Key result
Treatment with TEMPOL, SQ-29548, and phentolamine improved microvascular hematocrit and normalized its variability in Obese Zucker Rats, though it did not impact reduced PS.
Why the study?
Does targeted pharmacological intervention improve skeletal muscle microvascular hematocrit and perfusion heterogeneity in a rat model of metabolic syndrome?
Does targeted pharmacological intervention improve skeletal muscle microvascular hematocrit and perfusion heterogeneity in a rat model of metabolic syndrome?
Increased microvascular perfusion heterogeneity in metabolic syndrome reduces muscle microvascular hematocrit, which can be acutely improved by combined antioxidant and receptor antagonist therapy, though reduced surface area is not acutely reversible.
Does not inform clinical practice in metabolic syndrome; extends preclinical evidence on microvascular heterogeneity but leaves open human translation.
OBJECTIVE: To determine HMV and PS in skeletal muscle of OZR and evaluate the impact of increased microvascular perfusion heterogeneity on mass transport/exchange. METHODS: The in situ gastrocnemius muscle from OZR and LZR was examined under control conditions and following pretreatment with TEMPOL (antioxidant)/SQ-29548 (PGH2 /TxA2 receptor antagonist), phentolamine (adrenergic antagonist), or all agents combined. A spike input of a labeled blood tracer cocktail was injected into the perfusing artery. Tracer washout was analyzed using models for HMV and PS. HT was determined in in situ cremaster muscle of OZR and LZR using videomicroscopy. RESULTS: HMV was decreased in OZR versus LZR. While TEMPOL/SQ-29548 or phentolamine had minor effects, treatment with all three agents improved HMV in OZR. HT was not different between strains, although variability was increased in OZR, and normalized following treatment with all three agents. PS was reduced in OZR and was not impacted by intervention. CONCLUSIONS: Increased microvascular perfusion heterogeneity in OZR reduces HMV in muscle vascular networks and increases its variability, potentially contributing to premature muscle fatigue. While targeted interventions can ameliorate this, the reduced microvascular surface area is not acutely reversible.
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Butcher et al. (2014) studied Metabolic Syndrome. TEMPOL, SQ-29548, and phentolamine vs. Control conditions was evaluated on Microvascular hematocrit (HMV) and permeability-surface area product (PS). Treatment with TEMPOL, SQ-29548, and phentolamine improved microvascular hematocrit and normalized its variability in Obese Zucker Rats, though it did not impact reduced PS.
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