What is the clinical evidence from this study?

Study design: Other. Population: Ischemia/reperfusion injury (myocardial edema) (n=22). Intervention: 3% dextran vs. Standard buffer. Primary outcome: Left ventricular end-diastolic pressure (LVEDP) (p=<0.05).

What does this research mean for the field?

Reperfusion with hyperoncotic dextran reduces myocardial edema, which significantly mitigates post-ischemic left ventricular chamber stiffness and elevated coronary resistance. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine the role of myocardial edema in elevating left ventricular chamber stiffness and coronary vascular resistance after global ischemia and reperfusion.

December 1, 1986Journal of Molecular and Cellular CardiologyOpen Access

Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role of edema and effects of dextran

Q: What are the key findings of this study?

In isolated rabbit hearts, reperfusion with 3% dextran after ischemia significantly reduced left ventricular end-diastolic pressure (38 vs 51 mmHg, P<0.05) and water content compared to standard buffer.

Q: What does this research mean for the field?

Reperfusion with hyperoncotic dextran reduces myocardial edema, which significantly mitigates post-ischemic left ventricular chamber stiffness and elevated coronary resistance. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

Q: What question did this study set out to answer?

To determine the role of myocardial edema in elevating left ventricular chamber stiffness and coronary vascular resistance after global ischemia and reperfusion.

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Key result

Reperfusion with 3% dextran lowers LVEDP ~25% vs standard buffer in isolated rabbit hearts.

P<0.05
n=22

Why the study?

Does 3% dextran perfusion reduce LV chamber stiffness and coronary resistance in isolated rabbit hearts after global ischemia?

Population

Isolated buffer-perfused rabbit hearts subjected to 30 min global ischemia and 60 min reperfusion

Comparison

Perfusion with 3% dextran during 60 min… vs Perfusion with standard buffer during 60 min…

Design

Preclinical

Follow-up

60 min reperfusion

Authors

WVW VogelBoston University ACAdam CerelDeaconess Hospital CACarl S. ApsteinHeart Failure / Cardiomyopathy

Discussion

Member takes

Implication

May attenuate postischemic stiffness via edema reduction in isolated hearts; leaves open translation to clinical reperfusion strategies.

Key Points

To determine the role of myocardial edema in elevating left ventricular chamber stiffness and coronary vascular resistance after global ischemia and reperfusion.
Isolated buffer-perfused rabbit hearts with constant left ventricular volume were subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion.
Reperfused hearts received either standard buffer (n=8) or 3% dextran (n=8) to raise oncotic pressure and reduce tissue water content, alongside nonischemic controls (n=6).
Vasodilator responses to 2 minutes of hypoxia and 10⁻⁴ M adenosine were assessed after 15 and 30 minutes of ischemia to evaluate coronary vasomotion.
Untreated ischemic hearts exhibited marked left ventricular end-diastolic pressure (51 ± 4 mmHg) and water content (6.0 ± 0.1 ml/g dry weight; P < 0.001 vs. nonischemic at 11 ± 0.3 mmHg and 5.0 ± 0.1 ml/g dry weight), which were attenuated by dextran to 38 ± 3 mmHg (P < 0.05) and 5.2 ± 0.1 ml/g dry weight (P < 0.001).
Coronary resistance increased by 26% (2.0 ± 0.06 to 2.6 ± 0.06 mmHg/ml/min) in untreated ischemic hearts versus 16% (1.9 ± 0.09 to 2.2 ± 0.09 mmHg/ml/min) in dextran-treated hearts (P < 0.01).
After 30 minutes of ischemia, vasodilatory responses to hypoxia declined by 72% (P < 0.025) and responses to adenosine were abolished (P < 0.02), indicating dextran lowers coronary resistance via edema reduction rather than active vasodilation.

Structured PICO

Does 3% dextran perfusion reduce LV chamber stiffness and coronary resistance in isolated rabbit hearts after global ischemia?

Population

22 isolated buffer-perfused rabbit hearts subjected to 30 min global ischemia and 60 min reperfusion.

Intervention

Perfusion with 3% dextran during 60 min reperfusion

Comparator

Perfusion with standard buffer during 60 min reperfusion

Outcome

Left ventricular (LV) chamber stiffness (measured by LVEDP) and coronary resistancesurrogate

Main Result

Absolute Event Rate: 38% vs 51%

p-value: p=<0.05

Increasing oncotic pressure with dextran reduces myocardial edema, thereby decreasing post-ischemic ventricular chamber stiffness and coronary resistance.

Cite This Study

Vogel et al. (1986) studied Ischemia/reperfusion injury (myocardial edema) (n=22). 3% dextran vs. Standard buffer was evaluated on Left ventricular end-diastolic pressure (LVEDP) (p=<0.05). In isolated rabbit hearts, reperfusion with 3% dextran after ischemia significantly reduced left ventricular end-diastolic pressure (38 vs 51 mmHg, P<0.05) and water content compared to standard buffer.

synapsesocial.com/papers/6aa58407c34c6f6bfa64bd46 https://doi.org/10.1016/s0022-2828(86)80425-4

Topics

Heart failure HFrEF treatment

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Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role of edema and effects of dextran

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Topics

Post-ischemic cardiac chamber stiffness and coronary vasomotion: the role of edema and effects of dextran

Discussion

Member takes

Implication

Key Points

Structured PICO

Main Result

Cite This Study

Also Consider

Topics

Also Consider