Adenosine increases total venous capacitance in awake instrumented rats

M. R. Glick, J. D. Gehman, Joseph Gascho

Research output: Contribution to journalArticle

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Abstract

To determine the effect of adenosine on the venous system, mean circulatory filling pressure (MCFP) was determined during infusion of intravenous (i.v.) adenosine (66.5 to a maximum of 532 μg · kg-1 · min- 1) in 9 awake instrumented rats before and during ganglionic blockade with i.v. hexamethonium, 0.6 mg · kg-1 · min-1. MCFP, the equilibrated pressure (mm Hg) occurring when the circulation is arrested by transient inflation of a balloon in the right atrium, is inversely related to total venous capacitance. Both adenosine and hexamethonium caused a reduction in mean arterial pressure (MAP); heart rate (HR) decreased during adenosine infusion in the blocked, but not the unblocked, state. In the unblocked state, baseline MCFP was 6.5 ± 0.3 mm Hg; hexamethonium caused baseline MCFP to decrease to 5.3 ± 0.3 mm Hg. In both the unblocked and the blocked state, adenosine caused a dose-related decrease in MCFP [6.5 ± 0.3 to 5.5 ± 0.6 mm Hg (532 μg · kg-1 · min-1 adenosine dose) unblocked state; and 5.3 ± 0.3 to 4.3 ± 0.3 mm Hg (400 μg · kg-1 · min-1 adenosine dose) blocked state]. This decrease in MCFP induced by adenosine was highly significant. Intravenous adenosine, in an awake instrumented rat model, increases venous capacitance, with and without ganglionic blockade.

Original languageEnglish (US)
Pages (from-to)709-713
Number of pages5
JournalJournal of Cardiovascular Pharmacology
Volume19
Issue number5
StatePublished - Jan 1 1992

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Adenosine
Pressure
Hexamethonium
Economic Inflation
Cardiovascular System
Heart Atria
Intravenous Infusions
Arterial Pressure
Heart Rate

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Cardiology and Cardiovascular Medicine

Cite this

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title = "Adenosine increases total venous capacitance in awake instrumented rats",
abstract = "To determine the effect of adenosine on the venous system, mean circulatory filling pressure (MCFP) was determined during infusion of intravenous (i.v.) adenosine (66.5 to a maximum of 532 μg · kg-1 · min- 1) in 9 awake instrumented rats before and during ganglionic blockade with i.v. hexamethonium, 0.6 mg · kg-1 · min-1. MCFP, the equilibrated pressure (mm Hg) occurring when the circulation is arrested by transient inflation of a balloon in the right atrium, is inversely related to total venous capacitance. Both adenosine and hexamethonium caused a reduction in mean arterial pressure (MAP); heart rate (HR) decreased during adenosine infusion in the blocked, but not the unblocked, state. In the unblocked state, baseline MCFP was 6.5 ± 0.3 mm Hg; hexamethonium caused baseline MCFP to decrease to 5.3 ± 0.3 mm Hg. In both the unblocked and the blocked state, adenosine caused a dose-related decrease in MCFP [6.5 ± 0.3 to 5.5 ± 0.6 mm Hg (532 μg · kg-1 · min-1 adenosine dose) unblocked state; and 5.3 ± 0.3 to 4.3 ± 0.3 mm Hg (400 μg · kg-1 · min-1 adenosine dose) blocked state]. This decrease in MCFP induced by adenosine was highly significant. Intravenous adenosine, in an awake instrumented rat model, increases venous capacitance, with and without ganglionic blockade.",
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Adenosine increases total venous capacitance in awake instrumented rats. / Glick, M. R.; Gehman, J. D.; Gascho, Joseph.

In: Journal of Cardiovascular Pharmacology, Vol. 19, No. 5, 01.01.1992, p. 709-713.

Research output: Contribution to journalArticle

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AU - Gascho, Joseph

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AB - To determine the effect of adenosine on the venous system, mean circulatory filling pressure (MCFP) was determined during infusion of intravenous (i.v.) adenosine (66.5 to a maximum of 532 μg · kg-1 · min- 1) in 9 awake instrumented rats before and during ganglionic blockade with i.v. hexamethonium, 0.6 mg · kg-1 · min-1. MCFP, the equilibrated pressure (mm Hg) occurring when the circulation is arrested by transient inflation of a balloon in the right atrium, is inversely related to total venous capacitance. Both adenosine and hexamethonium caused a reduction in mean arterial pressure (MAP); heart rate (HR) decreased during adenosine infusion in the blocked, but not the unblocked, state. In the unblocked state, baseline MCFP was 6.5 ± 0.3 mm Hg; hexamethonium caused baseline MCFP to decrease to 5.3 ± 0.3 mm Hg. In both the unblocked and the blocked state, adenosine caused a dose-related decrease in MCFP [6.5 ± 0.3 to 5.5 ± 0.6 mm Hg (532 μg · kg-1 · min-1 adenosine dose) unblocked state; and 5.3 ± 0.3 to 4.3 ± 0.3 mm Hg (400 μg · kg-1 · min-1 adenosine dose) blocked state]. This decrease in MCFP induced by adenosine was highly significant. Intravenous adenosine, in an awake instrumented rat model, increases venous capacitance, with and without ganglionic blockade.

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