Elevation Of Aortic Pressure Research Articles

Renal vascular resistance and aortic pressure as determinants of sodium reabsorption.

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during aortic constriction, persistent increases in UNaV and urine flow rate were abolished during infusion of norepinephrine and after B.C.O. and V, and markedly reduced during infusion of angiotensin. These effects could not be attributed to changes in intrarenal hemodynamics. Thus increased sodium and water excretion following infusion of norepinephrine and angiotensin, and B.C.O. and V, can be largely attributed to an interplay of increased renal perfusion pressure and reduced preset renal vascular resistance.

Effects of Glucagon on a Multistressed Circulation

The effectiveness of intravenous glucagon in improving myocardial function during conditions when exceptional loads have been added has been evaluated in three groups of eight instrumented, anesthetized, open-chest dogs. Glucagon (5 mg/kg/min) was infused continuously for 20 minutes after a series of hemodynamic stresses had been applied. These stresses consisted of cardiovascular depression secondary to propranolol (2 mg/kg) and volume loading (20 ml/kg); experimental myocardial infarction produced by coronary artery ligation; and ligation of the thoracic aorta. Depression due to beta blockade alone resulted in significant increases in mean left atrial pressure and systemic vascular resistance and decreases in left ventricular dp/dt, right ventricular contractile force, heart rate, and cardiac output. The induction of myocardial infarction caused significant increase in mean atrial pressures and marked decreases in left ventricular systolic pressure, cardiac output, and stroke volume, while ligation of the thoracic aorta after myocardial infarction produced marked elevation of systemic vascular resistance, mean aortic pressure, left ventricular systolic pressure and decreases in heart rate as well. Significant hemodynamic improvement after the administration of glucagon was observed during each stress or combination of stresses, and consisted of marked increases in left ventricular dp/dt, right ventricular contractile force, heart rate, and cardiac output and decreases in mean right and left atrial pressures and in systemic vascular resistance. Elevation of aortic pressure and left ventricular systolic pressure, in addition, was seen in maximally stressed animals. Glucagon also attenuated rises in atrial pressure produced by volume loading of stressed animals. Improvement in hemodynamic variables was probably not due to the positive chronotropic actions of the drug, but due to its positive inotropic effects, since pacing to rates equivalent to those attained by the administration of glucagon did not improve significantly the hemodynamic status of the animals.

Cardiac mechanisms for regulating stroke volume during elevation of aortic blood pressure in dogs.

Cardiac output and stroke volume increased during elevation of aortic pressure at high adrenergic activity (constant isoproterenol infusion or stimulation of left stellate ganglion), but fell in control experiments and after propranolol administration, both in open-chest and conscious dogs. To examine the mechanisms involved, myocardial distances and ventricular volumes were measured with ultrasonic and thermodilution techniques, respectively. Enddiastolic volume always increased during elevation of aortic blood pressure. Myocardial shortening increased further at high adrenergic activity and fell in control experiments. The increase in myocardial shortening was not a consequence of increased delivery to the myocardium of circulating catecholamines, as reduction of coronary blood flow to control before elevation of aortic pressure did not reduce stroke volume. It is concluded that the stroke volume response to elevation of aortic blood pressure is the resultant of two effects: 1) a stroke-volume-increasin...

Hemodynamics of the carotid sinus reflex elicited by bilateral carotid occlusion in the conscious dog. Effect of - or -adrenergic blockade on the reflex response.

Flow velocity in the ascending aorta and aortic blood pressure were recorded continuously in healthy conscious dogs. Using implanted pneumatic cuffs the effect of bilateral carotid occlusion on heart rate, stroke volume, cardiac output, peak velocity, maximum acceleration, blood pressure, and total peripheral resistance (T.P.R.) was studied in the resting animal. Following carotid occlusion heart rate rose within 3–4 sec by 13 beats/min; during the steady state it exceeded the control by 8 beats/min. Cardiac output closely followed heart rate, since stroke volume decreased slightly (3–4%), mainly because of the elevated aortic pressure. During the first 3–4 sec cardiac output increased by 10–15% reaching a steady state level 8% above control. The initial fast increase of cardiac output caused mean aortic pressure to rise rapidly, while T.P.R. transiently decreased. Subsequently T.P.R. rose, causing a secondary slow increase of pressure. During the steady state blood pressure was elevated by 27 mm Hg (26%), T.P.R. by 12.1 mm Hg×l−1×min (20%). Maximum acceleration did not change with heart rate and was hardly affected (−1.5%) by the pressure rise. Peak velocity was little influenced by heart rate; it decreased by 7% mainly because of the elevated aortic pressure. β-blockade (0.5 mg/kg propranolol) affected T.P.R. only during control (+18%), but did not modify the time course of the reflex and its steady state changes. α-blockade (5.0 mg/kg phenoxybenzamine) decreased aortic mean pressure (5 mm Hg) and T.P.R. (7%) during control. Following carotid occlusion T.P.R. rose by the same amount, but much more slowly. Starting from the lower control the same pressure level was now obtained by a higher reflex increase of heart rate and cardiac output. It is concluded that the initial pressor response is initiated by an increase of cardiac output mediated by vagal inhibition. The secondary rise of blood pressure is predominantly caused by an increase of T.P.R. due to autoregulation in some vascular beds. The higher stroke work during the reflex is not accomplished by an increased contractility due to sympathetic activation.

Effect of Overload and Hyperbaric Oxygen on Protein Synthesis in Heart Muscle.

s1 May 1967Effect of Overload and Hyperbaric Oxygen on Protein Synthesis in Heart Muscle.Sidney S. Schreiber, M.D., F.A.C.P., Marcus A. Rothschild, M.D., F.A.C.P., Murray Oratz, Ph.D.Sidney S. Schreiber, M.D., F.A.C.P.Search for more papers by this author, Marcus A. Rothschild, M.D., F.A.C.P.Search for more papers by this author, Murray Oratz, Ph.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-66-5-1038_2 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptProlonged increase in left ventricle contractile action resulting from aortic hypertension or increased cardiac output is associated with hypertrophy and increased protein synthesis, but the mechanism stimulating synthesis is unclear. Using14C-labeled lysine, protein synthesis was measured in the perfused guinea pig heart. Increased fluid load or elevation of aortic pressure without increased load resulted in increased ventricular contractile action and increased14C-lysine incorporation into ventricle protein after 3 hr. Protein synthesis was also augmented in the absence of ventricular overload with increase in direct coronary perfusion. Because of the possible effect of oxygen availability due to increased coronary flow... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: New York, New York PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 May 1967Volume 66, Issue 5Page: 1038-1038KeywordsGuinea pigsHeartHyperbaric oxygenHypertensionLeft ventricleLysineMyocardiumOxygenProtein synthesisProteins ePublished: 1 December 2008 Issue Published: 1 May 1967 PDF downloadLoading ...

Hemodynamic Effects of Hyperbaric Oxygenation in Experimental Acute Myocardial Infarction

The hemodynamic effects of hyperbaric oxygenation were investigated in anesthetized dogs with acute myocardial embolism and infarction produced by injecting plastic spheres 325 micra in diameter. In 50 "control" animals with acute myocardial infarction induced while breathing either air at one atmosphere, 100% oxygen at one atmosphere or 7% oxygen at three atmospheres, 24-hour mortality was 85 to 90%. In 23 animals that received the same dose of microspheres and breathed 95 to 100% oxygen at three atmospheres for two hours following embolization, there was significantly less 24-hour mortality (30%), less ventricular fibrillation, and less advanced atrioventricular block. Hyperbaric oxygenation afforded protection against immediate mortality from ventricular fibrillation and also against later death, in shock, occurring within 24 hours of coronary embolization but after the immediate postembolization period had passed. In the animals exposed to hyperbaric oxygenation, declines of cardiac output and of central aortic pressure occurring 60 and 90 minutes after coronary embolization were significantly less than in the other animals. In normal animals, hyperbaric oxygenation reduced cardiac output moderately, increased systemic vascular resistance, and elevated aortic pressure slightly. The anatomic extent of the infarction did not differ detectably between the "control" animals and those treated with hyperbaric oxygenation. It is concluded that hyperbaric oxygenation provides protection against mortality in the early period after coronary embolization by preventing ventricular fibrillation. In addition, prevention of major declines in aortic pressure and cardiac output during the later postembolization period in the group with hyperbaric oxygenation was associated with diminished rates of late mortality.

Paradoxic Splitting of the Second Heart Sound in Systemic Hypertension: The Role of Myocardial Competence

Three cases of paradoxic splitting of the second heart sound in elderly hypertensive patients are presented. It would appear that in arterial hypertension this phenomenon is not so unusual as has been previously supposed. Its mechanism of development is obscure, but independent factors or the long-term myocardial consequences of the hypertensive state seem to be more frequently operative than an elevated aortic pressure per se in the production of this abnormality.

Vasodilation in skeletal muscle.

Blood flow was studied in dog hind-limb muscle isolated except for femoral and sciatic nerves. At constant perfusion pressure, elevation of aortic pressure produced by blood transfusion or intravenous epinephrine administration elicited a three- to fourfold increase in blood flow in perfused muscle. The blood flow increase evoked by epinephrine could be prevented by maintaining aortic pressure at control levels by means of a pressure compensator. Carotid artery occlusion had little effect on muscle blood flow whereas release of carotid occlusion produced marked increases. Cold or procaine block of the femoral or sciatic nerves resulted in little change in blood flow, whereas nerve section distal to the block produced large transient increases in flow. It is concluded that muscle blood flow increase after aortic pressure elevation is the result of active vasodilation and that increase in muscle blood flow after nerve section is due to stimulation of vasodilator fibers or direct stimulation of vascular smooth muscle by pressure changes produced by the twitch contraction associated with nerve section.

Local circulation in heart muscle studied with Na24 clearance method.

Neutral, isotonic Na24Cl solution was injected into the left ventricular wall of open-chest dogs. The disappearance of local radioactivity was recorded. Individual injections that exceeded 5 mm3 retarded Na clearance. The rate of Na clearance from individual deposits did not measure coronary flow in absolute terms; however, when one hemodynamic parameter was suddenly changed 50–200 sec after the injection of a radioactive deposit, the changed Na clearance slope reflected directional variations of coronary flow. In ischemic regions of self-perfused hearts, elevation of aortic pressure that was paralleled by increased left ventricular and central coronary pressures did not always result in more rapid Na clearance. Submitted on November 24, 1961

Effect of Nucleosides on Acute Left Ventricular Failure in the Isolated Dog Heart

The effect of nucleosides on acute left ventricular failure was studied in 15 isolated dog hearts. The unilateral failure was produced by exposure of the isolated left ventricle to elevated aortic pressure. Parameters of left ventricular function used to evaluate the control, failure and nucleoside periods included ventricular stroke work and output, contractility and distensibility. Adenosine and cytidine were found to be negative inotropic substances. Guanosine, inosine, thymidine and uridine were found to he positive inotropic substances, restoring the control level of ventricular function.