Role of the peripheral vasculature in changes in venous return caused by isoproterenol, norepinephrine, and methoxamine in anesthetized dogs.

Imai, Yutaka; Satoh, Keisuke; Taira, Norio

doi:10.1161/01.res.43.4.553

Cited by 68 publications

(41 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The opposite effect, i.e., relaxation after a prolonged increase in distending pressure (delayed compliance or viscoelastic creep), may be significant (358). By decreasing venous resistance due to relaxation of sphincters, e.g., in the hepatic vein, ,8-aclrenergic stimulation may centrally displace venous volume (163).…”

Section: Dynamic Responses To Posture Changesmentioning

confidence: 99%

Cardiovascular Adjustments to Gravitational Stress

Blomqvist

Stone

1983

Comprehensive Physiology

198

163

View full text Add to dashboard Cite

Section: Dynamic Responses To Posture Changesmentioning

confidence: 99%

Cardiovascular Adjustments to Gravitational Stress

Blomqvist

Stone

1983

Comprehensive Physiology

198

163

View full text Add to dashboard Cite

“…It has been suggested that there may be a sphincter mechanism regulating hepatic venous outflow (Knisely, Harding & Debacker, 1957;Greenway & Oshiro, 1973). However, the only physiological evidence in support of this has been indirect and has shown hepatic outflow to be influenced by various humoral stimuli (Imai, Satoh & Taira, 1978;Rutlen, Supple & Powell, 1981;Rothe, Flanagan & Maass-Moreno, 1990). No information was provided on where any potential site of obstruction to flow may have been.…”

Section: Introductionmentioning

confidence: 99%

Blood mobilization from the liver of the anaesthetized dog

Noble¹,

Drinkhill²,

Myers³

et al. 1998

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYThe abdominal circulation contains a high proportion of the total blood volume and this can change either passively in response to changes in vascular distending pressure or actively (termed a capacitance response) to changes in sympathetic nervous activity. The liver is the largest abdominal organ and this study was designed to evaluate its potential contribution to overall vascular capacitance and compliance. In chloralose anaesthetized dogs, the liver was vascularly isolated, perfused through the portal vein and hepatic artery at either constant pressures or constant flows and drained from the hepatic veins at constant pressure. Changes in vascular resistance were assessed from changes in inflow pressures or flows and hepatic blood volume was determined by differences between net inflow and outflow. During constant flow perfusion the change in hepatic volume (capacitance change) in response to supramaximal stimulation of sympathetic nerves at 16 Hz was (mean + S.E.M.) -2-40 + 0-61 ml (kg body weight)-'. This response was not significantly different during constant pressure perfusion. The changes in portal venous and hepatic arterial pressures during stimulation at constant flow perfusion were +0-67 + 0.13 and +4-92 + 0-67 kPa, respectively. The compliance of the liver, assessed as the change in volume to a change in hepatic venous pressure, was +544 + 0-18 ml kg-' kPa-. These results indicate that the liver has a major capacitance role, comparable to that of the canine spleen and, in addition, is highly compliant. No evidence was found to suggest that a sphincter on the hepatic outflow exists. Assuming similar responses occur in humans, who do not possess a large contractile spleen, the liver would be the most important controllable blood reservoir in the body.

show abstract

“…By using the open loop method, we have recently gained some insight into the role of vascular a and ;3 adrenergic receptors in changes related to venous return produced by sympathomimetic amines (12). In the present study in addition to nitroglycerin, 3 vasodilators, i.e., verapamil, trimetazidine, and 3,5-dicarbethoxy-2,6-dimethyl-4-(2-trifluoromethyl-phenyl)-1,4-dihydro pyridine (SK&F 24260) (13,14) were used, since in the previous studies (7,8) …”

mentioning

confidence: 99%

Differential effects of nitroglycerin, trimetazidine, verapamil and SK&F 24260 on venous return as revealed by the open-loop method in the dog.

1980

View full text Add to dashboard Cite

Abstract-To obtain detailed information concerning the effects of different vaso dilators on venous return, experiments were carried out on 28 dogs by the use of the open-loop method. Blood from the superior and inferior venae cavae was drained at the level of the tricuspid valve into a reservoir, from which blood was pumped into the right atrium at a constant flow rate. Changes in reservoir volume reflected a total blood shift from the experimental dog and indicated changes in venous return. Drugs were administered into the ascending aorta. Nitroglycerin (1-10 pg/kg) decreased systemic blood pressure, total peripheral resistance and venous return but scarcely altered heart rate. Trimetazidine (0.3-3 mg/kg) decreased systemic blood pressure, total peripheral resistance, venous return and heart rate. Verapamil (10-100 ug/kg) decreased systemic blood pressure, total peripheral resistance and heart rate, and increased venous return. SK&F 24260 (1-10 fig/kg) decreased systemic blood pres sure, total peripheral resistance and increased venous return. Only high doses (10 30 pg/kg) of SK&F 24260 reduced heart rate. Rigorous measurements of systemic output showed that nitroglycerin (10 pg/kg), trimetazidine (3 mg/kg), verapamil (100 pg/kg), SK&F 24260 (10 pg/kg) produced no change in this parameter. SK&F 24260 increased venous return even when sino-aortic baroreceptor reflex was eliminated, ruling out reflex venoconstriction as a possible cause of the increased venous return. The results suggest the following: [1] Vasodilators like SK&F 24260 and verapamil increase venous return by decreasing arterial and/or venous resistance. [2] If the effect which increases venous capacitance prevails over the effect which decreases ar terial and/or venous resistance, venous return is reduced as is the case of nitroglycerin and trimetazidine.Nitroglycerin reduces the left ventricular end-diastolic pressure and volume (1-4), and such is considered to be one of mechanisms responsible for the antianginal action of nitro glycerin (1, 2, 4-6). The reduction in these 2 parameters is thought to be due mainly to a decrease in venous return (3, 4). Thus, it was of interest to investigate the effect on venous return of other vasodilators used for prevention of attacks of angina pectoris. In previous studies (7,8) we demonstrated that some of vasodilators increased venous return whereas others decreased it. However, in those studies we measured venous return by noncannulating type flow probes of electromagnetic flow meters placed at the superior and the inferior vena cava in anesthetized open-chest dogs and did not control cardiac input (the closed-loop method). Thus, it was hardly discernible whether the observed change in venous return by a certain vasodilator would be due to its effect on vasculature or on the heart. Most

show abstract

Role of the peripheral vasculature in changes in venous return caused by isoproterenol, norepinephrine, and methoxamine in anesthetized dogs.

Cited by 68 publications

References 20 publications

Cardiovascular Adjustments to Gravitational Stress

Cardiovascular Adjustments to Gravitational Stress

Blood mobilization from the liver of the anaesthetized dog

Differential effects of nitroglycerin, trimetazidine, verapamil and SK&F 24260 on venous return as revealed by the open-loop method in the dog.

Contact Info

Product

Resources

About