Cardiac ischemia and impairment of vascular endothelium function in hearts from growth hormone-deficient rats: protection by hexarelin.
De Gennaro Colonna. V V; Rossoni. G G; Bernareggi. M M; Müller. E E EE; Berti. F F
Key Findings
- Hexarelin restores normal growth‑hormone function in GH‑deficient rats
- Hexarelin improves post‑ischemic heart contractility and reduces damage in both GH‑deficient and normal rats
- Hexarelin normalizes prostacyclin production and angiotensin‑II vasopressor activity, indicating better vascular endothelial function
Practical Outcomes
- If you already use hexarelin as a GH secretagogue, you might also be getting some heart‑protective benefits, but human data are missing. No clear human dosing protocol exists, so any use for cardiac protection would be experimental. Monitor cardiovascular health and consider that the main evidence is from animal studies before adding it for heart health alone.
Summary
In rats that lack growth hormone, giving the peptide hexarelin for two weeks not only fixed their hormone levels but also helped their hearts recover better after a simulated heart attack. Even normal rats got a boost in heart performance after a heart attack when given hexarelin, and this benefit didn’t depend on extra growth hormone. The study shows hexarelin can protect heart muscle and blood vessels, but it’s all in animals, not people yet.
Abstract
The ability of hexarelin, an effective growth hormone (GH)-releasing hexapeptide, to reverse the worsening of cardiac dysfunction in GH-deficient animals was studied in young male rats passively immunized by administration of an anti-GH-releasing hormone (GHRH) serum. Heart preparations from anti-GHRH serum-treated rats, undergoing low-flow ischemia and reperfusion, showed: (1) a progressive increase of left ventricular end-diastolic pressure during the ischemic period and a poor recovery of contractility at reperfusion with a consistent decrease of the left ventricular-developed pressure; (2) a decreased rate of formation of 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), a stable metabolite of prostacyclin, in perfusates from preischemic and reperfusion periods; (3) an increased vasopressor activity of angiotensin II. Hexarelin (80 microg/kg, bid, s.c.), administered for 15 days to anti-GHRH serum-treated rats, restored to normal the impaired somatotropic function and counteracted the ischemic damage, improving postischemic left ventricular developed pressure to values higher than those of controls. Furthermore, both the generation of 6-keto-PGF1alpha and the vasopressor activity of angiotensin II reverted to those of control preparations. Administration of hexarelin to control rats induced a considerable improvement of postischemic ventricular function of the perfused hearts which was similar to that present in preparations from anti-GHRH serum-treated rats given hexarelin. This protective activity was divorced from any further stimulation of somatotropic function. Collectively, these data indicate that, in GH-deficient rats, hexarelin is capable of restoring somatotropic function and has a beneficial effect in myocardial ischemia and reperfusion damage. In addition, the increased responsiveness of the coronary vasculature to angiotensin II and the decreased generation of prostacyclin in hearts from GH-deficient rats would indicate that for prevention of injury and dysfunction of the vascular endothelium a normal somatotropic function is mandatory.
Study Information
pubmed
1997
1997-09-10T00:00:00.000Z
10.1016/s0014-2999(97)01178-3