venous oxygen saturation, and cardiac output. The results of these experiments indicate that in the renal hypertensive animal, a therapeutically beneficial effect was derived from protoveratrine on the circulation by its ability to decrease the work of the heart (lowering the elevated mean arterial pressure) and the coronary vascular resistance while maintaining coronary blood flow and cardiac output within normal levels. The less advantageous effect of protoveratrine on circulation resulted from its respiratory inhibiting effect which reduced the arterial blood oxygen saturation. Although a small decline in coronary venous oxygen saturation was noted, the coronary flow and oxygen delivery in face of the reduced arterial oxygen saturation was apparently adequate to maintain a normal cardiac activity.

Effects of metabolic acidosis and alkalosis on coronary blood flow and myocardial metabolism in the intact dog

1961 ◽  
Vol 200 (3) ◽  
pp. 628-632 ◽  
Author(s):  
A. V. N. Goodyer ◽  
W. F. Eckhardt ◽  
R. H. Ostberg ◽  
M. J. Goodkind
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Metabolic Acidosis ◽  
Coronary Blood Flow ◽  
Venous Blood ◽  
Left Ventricular ◽  
Myocardial Uptake ◽  
Severe Metabolic Acidosis ◽  
Glucose Levels ◽  
Arterial Blood

Severe metabolic acidosis and alkalosis were induced in anesthetized dogs by the infusion of solutions of hydrochloric acid and sodium bicarbonate. Infusions of sodium chloride were administered to other dogs under the same experimental circumstances. Measurements were made of arterial blood pressure, heart rate, cardiac output and coronary blood flow, arterial blood pH, and the content of oxygen, total CO2, lactate, pyruvate and glucose in both arterial and coronary venous blood. The cardiac output and coronary blood flow were decreased by acidosis and increased by alkalosis, the changes induced by alkalosis. There were no significant changes of left ventricular efficiency. Acidosis increased blood glucose concentrations and interfered with the increased myocardial uptake of glucose expected at higher arterial glucose levels. Alkalosis increased blood lactate and pyruvate levels and, correspondingly, the myocardial uptake of these carbohydrate substrates. It is concluded that cardiac dynamic function (as indicated by measurements of cardiac efficiency and output and arterial pressure) is much less affected by severe metabolic acidosis in the intact animal than in the isolated perfused organ.

Coronary blood flow in vivo in the coho salmon (Oncorhynchus kisutch)

1993 ◽  
Vol 264 (5) ◽  
pp. R963-R971 ◽  
Author(s):  
M. Axelsson ◽  
A. P. Farrell
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Coho Salmon ◽  
Oncorhynchus Kisutch ◽  
Coronary Vascular Resistance ◽  
Aortic Blood ◽  
Aortic Blood Pressure

The effects of adrenergic agonists on dorsal aortic blood pressure, cardiac output, and coronary blood flow were studied in unrestrained coho salmon, Oncorhynchus kisutch. Resting coronary blood flow was 0.43 ml.min-1.kg body mass-1, which represented 1.1% of cardiac output or approximately 0.5 ml.min-1.g-1 compact ventricular mass calculated on 40% of total ventricle mass. Coronary blood flow was phasic and continuous throughout the cardiac cycle; flow seems to be affected by the ventricular contraction, with a peak flow occurring during diastole and a nadir in early systole. Epinephrine injections into the dorsal aorta resulted in a rapid increase in coronary blood flow in association with a rapid increase in dorsal aortic blood pressure. Subsequently there was also a slower increase in coronary vascular resistance, which could be blocked by phentolamine, indicating an alpha-adrenergic vasoconstriction. Isoprenaline injection produced an increase in coronary blood flow and a large reduction in coronary vascular resistance. The coronary vasodilatation was blocked by propranolol, indicating that it may be partly due to a beta-adrenergic vasodilatation. Preliminary results showed a marked increase in coronary blood flow associated with exposure to environmental hypoxia.

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