MENU
Anatomy
Anesthesiology
Biochemistry
Biomedical Informatics
Biophysics
Cell Biology
Clinical Cases
Dentistry
Dermatovenerology
Emergency Medicine
Family Medicine
Forensic Medicine
Gynecology and Obstetrics
Histology and Embryology
History of Medicine
Human Genetics
Hygiene
Infectious Diseases
Internal Medicine
Medical Deontology and Philosophy
Medical Psychology
Microbiology and Immunology
Neurology
Occupational Medicine
Oncology
Ophthalmology
Orthopaedics
Otorhinolaryngology
Pathology
Pathophysiology
Pediatrics
Pharmacology and Experimental Toxicology
Physical and Rehabilitation Medicine
Physiology
Psychiatry
Radiology
Social Medicine
Surgery
Toxicology
Research papers
Clinical research paper
Preclinical research paper
Sponsored articles
Archive » 1996 » 4 » | Archive » Medical field » Fields » Pharmacology and Experimental Toxicology » Archive » Medical field » Research papers » Preclinical research paper »

The Influence of Famotidine and Chloropyramine on Ischemic Rat Hearts

 
Abstract:

This post is also available in: enEnglish slSlovenščina (Slovenian)

In the present study the effects of either H1 antagonist chloropyramine or H2 antagonist famotidine were investigated in isolated Langendorff’s rat hearts. Ischemia lasted 60 minutes. Perfusion with either 10 μmol/L chloropyramine or 10 μmol/L famotidine was initiated 10 minutes before ischemia and lasted till the end of the experiments. Registered were left ventricular pressure, heart rate, Q, coronary flow and ECG. The temperature in the left ventricle was kept at 38.5 ± 0.5 °C. The extent of myocardial damage was assessed by the release rate of the enzyme lactate dehydrogenase. In control experiments chloropyramine had negative chronotropic effect and increased Q. Its addition decreased the coronary flow during reperfusion, caused bradycardia and did not influence the lactate dehydrogenase release. In control experiments famotidine had positive inotropic and positive chronotropic effects and decreased Q. In control experiments famotidine increased the coronary flow. During reperfusion famotidine induced tachycardia and fibrillation. Famotidine did not influence the lactate dehydrogenase release during reperfusion. Results of our experiments indicate that in the rat heart additionally to H1 receptors also H2 receptors might exist and that both of them could be involved in the myocardial damage induced by ischaemia and reperfusion.

Authors:
Burjak Mateja

Keywords:
myocardial ischemia – drug therapy, famotidine, histamine H1 antagonists

Cite as:
Med Razgl. 1996; 35: 473–89.

Download PDF >>
© 2019 Društvo Medicinski razgledi | Na vrh strani / To top ↑