Inotropic and chronotropic responses of the in vivo denervated dog myocardium to dobutamine

1976 ◽  
Vol 54 (4) ◽  
pp. 618-621 ◽  
Author(s):  
Chris P. Bolter ◽  
John R. Ledsome
Keyword(s):  
Heart Rate ◽  
Intravenous Infusion ◽  
Aortic Pressure ◽  
Inotropic Effect ◽  
Inotropic Response ◽  
Cardiac Denervation ◽  
Atrial Rate ◽  
Inotropic Activity ◽  
Mean Aortic Pressure

The inotropic and chronotropic responses to dobutamine (DBA) and isoprenaline (ISO) were examined in eight chloralose anaesthetised dogs. Following acute cardiac denervation, heart rate (HR) and contractility (dP/dtmax), measured at a fixed paced atrial rate, were recorded during intravenous infusion of incremental doses of DBA and ISO. Both DBA and ISO elicited increases in HR and dP/dtmax. The increases in dP/dtmax for a one beat per minute increase in HR was 102.0 ± 10.6 mm Hg/s (1 mm Hg (0 °C) = 133.322 Pa), during DBA infusion, and 61.5 ± 8.4 mm Hg/s during ISO infusion. It appeared that the relatively greater inotropic effect of DBA in comparison with ISO was the result of an augmentation of its inotropic activity. DBA infusion was accompanied by a significant increase in mean aortic pressure at all doses examined. An increase in afterload may account for part of the increased inotropic response to DBA.

Somatostatin modulates cholinergic neurotransmission in canine antral muscle

1988 ◽  
Vol 254 (2) ◽  
pp. G201-G209 ◽  
Author(s):  
C. B. Koelbel ◽  
G. van Deventer ◽  
S. Khawaja ◽  
M. Mogard ◽  
J. H. Walsh ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Substance P ◽  
Prostaglandin E2 ◽  
Positive Inotropic Effect ◽  
Mechanical Response ◽  
Inhibitory Effect ◽  
Inotropic Effect ◽  
Inotropic Response ◽  
Cholinergic Neurotransmission

Somatostatin has been shown to inhibit antral motility in vivo. To examine the effect of somatostatin on cholinergic neurotransmission in the canine antrum, we studied the mechanical response of and the release of [3H]acetylcholine from canine longitudinal antral muscle in response to substance P, gastrin 17, and electrical stimulation. In unstimulated tissues, somatostatin had a positive inotropic effect on spontaneous phasic contractions. In tissues stimulated with substance P and gastrin 17, but not with electrical stimulation, somatostatin inhibited the phasic inotropic response dose dependently. This inhibitory effect was abolished by indomethacin. Somatostatin stimulated the release of prostaglandin E2 radioimmunoreactivity, and prostaglandin E2 inhibited the release of [3H]acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of [3H]acetylcholine from unstimulated tissues by a tetrodotoxin-sensitive mechanism but inhibited the release induced by substance P and electrical stimulation. These results suggest that somatostatin has a dual modulatory effect on cholinergic neurotransmission in canine longitudinal antral muscle. This effect is excitatory in unstimulated tissues and inhibitory in stimulated tissues. The inhibitory effect is partially mediated by prostaglandins.

Peripheral circulatory control of preload-afterload mismatch with angiotensin in dogs

1987 ◽  
Vol 253 (1) ◽  
pp. H126-H132
Author(s):  
R. W. Lee ◽  
L. D. Lancaster ◽  
D. Buckley ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Arterial Compliance ◽  
Peripheral Circulation ◽  
Aortic Pressure ◽  
Venous Compliance ◽  
Mean Aortic Pressure

To determine whether changes in the venous circulation were responsible for preload-afterload mismatch with angiotensin, we examined the changes in the heart and the peripheral circulation in six splenectomized dogs after ganglion blockade during an angiotensin infusion to increase mean aortic pressure 25 and then 50%. The peripheral circulation was evaluated by measuring mean circulatory filling pressure (MCFP), arterial compliance, and venous compliance. A 25% increase in mean aortic pressure increased MCFP from 6.2 +/- 0.3 to 7.6 +/- 0.3 mmHg (P less than 0.001) but did not change cardiac output, heart rate, or stroke volume. Systemic vascular resistance increased (P less than 0.01) from 0.50 +/- 0.02 to 0.59 +/- 0.03 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.03 to 0.06 +/- 0.03 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.6 +/- 0.1 ml X mmHg-1 X kg-1, respectively. A 50% elevation in mean aortic pressure increased MCFP from 7.1 +/- 0.4 to 9.5 +/- 0.9 mmHg (P less than 0.001) but did not change heart rate. At this level of aortic pressure, cardiac output and stroke volume decreased (P less than 0.01) 12 and 19%, respectively, whereas systemic vascular resistance increased (P less than 0.001) from 0.48 +/- 0.03 to 0.83 +/- 0.05 mmHg X min X kg X ml-1. Arterial and venous compliances decreased (P less than 0.01) from 0.08 +/- 0.01 to 0.05 +/- 0.01 ml X mmHg-1 X kg-1 and from 2.1 +/- 0.1 to 1.4 +/- 0.1 ml X mmHg-1 X kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Estimation of total arterial compliance: an improved method and evaluation of current methods

1986 ◽  
Vol 251 (3) ◽  
pp. H588-H600 ◽  
Author(s):  
Z. Liu ◽  
K. P. Brin ◽  
F. C. Yin
Keyword(s):  
Diastolic Pressure ◽  
Arterial Compliance ◽  
Aortic Pressure ◽  
Arterial System ◽  
Windkessel Model ◽  
Total Arterial Compliance ◽  
Improved Methods ◽  
Mean Aortic Pressure

Determination of arterial compliance in vivo has long interested physiologists. Most current methods for estimating this parameter assume that compliance is constant, i.e., that arterial pressure-volume (P-V) relations are linear, and they also assume that diastolic aortic pressure decay is an exponential function of time. Both of these assumptions, however, are questionable. This study proposes improved methods of estimating compliance based on a Windkessel model of the arterial system but which utilize the area under the pressure tracing rather than the waveform itself. Formulations accounting for both linear and three hypothetical nonlinear arterial P-V relations (exponential, logarithmic, and parabolic) are presented. Data from patients with congestive heart failure and hypertension are used for illustration. Compliances assuming linear P-V relations are reasonably close to those assuming nonlinear P-V relations only at mean aortic pressure. At end-diastolic pressure the linear assumption underestimates and at peak systolic it overestimates the compliances obtained assuming nonlinear P-V relations. The simpler linear assumption still allows a first approximation to compliance, but we show that existing methods for obtaining compliance under this assumption have severe theoretical as well as practical shortcomings. Our proposed method avoids these shortcomings primarily because deviations from an exact exponential form of the pressure wave have less influence on these compliance estimates than currently used methods.

Effects of dietary fish oil on cardiovascular responsiveness to adrenergic agonists in spontaneously hypertensive rat

1993 ◽  
Vol 71 (7) ◽  
pp. 432-438 ◽  
Author(s):  
Jacquelyn M. Smith ◽  
Stephen J. Kopp ◽  
Dennis J. Paulson ◽  
June T. Daar
Keyword(s):  
Fish Oil ◽  
Spontaneously Hypertensive Rats ◽  
Aortic Pressure ◽  
Adrenergic Agonists ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Dietary Fish ◽  
Fish Oil Supplementation ◽  
Mean Aortic Pressure

To test the hypothesis that dietary fish oil supplementation decreases systolic blood pressure in hypertensive rats by modifying cardiovascular responsiveness to adrenergic agonists, spontaneously hypertensive rats (SHR) and Wistar–Kyoto rats (WKY) received either a corn or fish oil diet, 5% (g/kg) for 10 weeks. Mean aortic pressure was lower in fish oil treated (161 ± 7 mm Hg (1 mmHg = 133.3 Pa)) than corn oil treated (191 ± 6 mmHg) SHR. Although dietary fish oil supplementation decreased responsiveness to norepinephrine in isolated thoracic aorta from SHR, there was no change in cardiovascular responsiveness to the β1 agonist dobutamine or the α1, agonist phenylephrine when these adrenergic agonists were administered in vivo. However, dietary fish oil did decrease the spontaneous basal tone in aorta from both SHR and WKY. This study provides further evidence that dietary fish oil lowers blood pressure in an animal model genetically predisposed to hypertension. However, the mechanism for this decrease in mean aortic pressure in vivo does not appear to be related to modification of cardiovascular responsiveness to α1- or β1-adrenergic agonists and may be related to a decrease in basal vasomotor tone.Key words: fish oil, antihypertensive, spontaneously hypertensive rats, dobutamine, vascular smooth muscle.

Blockade of beta-adrenoceptor in control of blood pressure in fowl

1995 ◽  
Vol 269 (4) ◽  
pp. R914-R922 ◽  
Author(s):  
K. Kamimura ◽  
H. Nishimura ◽  
J. R. Bailey
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Aortic Pressure ◽  
Induced Hypotension ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Mean Aortic Pressure ◽  
Beta Adrenoceptor Blockers

Several avian species show elevated blood pressure (BP) and spontaneous atherogenesis in the aorta and other large arteries. The BP appears to be influenced by age, sex (higher in males), environment, and diet in some species. We reported previously that mean aortic pressure and heart rate, but not plasma renin activity (PRA), of conscious female domestic fowl were markedly reduced by propranolol. In the present study, we aimed to determine in conscious roosters whether 1) hypotension evoked by atenolol or practolol, which selectively inhibit cardiac beta-receptors in mammals, is more potent than that evoked by propranolol, and 2) the renin-angiotensin (ANG) system and/or catecholamines are involved in beta-adrenoceptor antagonist-induced hypotension. Mean arterial pressure (171.2 +/- 3.5 mmHg) and heart rate (281 +/- 4 beats/min) of chronically cannulated roosters (n = 38) were markedly reduced by acute infusion or repeated injections (14 days) of propranolol, atenolol, or practolol, but not by SQ-14,225 (ANG-converting enzyme inhibitor) or [Sar1, Thr8]ANG II (nonselective ANG receptor antagonist). None of the beta-adrenoceptor blockers, however, showed cardioselectivity. The resting PRA of conscious roosters (1.27 +/- 0.09 ng.ml-1.h-1, n = 38) was low and did not change significantly after chronic or acute treatment with beta-adrenoceptor blockers except for a slight decrease induced by practolol. PRA increased after SQ-14,225. The plasma levels (pg/ml) of norepinephrine (701.9 +/- 76.0), epinephrine (337.2 +/- 57.1), and dopamine (299.1 +/- 39.0) of conscious roosters were further increased by propranolol. Practolol also increased dopamine significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

The importance of nervous and humoral mechanisms in the control of cardiac performance in the Atlantic cod Gadus morhua at rest and during non-exhaustive exercise

1988 ◽  
Vol 137 (1) ◽  
pp. 287-301 ◽  
Author(s):  
M. Axelsson
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Gadus Morhua ◽  
Positive Inotropic Effect ◽  
Atlantic Cod ◽  
Inotropic Effect ◽  
Response Curves

The nervous regulation of heart rate and stroke volume in the Atlantic cod Gadus morhua was investigated both in vivo, during rest and exercise, and in vitro. The cholinergic and adrenergic influences on the heart were estimated in experiments with injections of atropine and sotalol. At rest the cholinergic and adrenergic tonus on the heart were 38% and 21%, respectively (ratio 1.81:1). At the end of an exercise period, the cholinergic tonus had decreased to 15% but the adrenergic tonus had increased to 28% (ratio 0.54:1). The results suggest that variation of the cholinergic tonus on the heart is a major factor in the regulation of the heart rate. In one group of fish, cardiac output was also measured, allowing calculation of stroke volume. Cardiac output increased significantly during exercise, and this effect persisted in the presence of both atropine and sotalol, although the increase in heart rate was reduced or abolished. The persisting increase in cardiac output during exercise is due to an increase in stroke volume, reflecting a Starling relationship. In the presence of the adrenergic neurone-blocking agent bretylium, a positive inotropic effect on isolated, paced atrial and ventricular strips was observed. In the atrial preparations the effect persisted after 24 h. The effect was prevented by pretreatment with sotalol or cocaine, but potentiated by phentolamine pretreatment. This shows that bretylium exerts its neurone-blocking action after being taken up into the adrenergic nerves, and suggests that the positive inotropic effect of bretylium observed in vivo is due to release of endogenous catecholamines. The concentration-response curves for adrenaline on isolated spontaneously beating atrial preparations showed that the concentrations of catecholamines necessary to produce appreciable effects on the heart are higher than the concentrations found in cod plasma during ‘stress’ situations (handling and exhaustive swimming).

Localization of Baroreceptors and Gain of the Baroreceptor-Heart Rate Reflex in the Lizard Trachydosaurus Rugosus

1980 ◽  
Vol 86 (1) ◽  
pp. 197-209
Author(s):  
P. J. BERGER ◽  
B. K. EVANS ◽  
D. G. SMITH
Keyword(s):  
Heart Rate ◽  
Dominant Role ◽  
Aortic Pressure ◽  
Systemic Arterial Pressure ◽  
Cardiac Response ◽  
Percentage Increase ◽  
Aortic Blood Pressure ◽  
Change In Mean ◽  
Mean Aortic Pressure ◽  
Adrenergic Neurone

1. The location of arterial baroreceptors was studied in unanaesthetized Trachydosaurus rugosus by inflation of strategically placed perivascular cuffs. There was no evidence for baroreceptors at the site homologous with the carotid sinus of mammals or at the site homologous with the aortic arch baroreceptors of mammals and birds. The baroreceptors of T. rugosus probably lie in the truncus arteriosus. 2. When the sensitivity or gain of the cardiac response to changes in systemic arterial pressure was expressed as change in heart period per unit change in mean aortic blood pressure, the value for 6 animals was 1370 ms/kPa (100 ms/mmHg). This is very much greater than reported values for rabbits. If, instead, gain was calculated as the percentage increase in heart rate per unit fall in mean aortic pressure, a mean gain of 98%/kPa (7.2%/mmHg) was obtained. It is suggested that the latter method provides the better comparative value. 3. Adrenergic neurone blockade with bretylium and muscarinic blockade with atropine or hyoscine indicated that sympathetic fibres probably play the dominant role in generating the gain of the cardiac baroreflex.

Effect of Catecholamines, l-Epinephrine and l-Norepinephrine on Coronary Flow and Oxygen Metabolism of the Myocardium

1958 ◽  
Vol 193 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Harold Feinberg ◽  
Louis N. Katz
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Oxygen Consumption ◽  
Coronary Flow ◽  
Myocardial Oxygen Consumption ◽  
Oxygen Metabolism ◽  
Aortic Pressure ◽  
Coronary Vasodilatation ◽  
Oxygen Difference ◽  
Mean Aortic Pressure

The effect of continuously infused intravenous l-epinephrine and l-norepinephrine (0.1–2.5 gamma/kg/min.) was determined in the open-chest, anesthetized dog prepared for measurement of total coronary flow. Coronary blood flow, myocardial oxygen availability and coronary venous oxygen content consistently increased after catecholamine administration despite wide fluctuations, above and below control values, in heart rate and mean aortic pressure at constant cardiac output. Thus, there was a significant decrease in the coronary arteriovenous oxygen difference after catecholamine administration. The increase in coronary flow and decrease in the coronary A-V oxygen difference were seen even when blood pressure and heart rate were lowered. It is concluded that the departure from the usual relationship between coronary flow and myocardial oxygen consumption is attributable to coronary vasodilatation. However, myocardial oxygen consumption is still the primary factor controlling coronary flow during catecholamine action.

Beat-to-beat estimation of peripheral resistance and arterial compliance during pressure transients

1987 ◽  
Vol 252 (6) ◽  
pp. H1275-H1283 ◽  
Author(s):  
G. P. Toorop ◽  
N. Westerhof ◽  
G. Elzinga
Keyword(s):  
Heart Rate ◽  
Arterial Compliance ◽  
Peripheral Resistance ◽  
Estimation Method ◽  
Aortic Pressure ◽  
Autonomous Nervous System ◽  
Mean Flow ◽  
Arterial Tree ◽  
Total Arterial Compliance

We have used a computer-based parameter estimation method to obtain peripheral resistance, total arterial compliance, and characteristic resistance from the measurement of aortic pressure and flow in the open-thorax cat, assuming the three-element windkessel as a model of the systemic arterial tree. The method can be applied on a beat-to-beat basis in the steady state and in transients. We have validated this method by analyzing nonsteady-state data obtained from an electrical analog with fixed values of the resistances and compliance and by showing that the values obtained by this procedure were within 5% of the fixed values of the circuit. Changes in total peripheral resistance and arterial compliance were studied before, during, and after acute heart rate changes in five open-thorax cats with blocked autonomous nervous system. As expected, the peripheral resistance, estimated during the heart rate transient [3.93 +/- 0.94 (SE) kPa X ml-1 X s] was the same as before the transient (3.53 +/- 0.83 kPa X ml-1 X s); total arterial compliances were also identical (0.28 +/- 0.04 vs. 0.27 +/- 0.03 ml/kPa). In six cats without nervous blockade we obtained similar results. Calculation of peripheral resistance during transients from the mean pressure-to-mean flow ratio, i.e., without correction for arterial compliance, suggested changes in resistance values of less than or equal to 57%, which shows that correction is necessary. The findings indicate that peripheral resistance and total arterial compliance can be estimated in vivo on a beat-to-beat basis, even during hemodynamic transients.

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