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Health Care Reform↗
Biomedical subjects
R L Crum
Publications and source records attributed to R L Crum.
Cardiovascular and neurohumoral responses following burn injury.
Cardiovascular and endocrine responses were evaluated in 12 adult patients over a 5-day period following 30% to 66% burn injury. Heart rate, mean arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac output, systemic vascular resistance, and stroke volume were measured. Plasma concentrations of angiotensin II, atrial natriuretic peptide, vasopressin, neuropeptide Y, norepinephrine, and epinephrine were measured. On the day of burn injury, systemic vascular resistance was markedly elevated, and stroke volume and cardiac output were low, but all normalized by day 3, and cardiac output and stroke volume increased by day 5 without significant changes of central venous pressure or pulmonary capillary wedge pressure. Mean arterial pressure and heart rate did not change significantly over the 5-day period. Vasopressin, angiotensin II, neuropeptide Y, norepinephrine, and epinephrine concentrations in plasma were elevated on admission. Vasopressin concentrations were elevated 50 times normal on admission and returned to normal levels by days 4 to 5. Plasma atrial natriuretic peptide concentrations were normal on admission and increased significantly on days 3 to 5. The reciprocal relationship between systemic vascular resistance and cardiac output and between vasopressin and atrial natriuretic peptide correlate with each other and the observed physiologic events that occurred following burn injury and resuscitation. All of these changes in cardiac performance occurred without significant alterations in preload or afterload as measured by central venous pressure, pulmonary capillary wedge pressure, and mean arterial pressure. Increases in plasma levels of atrial natriuretic peptide correlated with the increased stroke volume and cardiac output observed in these patients. The results of this study are consistent with the conclusion that the extreme elevations of plasma vasopressin levels contribute to the vascular complications of increased systemic vascular resistance and decreased cardiac output and contractility seen following burn injury.
Adult↗
Distinction of NPY receptors in vitro and in vivo. II. Differential effects of NPY and NPY-(18-36).
We have studied the hemodynamic effects of neuropeptide Y (NPY) and its COOH-terminal fragment NPY-(18-36) in conscious rats. Intra-arterial injection of NPY rapidly elevated systemic vascular resistance (SVR), which remained high for greater than 30 min. Cardiac output (CO) decreased, and it remained low for greater than 30 min. Accordingly, blood pressure rose only transiently and returned to base-line values within 5 min. The reduction of CO could be attributed to a decreased stroke volume with an only marginal reduction of heart rate. Thus a direct cardiodepressive effect of NPY rather than baroreflex activation appears to be the major cause of the reduced CO. In vitro experiments excluded the possibility that NPY has direct negative inotropic effects and suggest that its cardiodepressive action is caused by coronary vasoconstriction or by presynaptic inhibition of norepinephrine release. Intra-arterial injections of NPY-(18-36) caused different hemodynamic effects. NPY-(18-36) decreased CO in a manner similar to that seen with NPY but initially did not elevate SVR, resulting overall in a reduced blood pressure. Only later, when blood pressure was reduced, was an elevation of SVR observed, which could be associated with increased plasma levels of catecholamines, angiotensin II, vasopressin, and NPY. Thus NPY-(18-36) mimics the cardiac effects of NPY but does not elicit its vascular effects. As NPY-(18-36) discriminates between NPY receptor subtypes in vitro, we conclude that the cardiac and vascular effects of NPY are mediated by distinct receptor subtypes.
Animals↗
Effects of morphine and opioid peptides on plasma levels of atrial natriuretic peptide.
The effect of opiate ligand administration on plasma levels of atrial natriuretic peptide (ANP) was studied in awake, freely moving Sprague-Dawley rats. Prior to and following the intracerebroventricular (icv) or central venous (iv) injection of morphine (MS), leu-enkephalin (Leu-enk), dynorphin (Dyn) or beta-endorphin (B-endor), plasma samples were obtained for measurement of ANP concentrations by radioimmunoassay. MS was 10 times more potent when given icv than when given iv to increase plasma ANP levels. Icv injection of Leu-enk decreased plasma ANP concentrations. Dyn and B-endor administration (iv or icv) did not alter the plasma concentration of ANP. These effects of MS and Leu-enk on plasma concentrations of ANP appear to be mediated through actions on the central nervous system. MS, Leu-enk, B-endor, and Dyn given icv, produced elevations of plasma norepinephrine (NE) and epinephrine (Epi) concentrations. When MS was given icv, mean Epi and NE plasma levels increased 10-50 times the increases noted with B-endor, Leu-enk and Dyn. A role of catecholamines in mediating MS-stimulated ANP release is supported by the observation that ganglionic blockade with chlorisondamine significantly attenuated the increase of plasma ANP levels. MS, but not B-endor, Leu-enk and Dyn, acts within the brain to increase plasma levels of ANP. MS-induced elevations of plasma ANP levels may be dependent on an intact autonomic nervous system.
Animals↗