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In vivo analysis of microvascular injury after myocardial cryothermia
H Huwer1, N Nikoloudakis, J Rissland
1Department of Thoracic and Cardiovascular Surgery, University of Saarland, Homburg/Saar, D-66421, Germany.
Abstract:
We studied microvascular injury after myocardial cryothermia in rats using intravital fluorescence microscopic techniques. Cryolesions were induced to the right ventricle by freezing with -160 degrees C (probe diameter: 5 mm) for a total of 5 min. Fluorescence microscopy was performed at 15, 30, 60, 90, and 120 min as well as at 3 and 7 days after cryothermia. Analysis of the epicardial microvasculature 15 min after cryothermia revealed an area of 24.6 +/- 3.8 mm2 of nonperfused tissue, which was reduced to 5.3 +/- 1.5 mm2 (P < 0.05) after the initial 2-h observation period. Vital microscopic images of reperfused tissue characteristically demonstrated extravasation of the macromolecular fluorescent tracer FITC-dextran (21.7 +/- 3.4 mm2), suggesting substantial loss of endothelial integrity. In vivo propidium iodide staining confirmed membrane damage of microvascular endothelial cells. Three days after cryoinjury the area of nonperfused tissue was reduced further to 1.1 +/- 0.4 mm2 in the center of the lesion, while the area of perfused tissue with disruption of endothelial integrity was found significantly increased to 47.4 +/- 5.9 mm2 (P < 0.05) toward the periphery. Analysis at 7 days revealed endothelial repair at the periphery of the cryolesion, but now a central necrotic area was found demarcated (nonperfused), presenting with a size (26.0 +/- 3.5 mm2) similar to that shown during the very early (15 min) reperfusion period. Our study demonstrates recovery of microvascular perfusion during the first hours and days after myocardial cryothermia. This is, however, associated with endothelial injury, i.e., damage of plasma membrane and loss of barrier function. Infarction with capillary perfusion failure is evident at 7 days with a size which strikingly corresponds to the sizeof nonperfused tissue observed immediately after cryointervention.
Insights
Myocardial cryothermia causes microvascular injury and endothelial damage in rats. While perfusion recovers initially, infarction with capillary failure reappears by day 7.
Area of Science:
- Cardiovascular Biology
- Microcirculation Research
- Cryobiology
Background:
- Myocardial cryothermia is a procedure that can lead to tissue damage.
- Understanding microvascular responses to cryoinjury is crucial for developing therapeutic strategies.
- Previous studies have not fully elucidated the temporal dynamics of microvascular integrity post-cryothermia.
Purpose of the Study:
- To investigate the microvascular injury and repair processes following myocardial cryothermia in a rat model.
- To characterize the changes in microvascular perfusion and endothelial integrity over time.
- To correlate early nonperfused tissue size with later infarction size.
Main Methods:
- Induction of cryolesions on the right ventricle of rats using a -160°C probe for 5 minutes.
- Intravital fluorescence microscopy to assess microvascular perfusion and endothelial integrity.
- Use of FITC-dextran and propidium iodide to evaluate vascular permeability and cell membrane damage.
- Serial observations at 15 minutes, 2, 3, and 7 days post-cryoinjury.
Main Results:
- Initially, cryolesions resulted in significant nonperfused tissue (24.6 mm²), which decreased within 2 hours.
- Reperfusion was accompanied by substantial extravasation of FITC-dextran (21.7 mm²), indicating loss of endothelial barrier function.
- By day 7, a central necrotic area (26.0 mm²) reappeared, similar in size to the initial nonperfused area, despite peripheral endothelial repair.
Conclusions:
- Myocardial cryothermia induces significant microvascular injury and endothelial dysfunction.
- Initial recovery of microvascular perfusion is transient and associated with persistent endothelial damage.
- Capillary perfusion failure and infarction are evident at 7 days, mirroring the initial nonperfused tissue size.