Increased effective vascular compliance and venous pooling of intravascular volume during sustained venodilation in conscious dogs

Holtz, J.; Bassenge, E.; Kinadeter, H.; Kolin, Alexander

doi:10.1007/bf01908056

Cited by 14 publications

(7 citation statements)

References 29 publications

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“…(Sigma Chemical, Munich, FRG) and by semilogarithmic extrapolation of arterial plasma concentration at injection time from several plasma samples, analyzed photometrically at 578 nm, obtained 10-40 minutes after the injection. [12][13][14][15][16][17][18] hours after the final diclofenac injection, these dogs were anesthetized and prepared for measurement of compliance under ganglionic and ,Badrenergic blockade as described for protocols 1-7. Compared with the effects of norepinephrine infusion in the same model, the COI in protocols 1 and 2 caused preferential venoconstriction.…”

Section: Measurementsmentioning

confidence: 99%

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

et al. 1988

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Because prostacyclin is a rather potent venodilator in vivo, we analyzed the effect of cyclooxygenase inhibition on venous tone in 14 anesthetized dogs during ganglionic and ,8-adrenergic blockade and atraumatic conditions. Effective vascular stiffness (a reciprocal of effective vascular compliance) as a variable of integrated venous tone was 0.30 + 0.01 mm Hg* kg/ml (n=35) and was augmented up to twofold by diclofenac (1, 3, and 10 mg/kg i.v.), ibuprofen (6 and 60 mg/kg), or indomethacin (5 mg/kg) parallel to augmentations in central venous pressure, while the rise in arterial pressure was less than half of the increase induced by equivenoconstrictor dosages of norepinephrine. After preconstriction by indomethacin or diclofenac, nitroglycerin (1.5 ,g/kg/min) lowered effective vascular stilfness (by 24+±2% or 23+± 5%, respectively), similarly as during preconstriction by norepinephrine (by 24 4%). Long-term cyclooxygenase inhibition (diclofenac 2 X 1 mg/kg/day for 4 days) did not modify arterial pressure, heart rate, or hematocrit levels in conscious dogs at rest, but it lowered plasma volume to 52.54±1.9 ml/kg (sham treatment: 59.1+±1.6 ml/kg, p

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Section: Measurementsmentioning

confidence: 99%

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

et al. 1988

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“…First, the VOL 8, No 11, NOVEMBER 1986 a-agonists did not significantly decrease cardiac output (see Table 3). Second, the increased central venous pressure values during administration of a-agonists were always well within the normal range found in conscious dogs 22 and were not in a range consistent with cardiac failure. Third, in experiments similar to the ones presented, which were performed in dogs equipped with chronic aortic flowmeters, cardiac output never changed inversely with the cycle of volume changes, neither under control conditions nor during an infusion of norepinephrine, 0.15 /ug/kg/min.…”

Section: Discussion Critique Of the Modelmentioning

confidence: 67%

“…Under ganglionic blockade, effective vascular compliance was higher and central venous pressure was lower than those in untreated conscious dogs. 22 Basal data during prazosin (Protocols 3 and 4) were not different from those in control Protocols 1 and 2. With rauwolscine, a higher mean arterial (p<0.05) and slightly higher central venous pressure (not significant) were observed, while effective vascular compliance tended to be lower (not significant) than that in the control Protocols 1 and 2).…”

Section: Selective A-agonists and Effective Vascular Compliance (Protmentioning

confidence: 80%

“…At equipotent doses with respect to arterioles, both selective a-agonists also yield equivalent effects on the low pressure system (see Figures 2 and 3), with the higher agonist doses increasing effective vascular stiffness and central venous pressure to about physiological levels. 22 The tendency of a rauwolscine-induced arterial and venous vasoconstriction (though not significant in all protocols) might have resulted from a central sympathoexcitation that is not completely suppressed by the ganglionic blockade. This interpretation is supported by the lack of such a pressor effect of rauwolscine in anesthetized dogs with spinal transsection 12 and by the transient augmentation of the norepinephrine release rate observed in the present study.…”

Section: Pharmacological Characterization Of A-adrenergic Receptors Imentioning

confidence: 87%

“…On the other hand, the measurement of effective vascular compliance provides, in the intact animal, more direct information on capacitance vessel tone than do measurements of indirect parameters such as central venous pressure and cardiac output. Furthermore, this approach has been applied in conscious animals 22 and in humans; 3 ' 21 thus, the data from our model can be compared directly with values obtained under strictly physiological conditions. Nevertheless, several possible limitations of this model must be discussed.…”

Section: Discussion Critique Of the Modelmentioning

confidence: 99%

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Postsynaptic alpha 1- and alpha 2-adrenergic receptors in adrenergic control of capacitance vessel tone in vivo.

Elsner¹,

Stewart²,

Sommer³

et al. 1986

Hypertension

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SUMMARY The involvement of postsynaptic a 2 -adrenergic receptors in the adrenergic constriction of the capacitance vessels was studied in anesthetized, spontaneously breathing dogs under ganglionic blockade (hexamethonium, 10 mg/kg + 10 mg/kg/hr; methylatropine, 0.5 mg/kg). Effective vascular compliance was measured as an indicator of venous tone (blood volume was varied by ± 4 ml/kg in an 11-minute cycle of infusion, withdrawal, withdrawal, and reinfusion) and was calculated from the correlation between the observed changes in central venous pressure and the changes in blood volume. Sympathetic activity and central venous pressure were lower and effective vascular compliance was higher than values in untreated conscious dogs. The a 2 -agonist UK 14,304 (5-bromo-6-[imidazolin-2-ylamino]-quinoxaline; 0.04 and 0.12 //.g/kg/min; n = 6) dose-dependently lowered compliance and increased central venous pressure to levels found in conscious dogs, as did the ai-agonist methoxamine (10 and 30 ^ig/kg; n = 6). Rauwolscine (a 2 -antagonist), 0.3 mg/kg, significantly attenuated the effects of UK 14,304, but not those of methoxamine, while prazosin (a!-antagonist), 0.12 mg/kg, attenuated the effects of methoxamine, but not those of UK 14,304 (n = 6 each). Under /3-blockade (nadolol, 2 mg/kg; a = 12) venous tone was increased to about physiological levels by norepinephrine, 0.15 yug/kg/min i.v., or by neuronal norepinephrine release induced by tyramine, 10 /ng/kg/min i.v. These increases were significantly attenuated by prazosin as well as by rauwolscine and were abolished by a combination of both. These results indicate that postsynaptic a 2 -adrenergic receptors (in addition to a r adrenergic receptors) are functional in the venous system in vivo and contribute substantially to adrenergic sympathetic and humoral regulation of venous tone. (Hypertension 8: 1003(Hypertension 8: -1014(Hypertension 8: , 1986 KEY WORDS • total effective vascular compliance • venous tone • vascular a 2 -adrenergic receptors • capacitance vessel constriction • rauwolscine • prazosin A BNORMALITIES in venous function feature / \ prominently in the pathophysiological A. \ . changes found in various types of experimental hypertension 1 ' 2 as well as in hypertensive patients, 3 -4 and augmented venous tone is a key link underlying the postulated pathophysiological role of natriuretic hormone in hypertension.3 The abnormalities in venous function include increased sensitivity to

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Molsidomine: Alternative Approaches To Treat Myocardial Ischemia

Nitz¹,

Fiedler²

1987

Pharmacotherapy

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The long-acting antianginal drug molsidomine has been shown experimentally to reduce myocardial infarct size when administered prior to or after cardiac insult. This is due to several drug actions. Dilation of postcapillary capacitance vessels diminishes venous return, preload, heart dimensions, and myocardial oxygen consumption. Relaxation of stenosed conductive coronary arteries increases the perfusion of myocardial areas at risk of infarction due to enhanced collateral circulation. Increased regional blood supply nourishes predominantly subendocardial cardiac muscles as a result of reduction of extravascular coronary pressure, and resistance. The stable heart rate and cardiac contractility favor improved heart performance. The inhibition of platelet aggregation in vivo by molsidomine or its active metabolites, SIN-1 and SIN-1A, is linked to the stimulation of prostacyclin synthesis, inhibition of thromboxane release with induction of thrombosis and vasoconstriction, and enhanced concentrations of cyclic guanosine monophosphate. Dilation of coronary arteries after intracoronary administration of SIN-1, with inhibition of platelet aggregation by restrained release of adenosine diphosphate and stabilization of platelet membranes, facilitates the recanalization of stenosed arteries and reduces coronary muscle tone at the site of thrombosis. Activation of the human fibrinolytic system and drug-induced release of a plasminogen activator favor dysaggregatory effects. The drug's inhibiting actions on lipoxygenase products of arachidonate (e.g., 12-hydroperoxy-eicosatetraenoic acid and leukotrienes) may shift prostaglandin catabolism to cyclooxygenase products (e.g., prostacyclin) that protect against the expansion of ischemia and the induction of coronary spasm. Experimentally, the hemodynamic effectiveness of molsidomine can be antagonized by catecholamines (afterload effects) and dihydroergotamine (preload and afterload effects) respectively. Further clinical investigations will clarify the application of these mechanisms for the therapeutic success of the drug in human myocardial infarction.

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Increased effective vascular compliance and venous pooling of intravascular volume during sustained venodilation in conscious dogs

Cited by 14 publications

References 29 publications

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

Preferential venoconstriction by cyclooxygenase inhibition in vivo without attenuation of nitroglycerin venodilation.

Postsynaptic alpha 1- and alpha 2-adrenergic receptors in adrenergic control of capacitance vessel tone in vivo.

Molsidomine: Alternative Approaches To Treat Myocardial Ischemia

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