[Limitation of disorders of the contractile function of the nonischemic areas of the myocardium during infarct by using the delta-sleep peptide and its cyclic derivative].
Meerson. F Z FZ; Zaiats. V I VI; Pshennikova. M G MG; Bozhko. A P AP
Key Findings
- Pretreatment with DSP or cDSP (20 µg/kg) reduced the drop in atrial flexibility and contractility after induced heart attacks in rats.
- s susceptibility to hypoxia and calcium overload.",
Practical Outcomes
- While the results hint that delta‑sleep peptide might blunt stress‑related heart damage, the study is limited to rats and uses a pre‑emptive dosing strategy that isn’t feasible for most people. No human safety or dosing data exist, so biohackers cannot yet apply this as a protocol for heart health or stress management.
Summary
In a rat study, giving a tiny dose of delta‑sleep peptide (DSP) or its cyclic version an hour before a heart attack helped keep the heart's right atrium more flexible and better at contracting, and made it less vulnerable to low oxygen and too much calcium. The authors think this protection comes from dampening the stress response that usually follows a heart attack.
Abstract
The effect of pretreatment with delta-sleep peptide (DSP) and its cyclic analogue (cDSP) on right-atrial myocardial distensibility and contractility disturbances in left-ventricular infarction (according to Selye) was studied in Wistar rats. These peptides, administered in a 20 micrograms/kg dose, 1 hour before the induction of experimental infarction, significantly limited the infarct-related depression of atrial distensibility and contractility, and also reduced atrial resistance to hypoxia and excessive calcium. Since infarction-associated disorders of myocardial structure and function in non-ischemic regions of the heart are due to the emotional-painful stress that accompanies the infarction, it can be assumed that the protective effect of DSP and cDSP consists in limiting the stress-induced response.
Study Information
pubmed
1985