Influence of Epinephrine and Norepinephrine on Respiratory Variations in Vascular Pressures

1956 ◽  
Vol 186 (2) ◽  
pp. 365-368 ◽  
Author(s):  
D. M. MacCanon ◽  
Steven M. Horvath
Keyword(s):  
Left Ventricular ◽  
Respiratory Cycle ◽  
Before And After ◽  
Isolated Points ◽  
Anesthetized Dogs ◽  
Vasomotor Activity ◽  
Control Patterns

Comparisons were made between the respiratory variations in right and left ventricular and femoral arterial pressures of anesthetized dogs before and after the administration of l-epinephrine and l-norepinephrine. These analyses revealed significant deviations from control patterns following administration of these pressor drugs, but only at isolated points in the respiratory cycle. Many of these alterations could only be explained on the basis of alterations in cardiac and/or vasomotor activity.

Optimal matching between canine left ventricle and afterload

1988 ◽  
Vol 254 (6) ◽  
pp. H1051-H1058
Author(s):  
E. S. Myhre ◽  
A. Johansen ◽  
H. Piene
Keyword(s):  
Systolic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Stroke Work ◽  
External Work ◽  
Volume Load ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Volume Relationship ◽  
Optimal Values

A parabolic relationship exists between ventricular external work and arterial load at given preload and contractility. Previous data indicate that the working point falls close to the parabola optimum. By combining the left ventricular (LV) end-systolic pressure-volume relationship (ESPVR) and an equation describing external stroke work, optimum values of stroke volume (SV), the slope (Emax) of the ESPVR, and arterial resistance (Rp) corresponding with the optimum (i.e., mSV, mEmax, mRp) were obtained. Experiments in anesthetized dogs were performed to test whether mSV, mEmax, and mRp also correspond to observed SV, Emax, and Rp at three different levels of volume load (right atrial pressure, RAP) before and after acute depression of LV contractility. Comparisons of observed and optimal values of SV, Emax, and Rp were made before and after LV depression. Before embolization, the ratios were SV/mSV 1.10–1.20 (RAP 5–15 mmHg); Emax/mEmax 1.21–1.41; and Rp/mRp 0.84–0.69. After LV depression, SV/mSV was 0.80–0.83, Emax/mEmax was 0.78–0.71, and Rp/mRp was 1.56–1.46. The ratios were all significantly changed (P less than 0.01) by the induced LV depression. The present analysis may offer a new tool to detect nonoptimal relations between cardiac and arterial functions.

Increased myocardial contractility during endotoxin shock in dogs

1985 ◽  
Vol 249 (4) ◽  
pp. H715-H722 ◽  
Author(s):  
P. M. Kober ◽  
J. X. Thomas ◽  
R. M. Raymond
Keyword(s):  
Myocardial Contractility ◽  
Salmonella Enteritidis ◽  
Systolic Pressure ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Terminal Phase ◽  
Endotoxin Administration ◽  
Before And After ◽  
Anesthetized Dogs

The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (Ees) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella enteritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 +/- 44 min). There were no significant changes in Ees in control dogs (17 +/- 3 mmHg/mm), which were hemodynamically stable for 4 h. Ees was significantly increased in endotoxic dogs even into the late stages of shock (41 +/- 11 mmHg/mm, P less than 0.01). Only during the terminal phase did Ees fall significantly below control (11 +/- 2 mmHg/mm, P less than 0.05). End-diastolic diameter decreased following endotoxin administration (P less than 0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was not depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.

Adenosine deaminase attenuates norepinephrine-induced coronary functional hyperemia

1988 ◽  
Vol 254 (3) ◽  
pp. H417-H424 ◽  
Author(s):  
H. F. Downey ◽  
G. F. Merrill ◽  
S. Yonekura ◽  
N. Watanabe ◽  
C. E. Jones
Keyword(s):  
Adenosine Deaminase ◽  
Left Ventricular ◽  
Atrial Pacing ◽  
Functional Hyperemia ◽  
Flow Response ◽  
O2 Extraction ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Elevated Rate ◽  
Myocardial Oxygen Extraction

Responses to norepinephrine (NE) before and after treatment with adenosine deaminase (ADA) were examined in anesthetized dogs. In four dogs repeatable changes in coronary blood flow, myocardial oxygen extraction and consumption, left ventricular +dP/dtmax, and heart rate (HR) were demonstrated during two successive intracoronary infusions of 0.13 micrograms.kg-1.min-1 NE. In eight dogs, the NE-induced hyperemia was decreased from +150 to +67%, the change in myocardial oxygen consumption (MVo2) was attenuated from +177 to +101% by ADA, and the increase in HR was reduced from +28 to +16%. In six dogs, the increase in HR caused by NE before ADA was maintained after ADA by atrial pacing. The NE-induced hyperemia and the increase in MVo2 were again decreased by ADA. Similar results were observed in 12 other dogs with hearts paced at a constant, elevated rate during control as well as during both infusions of NE. In all groups, the O2 extraction response to increased MVo2 increased and the flow response decreased after ADA. In six dogs nitroprusside was infused during NE after ADA. When coronary flow was restored to the same level observed before deaminase, MVo2 was not diminished. These results support a role for adenosine in the coronary functional hyperemia accompanying NE activation of the canine myocardium.

scholarly journals Altered LV inotropic reserve and mechanoenergetics early in the development of heart failure

2000 ◽  
Vol 278 (3) ◽  
pp. H698-H705 ◽  
Author(s):  
Sumanth D. Prabhu ◽  
Gregory L. Freeman
Keyword(s):  
Heart Failure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Short Term ◽  
Before And After ◽  
Autonomic Blockade ◽  
Anesthetized Dogs ◽  
Rapid Ventricular Pacing ◽  
Volume Relation

To test the hypothesis that alterations in left ventricular (LV) mechanoenergetics and the LV inotropic response to afterload manifest early in the evolution of heart failure, we examined six anesthetized dogs instrumented with LV micromanometers, piezoelectric crystals, and coronary sinus catheters before and after 24 h of rapid ventricular pacing (RVP). After autonomic blockade, the end-systolic pressure-volume relation (ESPVR), myocardial O2 consumption (MV˙o 2), and LV pressure-volume area (PVA) were defined at several different afterloads produced by graded infusions of phenylephrine. Short-term RVP resulted in reduced preload with proportionate reductions in stroke work and the maximum first derivative of LV pressure but with no significant reduction in baseline LV contractile state. In response to increased afterload, the baseline ESPVR shifted to the left with maintained end-systolic elastance ( E es). In contrast, after short-term RVP, in response to comparable increases in afterload, the ESPVR displayed reduced E es ( P < 0.05) and significantly less leftward shift compared with control ( P< 0.05). Compared with the control MV˙o 2-PVA relation, short-term RVP significantly increased the MV˙o 2 intercept ( P< 0.05) with no change in slope. These results indicate that short-term RVP produces attenuation of afterload-induced enhancement of LV performance and increases energy consumption for nonmechanical processes with maintenance of contractile efficiency, suggesting that early in the development of tachycardia heart failure, there is blunting of length-dependent activation and increased O2requirements for excitation-contraction coupling, basal metabolism, or both. Rather than being adaptive mechanisms, these abnormalities may be primary defects involved in the progression of the heart failure phenotype.

Postsystolic shortening of ischemic myocardium: a mechanism of abnormal intraventricular filling

2003 ◽  
Vol 284 (6) ◽  
pp. H2343-H2350 ◽  
Author(s):  
Stig Urheim ◽  
Thor Edvardsen ◽  
Kjetil Steine ◽  
Helge Skulstad ◽  
Erik Lyseggen ◽  
...  
Keyword(s):  
Wall Motion ◽  
Diastolic Pressure ◽  
Color Doppler ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Segment Length ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Apical View ◽  
Velocity Changes

Acute myocardial ischemia has been associated with abnormal filling patterns in the left ventricular (LV) apex. We hypothesized that this may in part be due to postsystolic shortening of ischemic apical segments, which leads to reversal of early diastolic apical flow. Fourteen open-chest anesthetized dogs were instrumented with micromanometers in the LV apex and left atrium and myocardial sonomicrometers in the anterior apical LV wall. Intraventricular filling by color Doppler and wall motion by strain Doppler echocardiography (SDE) were assessed from an apical view. Measurements were taken before and after 5 min of left anterior descending coronary artery (LAD) occlusion. In four dogs, we measured the pressure difference between the LV apex and outflow tract. At baseline, peak early diastolic flow velocities in the distal one-third of the LV were directed toward apex (9.2 ± 1.6 cm/s). After LAD occlusion, the velocities reversed (−2.3 ± 0.4 cm/s, P < 0.01), indicating that blood was ejected from the apex toward the base during early filling. This interpretation was confirmed by wall motion analysis, which showed postsystolic shortening of apical myocardial segments. The postsystolic shortening represented 9.7 ± 1.7% ( P < 0.01) and 14.2 ± 2.4% ( P < 0.01) of end-diastolic segment length by SDE and sonomicrometry, respectively. Consistent with the velocity changes, we found reversal of the early diastolic pressure gradient from the LV apex to outflow tract. In the present model, acute LAD occlusion resulted in reversal of early diastolic apical flow, and this was attributed to postsystolic shortening of dyskinetic apical segments. The clinical diagnostic importance of this finding remains to be determined.

Cardiac Effects of Coronary Arteriography with Electrolyte Addition to Iohexol

1994 ◽  
Vol 35 (1) ◽  
pp. 77-82 ◽  
Author(s):  
H. K. Pedersen ◽  
E. A. Jacobsen ◽  
H. Refsum ◽  
N. E. Kløw
Keyword(s):  
Heart Failure ◽  
Contrast Media ◽  
Cardiac Electrophysiology ◽  
Coronary Arteriography ◽  
Left Ventricular ◽  
Monophasic Action Potential ◽  
Initial Decrease ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Nonionic Contrast Media

Electrolyte addition to nonionic contrast media has been suggested to further reduce the incidence of ventricular fibrillation during coronary arteriography. The present study was designed to investigate the effects of adding 30 mM NaCl, 0.9 mM KCl, 0.15 mM CaCl2 and 0.1 mM MgCl2 to iohexol on cardiac electrophysiology and hemodynamics (iohexol + electrolytes = IPE). Contrast media were injected into the left main coronary artery in 9 open-chest, anesthetized dogs before and after induction of acute ischemic heart failure. IPE increased left ventricular inotropy (LV dP/dtmax) with no initial decrease, even during heart failure. During heart failure IPE induced the same hemodynamic effects as iohexol without electrolyte addition. IPE slightly lengthened epicardial monophasic action potential duration before heart failure. We conclude that IPE appears to be well tolerated hemodynamically. The electrophysiologic differences between IPE and iohexol are small when the injection time is not longer than 5 s.

Influence of the pericardium on right and left ventricular filling in the dog

1987 ◽  
Vol 63 (3) ◽  
pp. 1025-1032 ◽  
Author(s):  
D. Assanelli ◽  
W. Y. Lew ◽  
R. Shabetai ◽  
M. M. LeWinter
Keyword(s):  
Right Ventricular ◽  
Diastolic Pressure ◽  
Left Ventricular ◽  
Before And After ◽  
Data Points ◽  
Anesthetized Dogs ◽  
Proportional Contribution ◽  
Left And Right ◽  
Ventricular Filling ◽  
Absolute Contribution

We compared the influence of the pericardium on left and right ventricular (LV, RV) filling by measuring LV and RV pressures and segment lengths (SL, LV free wall, and RV inflow and outflow tracts) in six open-chest, pentobarbital sodium-anesthetized dogs before and after pericardiectomy. End-diastolic pressure (EDP) was varied by partial caval occlusion and dextran infusion. At each site the ln EDP-SL relation was fitted by linear regression and characterized by its slope and 1-Torr EDP intercept. The slope and 1-Torr intercept of the LV ln EDP-SL relation changed variably after pericardiectomy, but in each dog a change occurred that shifted this relation downward. In contrast, the RV inflow tract slope invariably decreased significantly after pericardiectomy, whereas its intercept was unchanged in all but one dog. The RV outflow tract results were similar to the inflow tract but less consistent. By the use of the raw EDP-SL data points, we calculated that the absolute contribution of the pericardium to EDP (i.e., the effective pericardial surface pressure) was similar at the three sites. However, as EDP values increased the proportional contribution of the pericardium to right ventricular end-diastolic pressure (RVEDP) increased, whereas that to left ventricular end-diastolic pressure (LVEDP) remained relatively constant. As a result, at the higher EDP values tested, the pericardium was responsible for a larger proportion of RVEDP than LVEDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Thermodilution studies of ventricular volume changes due to isoproterenol and bleeding

1963 ◽  
Vol 18 (1) ◽  
pp. 129-133 ◽  
Author(s):  
J. David Bristow ◽  
Richard E. Ferguson ◽  
Fredric Mintz ◽  
Elliot Rapaport
Keyword(s):  
Ventricular Volume ◽  
Left Ventricular ◽  
Indicator Dilution ◽  
Dilution Method ◽  
Volume Changes ◽  
Thermodilution Technique ◽  
End Diastolic Volume ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Ventricular Dimensions

The effects of intravenous isoproterenol on left ventricular stroke and on end-systolic and end-diastolic volumes were studied in anesthetized dogs before and after bleeding. Volumes were measured by a thermodilution technique. In this indicator-dilution method a small amount of cooled blood is rapidly injected into the ventricle, and the washout of cold from the ventricle is sensed by a thermistor catheter at the root of the aorta. Control values showed that approximately two-thirds of the end-diastolic volume remained in the ventricle at the end of systole. Bleeding decreased all three volumes. Isoproterenol consistently increased ventricular emptying, as shown by the fall in the proportion of the end-diastolic volume which remained at end systole. This effect did not depend on an increase or decrease in the end-diastolic volume itself. End-systolic force-circumference relationships were derived from a consideration of idealized ventricular dimensions. A linear relationship between these calculated values was not altered by isoproterenol. Submitted on July 5, 1962

Pulmonary injury depresses cardiac systolic function through Starling mechanism

1986 ◽  
Vol 251 (4) ◽  
pp. H722-H733 ◽  
Author(s):  
J. E. Calvin ◽  
R. W. Baer ◽  
S. A. Glantz
Keyword(s):  
Diastolic Pressure ◽  
Systolic Function ◽  
Left Ventricular ◽  
Stroke Work ◽  
Volume Loading ◽  
Lung Hyperinflation ◽  
Microvascular Injury ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Heart Size

To determine whether pulmonary microvascular injury or lung hyperinflation changes left ventricular (LV) performance and whether ventricular interaction plays a role in mediating such changes, we studied seven open-chest, closed-pericardium, anesthetized dogs before and after right ventricular (RV) injections of 150- to 200-micron glass beads. Because people with pulmonary disease are often treated with positive end-expiratory pressure, we also hyperinflated the lungs before and after creating the pulmonary microvascular injury. Measurements of LV and RV pressures and dimensions were taken at end expiration during the basal state, during lung hyperinflation, and after microvascular injury at RV end-diastolic pressures of 5, 10, and 15 mmHg produced by volume loading. Acute volume loading produced upward shifts in the LV diastolic pressure-size curve both before and after microvascular injury. Neither microvascular injury nor lung hyperinflation substantially affected the LV diastolic pressure-size relationship. LV end-diastolic size determined LV stroke work with no consistent independent influence of microvascular injury or lung hyperinflation. Neither microvascular injury nor lung hyperinflation depressed systolic performance beyond that associated with changes in end-diastolic heart size.

Effects of myocardial contraction on ultrasonic backscatter before and after ischemia

1984 ◽  
Vol 247 (3) ◽  
pp. H478-H483 ◽  
Author(s):  
B. Barzilai ◽  
E. I. Madaras ◽  
B. E. Sobel ◽  
J. G. Miller ◽  
J. E. Perez
Keyword(s):  
Coronary Occlusion ◽  
Cardiac Cycle ◽  
Myocardial Contraction ◽  
Left Ventricular ◽  
Normal Myocardium ◽  
Integrated Backscatter ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Ultrasonic Backscatter ◽  
Contraction And Relaxation

To determine whether contraction and relaxation influence quantitative myocardial ultrasonic backscatter we measured systolic and diastolic integrated backscatter separately in 10 pentobarbital-anesthetized dogs with defined, paced heart rates, before and after coronary occlusion. Data were acquired from intramural sites by coupling a broadband 5-MHz transducer to the left ventricular epicardium. Integrated backscatter was obtained from seven sequential ECG gated intervals throughout the cardiac cycle over the frequencies of 2.5-7.5 MHz and referenced to values obtained with a steel reflector. Before coronary occlusion myocardium in all dogs exhibited a decrease in integrated backscatter from end diastole to end systole (P less than 0.05) in control zones and in zones destined to become ischemic (P less than 0.05). Thirty minutes after occlusion integrated backscatter did not change in control zones but was elevated in ischemic zones with blunting of the diastolic-to-systolic variation. Thus myocardium undergoing contraction exhibits a decrease in integrated backscatter, and measurement of integrated backscatter at end systole differentiates ischemic from normal myocardium.

Sign in / Sign up

Export Citation Format

Share Document