Hemorrhagic Hypotension Alters Circulating and Myocardial Enkephalins and Catecholamines

dc.contributor.advisorCaffrey, James
dc.contributor.committeeMemberNapier, Leslie
dc.contributor.committeeMemberYoshishige, Darice
dc.creatorMateo, Zaira
dc.description.abstractMateo, Zaira, Hemorrhagic hypotension alters circulating and myocardial enkephalins and catecholamines. Master of Science (Biomedical Sciences). November, 1994. A variety of plasma and intrinsic cardiac enkephalins were extracted, chromatographed and assayed under control conditions and during two hours of hemorrhagic hypotension. The animals were anesthetized, instrumented and sufficient blood was withdrawn as required to reduce mean arterial pressure and maintain it at 40 mmHg. Central venous blood samples were obtained 15 minutes before and at 30 minute intervals during the experiment. Arterial blood gases remained stable throughout the experiment while pH declined from above 7.4 to near 7.1. Heart rate rose gradually by 100 bpm. Plasma catcholamines were unchanged during two hour time-controls. Plasma norepinephrine and epinephrine increased by 6 and 100 fold respectively, during the first hour of hypotension and remained high through the second hour. All eight enkephalin immunoreactivities monitored were unchanged during the time-controls. Plasma met-enkephalin (ME) and Peptide-F both gradually increased by 70-100% during the hypotension. Plasma Met-enkephalin-Arg-Phe (MEAP) and Peptide-B concentrations increased 4-5 fold during the same interval. Proenkephalin and other large enkephalin containing peptids though present, were unchanged during hypotension. Myocardial norepinephrine was preferentially concentrated about 3:1 in the atria. Both atrial and ventricular concentrations were reduced by one third or more following two hours of hypotension. Proenkephalin and peptide-B accounted for 75% of the intrinsic enkephalins and their ventricular concentrations were 3 to 4 times atrial concentrations in the same hearts. Intrinsic cardiac MEAP concentrations were 15-25 times higher than comparable ME concentrations in the same myocardial regions. Hypotension produced a significant increase in Peptide-B and proenkephalin compared to controls. The increase was consistent throughout the heart, thus maintaining the preferential concentration in the ventricles. Myocardial ME, MEAP and Peptide-F were largely unchanged in hypotensives compared to time-controls. The data demonstrate the preferential processing and retention of MEAP rather than ME-immunoreactive enkephalins in heart tissue. The data also indicate the responsiveness of MEAP-ir to changes in the circulatory environment and their subsequent appearance in plasma during hemorrhagic hypotension. Prior data suggests that intrinsic cardiac enkephalins may actively regulate either vagal control of the heart or sympathetic control of vasomotor tone.
dc.subjectCardiovascular System
dc.subjectCirculatory and Respiratory Physiology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectHemorrhagic hypotension
dc.subjectcirculating enkephalins
dc.subjectmyocardial enkephalins
dc.subjectplasma catecholamines
dc.subjectcardiac enkephalins
dc.subjectheart tissue
dc.subjectvagal control
dc.subjectsympathetic control
dc.titleHemorrhagic Hypotension Alters Circulating and Myocardial Enkephalins and Catecholamines
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineBiomedical Sciences
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameMaster of Science


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