The pituitaries and adrenals of 30 patients died from extensive fresh myocardial infarction and of 25 patients died from other diseases were studied. In myocardial infarction the mean weight of the above glands was significantly higher than in other diseases. In most cases an increase in number of pituitary ACTH-cells was observed with the immunoperoxidase method. In non-cardiogenic shock (another 9 cases) gland weight was also increased but without a significant increase in the number of ACTH-cells. Hyperactivity of the anterior pituitary-adrenal system is due to a number of known factors. It may be assumed that patients who have infarction are either exposed to an extraordinary amount of stress stimuli or are more susceptible to stress than normal subjects. The findings may indicate the morphological basis of this situation. Of the shock phenomena, incomplete necrosis and haemorrhage of the adrenal cortex are frequent. In the pituitary neural lobe the neurosecretory material, which proved to be vasopressin with the PAP-method, was found to be increased more frequently in myocardial infarction than after other diseases.

Download full-text PDF

Source

Publication Analysis

Top Keywords

myocardial infarction
16
patients died
8
increase number
8
infarction
5
immunocytochemical investigation
4
investigation acth-cells
4
acth-cells vasopressin
4
vasopressin pituitaries
4
pituitaries humans
4
humans died
4

Similar Publications

Background: He's team have recently developed a new Coronary Artery Tree description and Lesion EvaluaTion (CatLet) angiographic scoring system, which is capable of accounting for the variability in coronary anatomy, and risk-stratifying patients with coronary artery disease. Preliminary studies have demonstrated its superiority over the the Synergy between percutaneous coronary intervention with Taxus and Cardiac Surgery (SYNTAX) score with respect to outcome predictions for acute myocardial infarction (AMI) patients. However, there are fewer studies on the prognostic in chronic coronary artery disease(CAD).

View Article and Find Full Text PDF

Background: Myocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.

View Article and Find Full Text PDF

Myocardial infarction is a condition where the heart muscle is damaged due to clogged coronary arteries. There are limited treatment options for treating myocardial infarction. Microneedle patches have recently become popular as a possibly viable therapy for myocardial.

View Article and Find Full Text PDF

Cardiomyocytes can be implanted to remuscularize the failing heart. Challenges include sufficient cardiomyocyte retention for a sustainable therapeutic impact without intolerable side effects, such as arrhythmia and tumour growth. We investigated the hypothesis that epicardial engineered heart muscle (EHM) allografts from induced pluripotent stem cell-derived cardiomyocytes and stromal cells structurally and functionally remuscularize the chronically failing heart without limiting side effects in rhesus macaques.

View Article and Find Full Text PDF

Acute myocardial infarction (AMI) remains one of the most common causes for cardiogenic shock (CS), with high inpatient mortality (40-50 %). Studies have reported the use of pulmonary artery catheters (PACs) in decompensated heart failure, but contemporary data on their use to guide management of AMI-CS and in different SCAI stages of CS are lacking. We investigated the association of PACs and clinical outcomes in AMI-CS.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!