Hypothalamo–pituitary–adrenal axis response to coronary artery embolization: an ovine model of acute myocardial infarction

Abstract

Although previous studies have described the hypothalamo-pituitary-adrenal (HPA) response to the stress of acute myocardial infarction, it is not possible to study the hormone changes immediately after infarction in humans. Accordingly, we have examined the HPA response to microembolization of coronary arteries in 13 sheep compared with 5 sham control sheep. Plasma vasopressin (AVP; P < 0.001), ACTH (P = 0.005) and cortisol (P = 0.005) were all increased 2 h (first sample time) after embolization. Plasma ACTH and cortisol levels returned to baseline levels by 6 h but plasma AVP levels did not return to baseline levels until more than 12 h after embolization. Plasma corticotrophin-releasing hormone (CRH) showed no significant change in response to embolization. In a subset of six animals which were sampled more frequently, the peak responses for plasma AVP, ACTH and cortisol occurred at 40 min after embolization. The maximum responses in any individual sheep observed at this time point were 744 pmol/l for AVP, 144 pmol/l for ACTH and 492 nmol/l for cortisol. CRH levels tended to increase across the first hour but these changes were not statistically significant. In conclusion, the stress hormone responses to microembolization of the coronary arteries have been defined in an ovine model of myocardial infarction. This model is suitable for studying the effects of novel treatments to reduce the stress of myocardial infarction.

Combination of Copeptin and Troponin Assays to Rapidly Rule Out Non‐ST Elevation Myocardial Infarction in the Emergency Department

“…Initial plasma levels of arginine‐vasopressin measured within 6 hours of the onset of symptoms were highly elevated and then declined during the following 3 days. In sheep, experimental coronary embolization led to a very early rise in plasma arginine‐vasopressin, which was maximal at 40 minutes after embolization, and then decreased, but remained elevated for more than 12 hours 26 . The magnitude of this maximum response was comparable with levels seen in humans on ED presentation to hospital with AMI 25 .…”

Postmortem biochemistry and immunohistochemistry of adrenocorticotropic hormone with special regard to fatal hypothermia

“…These findings suggest that a dysfunctional HPA axis contributes to an acute cardiac attack [33,34].…”

Elevation of Plasma Copeptin in Acute Myocardial Infarction in Pigs is Related to Changes in Mean Arterial Blood Pressure but not to Myocardial Ischemia

“…Results from animal models show that hypotension causes an immediate induction of AVP-gene transcription and that induced hypotension in humans leads to a significant increase in plasma vasopressin [12,13]. An increase of plasma vasopressin was also shown in the setting of myocardial infarction due to microembolization in an ovine model [14]. In accordance with these findings, in our model of reperfused experimental AMI in pigs, the infarction-related decrease of MAP seems to be the trigger for the increase of copeptin levels.…”