Stopped-flow epicardial lymph pressure is affected by left ventricular pressure in anesthetized goats

1993 ◽  
Vol 264 (5) ◽  
pp. H1624-H1628 ◽  
Author(s):  
Y. Han ◽  
I. Vergroesen ◽  
J. A. Spaan
Keyword(s):  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beating Heart ◽  
Ventricular Pressure ◽  
Stopped Flow ◽  
Pressure Waveform ◽  
Descending Aorta ◽  
Aortic Clamping ◽  
The Relationship

We measured epicardial lymph pressure (Plymph) in the anesthetized goat (n = 5 goats). To study the transmission of systolic left ventricular pressure (PLV) to Plymph, the effect of an increase in PLV caused by clamping of the descending aorta on Plymph was evaluated. Peak systolic PLV was 131 +/- 4 (+/- SE) mmHg during control (43 beats) and 188 +/- 4 mmHg when elevated due to aortic clamping (157 beats). Peak systolic Plymph was 24.8 +/- 1.0 and 34.8 +/- 1.1 mmHg during control and elevated PLV, respectively. In the first beat of elevated PLV, peak Plymph did not change, although the pressure waveform did. In the subsequent beats, Plymph increased proportionally with increased PLV. When PLV was decreased back to control, Plymph also decreased but did not reach control level until after three beats. The relationship between normalized Plymph and normalized PLV is given by Plymph = 0.70 x PLV + 0.09. The results show that PLV does affect Plymph in a normal beating heart.

scholarly journals Influence of dual ETA/ETB-receptor blockade on coronary responses to treadmill exercise in dogs

2000 ◽  
Vol 89 (5) ◽  
pp. 2041-2048 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Peter Cernacek ◽  
Michel Lavallée
Keyword(s):  
Coronary Sinus ◽  
Adrenergic Receptor ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Receptor Blockade ◽  
Etb Receptor ◽  
Dual Blockade ◽  
The Relationship

We hypothesized that endothelin (ET) release during exercise may be triggered by α-adrenergic-receptor activation and thereby influence coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min−1 · g−1) and in a fall ( P < 0.01) in coronary sinus O2saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas myocardial O2 consumption (MV˙o 2) increased (109 ± 13% from 145 ± 16 μl O2 · min−1 · g−1). Tezosentan, a dual ETA/ETB-receptor blocker, slightly reduced mean arterial pressure (MAP) and increased heart rate throughout exercise. The relationship between coronary sinus O2 saturation and MV˙o 2 was shifted upward ( P < 0.05) after tezosentan administration; i.e., as MV˙o 2 increased during exercise, coronary sinus O2 saturation was disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases ( P < 0.05) in left ventricular pressure, the first derivative of left ventricular pressure over time, and MAP during exercise. As MV˙o 2 increased during exercise, coronary sinus O2 saturation levels after tezosentan became superimposable over those observed before ET-receptor blockade. Thus dual blockade of ETA/ETBreceptors alters coronary hemodynamics and O2 metabolism during exercise, but ET activity failed to increase beyond baseline levels.

Nature of [Ca2+]i transients during ventricular fibrillation and quinidine treatment in perfused rat hearts

1994 ◽  
Vol 266 (4) ◽  
pp. H1473-H1484
Author(s):  
S. Kojima ◽  
J. Wikman-Coffelt ◽  
S. T. Wu ◽  
W. W. Parmley
Keyword(s):  
Ventricular Fibrillation ◽  
Control Level ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Acetoxymethyl Ester ◽  
Ecg Signals ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Electrocardiogram Ecg ◽  
The Relationship

We studied intracellular Ca2+ concentration ([Ca2+]i) and the electrocardiographic signals during pacing-induced ventricular fibrillation (VF) and quinidine treatment (0.4 mg/min) using surface fluorometry in indo 1-acetoxymethyl ester (AM)-loaded perfused rat hearts. [Ca2+]i was evaluated as the indo 1 fluorescence ratio (F400/F510) and expressed as a percentage of the control amplitude of F400/F510 transients. F400/F510 increased to approximately 250% during 2- (n = 14) or 20-min (n = 9) VF. Quinidine significantly decreased F400/F510 by 60% after 2-min VF; however, this effect was blunted after 20-min VF. After 2-min VF, F400/F510 and left ventricular pressure recovered almost to the control level. However, recovery of F400/F510 and ventricular function was poor after 20-min VF. The relationship between [Ca2+]i and the electrocardiogram (ECG) during VF was evaluated by power spectrum analysis of F400/F510 and ECG signals. During VF (25 +/- 3 Hz) with high irregularity, there were no clear [Ca2+]i transients (n = 110). When the cardiac rhythm (22 +/- 3 Hz) was regular, including ventricular tachycardia, there were recognizable [Ca2+]i signals with dominant frequencies that were the same (n = 2), one-half (n = 12), or one-third (n = 1) of the ECG frequencies. The highest frequency of the [Ca2+]i transients was 19 Hz. During quinidine treatment, the VF rate decreased significantly, and clear [Ca2+]i transients were noted in all records responding to every one or two ECG signals. The conclusions were the following: 1) [Ca2+]i responds to electrical signals rapidly (up to 19 Hz) during VF. This fast [Ca2+]i response is a probable cause of high [Ca2+]i during VF. 2) Quinidine decreased [Ca2+]i after 2-min VF possibly in part by slowing the VF and [Ca2+]i transients rates. 3) 20-min VF caused [Ca2+]i overload and poor functional recovery after defibrillation.

Intramyocardial blood volume change in first moments of cardiac arrest in anesthetized goats

1987 ◽  
Vol 253 (2) ◽  
pp. H307-H316 ◽  
Author(s):  
I. Vergroesen ◽  
M. I. Noble ◽  
J. A. Spaan
Keyword(s):  
Cardiac Arrest ◽  
Blood Volume ◽  
Volume Change ◽  
Venous Pressure ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Beating Heart ◽  
Ventricular Pressure ◽  
The Mean ◽  
Change In Mean

The effect of cardiac relaxation on the intramyocardial blood volume was studied by measuring the integrated difference between arterial inflow and great cardiac venous outflow. In nine anesthetized goats, the left main coronary artery was perfused under constant pressure. The great cardiac vein was drained under pressure control. The venous flow signal was amplified so that the integrated intramyocardial blood volume was constant in the beating heart. With normal vasomotor tone, the mean change in vascular volume was 3.01 +/- 0.18 (SE) ml/100 g left ventricle (LV); 67% of the volume change was achieved in 1.60 +/- 0.09 s. For the fully dilated bed (adenosine infusion), the values were 4.13 +/- 0.33 ml/100 g and 0.96 +/- 0.06 s, respectively. The volume change could be correlated with the venous pressure during cardiac arrest (Pvd) and the change in mean left ventricular pressure after cardiac arrest (r = 0.95). The correlation improved when data were selected for Pvd less than 6 mmHg to r = 0.98. We assumed that the change in vascular transmural pressure can be approximated as half the mean left ventricular pressure change. The intramyocardial vascular compliance was then estimated as 0.104 +/- 0.012 and 0.146 +/- 0.028 ml X mmHg-1 X 100 g-1 for control and adenosine conditions, respectively. The long time constants excluded the large epicardial veins as the site of volume change; they were much longer than the duration of diastole in the beating heart. We conclude that the intramyocardial vascular compartment is capable of volume expansion on the order of 20% of its normal volume when myocardial compression by ventricular systole is suspended.

Harmonic Analysis of the Left Ventricular Pressure Waveform of the Primate

Cardiology ◽  
1978 ◽  
Vol 63 (2) ◽  
pp. 79-93 ◽  
Author(s):  
David M. Mirvis ◽  
Gary S. Kopf ◽  
Erik W. Potalla
Keyword(s):  
Harmonic Analysis ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Pressure Waveform

Enkephalin lowers vascular resistance in dog hindlimb via a peripheral nonlimb site

1991 ◽  
Vol 260 (2) ◽  
pp. H386-H392 ◽  
Author(s):  
J. L. Caffrey ◽  
H. Gu ◽  
B. A. Barron ◽  
J. F. Gaugl
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Opiate Receptors ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Sharp Decline ◽  
Descending Aorta ◽  
A Site

The intravenous administration of methionine enkephalin in anesthetized dogs produces an abrupt decline in mean arterial pressure, left ventricular pressure, and the maximal rate of left ventricular pressure development. All of these changes are prevented by receptor blockade with the opiate antagonist, naloxone. To evaluate peripheral vascular contributions to these responses, experiments were conducted in a constant pressure-isolated perfused hindlimb. In this model, the sharp decline in mean arterial pressure associated with enkephalin injection (5 micrograms/kg iv) coincided with an equally sharp decline in vascular resistance (rise in blood flow) in the hindlimb. Both were blocked by naloxone pretreatment (1 mg/kg). When equal doses of enkephalin were administered directly into the femoral inflow (external iliac artery), both arterial pressure and hindlimb flow responses were all but eliminated. This observation ruled out significant direct vascular interactions in the response and indicated a site of action outside the hindlimb. Additional catheters were placed in the bracheocephalic artery and descending aorta to permit the comparison of arterial injections conducted, respectively, into the cerebral or abdominal circulations. Injections introduced into the descending aorta consistently produced the greatest response, followed by injections (in descending order of effectiveness) into the jugular, the brachiocephalic, and external iliac. The response in the hindlimb vasculature was initiated at a site somewhere between the diaphragm and terminal aorta. The vascular response to enkephalin was subsequently eliminated by blocking ganglionic transmission with the nicotinic antagonist mecamylamine. These observations suggest that the opioids probably interrupt local vasomotor traffic via opiate receptors in regional sympathetic ganglia or in the spinal cord.

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