Rise In Systemic Arterial Pressure Research Articles

THE EFFECT OF SYMPATHOMIMETIC AMINES ON FEMORAL ARTERIAL BLOOD FLOW IN THE CAT

Abstract : Changes in the blood flow through the unopened femoral arteries of anaesthetized cats after the local intra-arterial and intravenous injection of adrenaline, noradrenaline, phenylephrine, metaraminol, methylamphetamine, mephentermine, methoxamine and isoprenaline have been determined by an electromagnetic method. The simultaneous recording of mean aortic pressure enabled changes in femoral vascular resistance to be calculated. Local intraarterial injection of isoprenaline reduced, while noradrenaline, phenylephrine, metaraminol, methoxamine and methylamphetamine increased, femoral vascular resistance. Adrenaline and mephentermine produced variable resistance changes. Those agents which increased femoral vascular resistance when given intra-arterially frequently reduced resistance when given intravenously. This reduction accompanied the rise in systemic arterial pressure, but in many animals adrenaline, noradrenaline, phenylephrine and metaraminol frequently induced a further reduction in resistance as the pressor effect declined. These observations are discussed in relation to the current theories of the mechanism of vasodilatation produced by sympathomimetic amines. (Author)

Mechanism and pharmacology of shock due to rattlesnake venom in sheep.

Acute hypotension produced by the intravenous injection of 20 μg/kg of rattlesnake (Crotalus atrox) venom in sheep was spontaneously restored within frac12—2 hr (crotalin collapse). Slow continuous intravenous infusion of larger doses of crotalin produced a fall in cardiac output and systemic arterial pressure, hemoconcentration, and hypoventilation. This condition could only be reversed by therapeutic intervention and was termed “crotalin shock.” Administration of antivenin in crotalin shock proved to be ineffective. Intravenous dextran infusion restored cardiac output and accentuated respiratory depression. Administration of steroids in conventional therapeutic doses resulted in a rise in systemic arterial pressure and alveolar ventilation with little change in blood flow. Simultaneous administration of dextran and corticosteroids gave better results than either material used alone. Continuous intravenous infusion of isoproterenol improved alveolar ventilation and restored spontaneous breathing in some cases of crotalin-induced respiratory arrest. dextran; ventilation; steroids; antivenin; isoproterenol; respiratory failure; hemoconcentration Submitted on September 29, 1964

Influence of Autonomic Blockade on Aconitine Induced Pulmonary Edema.

Summary1. Bilateral injection of aconitine into the preoptic areas of rats results in a marked rise in systemic arterial pressure and a rise in pulmonary venous pressure followed or accompanied by ...

COMPARATIVE STUDY OF EFFECTS OF LEVARTERENOL AND METHOXAMINE IN SHOCK ASSOCIATED WITH ACUTE MYOCARDIAL ISCHEMIA IN DOGS

Coronary arterial injections of levarterenol in dogs in shock from acute experimental myocardial ischemia (by selective coronary embolization with lycopodium spores) directly increased myocardial contraction and resulted in a lowering of both atrial and pulmonary arterial pressures while at the same time raising systemic arterial pressure. Appropriate intravenous administration of the same drug had similar effects and produced a greater rise in systemic arterial pressure. Methoxamine, when administered intravenously, elevated the lowered systemic arterial pressure, but produced a further elevation in the already high atrial and pulmonary arterial pressures. These experiments demonstrate that during acute myocardial ischemia with arterial hypotension, and even in the presence of elevated atrial and pulmonary pressures, a more favorable effect, i.e., increased systemic pressure at lower atrial and pulmonary pressures, is achieved by employing a pressor amine with a direct cardiac stimulating action which increases myocardial contraction in addition to a peripheral vasoconstricting effect. By selective coronary arterial injections, levarterenol has been shown to have a direct cardiac stimulating effect, and therefore satisfies the above requirement, whereas methoxamine does not, since it fails to stimulate myocardial contraction, or actually depresses it, when given into the same site.

The lung as the main target organ in the acute phase of transfusion reaction in sheep

Summary Pulmonary complications arising from the transfusion of small amounts of incompatible blood were studied in sheep. The main features of the nonfatal response consisted of a rise in pulmonary arterial and pulmonary arterial wedge pressures (with left atrial pressure unchanged), arterial hypoxemia, fall in lung compliance and hyperventilation. If death occurred it was due to systemic collapse and respiratory arrest. Systemic hypotension in these cases appeared to be due to acute obstructive pulmonary hypertension, whereas arterial hypoxemia resulted from the compliance fall produced by terminal airway closure. The injection or inhalation of isoproterenol resulted in a fall in pulmonary arterial pressure, and a rise in cardiac output, lung compliance and arterial oxygen saturation. In animals with transfusion-induced respiratory arrest and shock (resistant to vasopressor agents), intravenous isoproterenol produced a prompt rise in systemic arterial pressure and restored spontaneous breathing. It is suggested that in incompatible blood transfusion, or in any other situation conducive of massive red cell destruction, a humoral agent is released from the lysed red cells producing airway closure and pulmonary vaso constriction. The latter, if sufficiently severe, may cause systemic collapse. The beneficial effect of isoproterenol appears to be due to its positive inotropic action and to its dilator effect on lung vessels and airways.

Pressor effect of increased cerebrospinal fluid pressure and vertebral artery occlusion with and without anesthesia.

The intracranial pressures of conscious, lightly anesthetized and fully anesthetized dogs were altered by means of previously implanted intraventricular cannulas, while systemic arterial pressures were simultaneously measured. One vertebral artery was occluded in all these experiments by the catheter used to record aortic pressure. Increased intracranial pressure, which probably acts by reducing cerebral blood flow, caused a rise in systemic arterial pressure whose magnitude depended on the presence and depth of anesthesia. When anesthesia was not used, but when the animals were resting quietly, a significant pressor response occurred within the physiological range of CSF pressure. The response was typically of slow onset, developing over a period of one half to two minutes. It was reproducible, but tended to diminish gradually in the course of several hours if the experiment was continued, although it could be restored if CSF pressure was further increased. The pulse rate tended to increase slightly, or remain the same, providing CSF pressure was not increased too greatly or too rapidly. Respiratory effects were variable, but most commonly a slightly increased rate and depth of respiration occurred at first, with a return towards normal as the systemic arterial pressure rose. Similar responses were seen during bilateral artery occlusion, by means of previously implanted inflatable cuffs, in dogs whose carotid sinuses had been excised. These effects were also slow in onset, and were accompanied by comparable respiratory changes. In anesthetized animals with intact carotid arteries, bilateral vertebral artery occlusion produced negligible pressor effects, but was found to augment the response to increased intracranial pressure. Observations in four dogs with chronic experimental renal hypertension did not reveal notable differences, except that these animals may be less sensitive than normal to increases in intracranial pressure. The results of these experiments are compatible with the hypothesis that basal systemic arterial pressure during sleep in some degree depends on the cerebrovascular resistance, although it will be important to determine the nature of the slow adaptation seen in these experiments. If this adaptation is brought about by compensatory cerebral vasodilation, this investigation is in accord with the concept of Dickinson and Thomson that some forms of chronic high blood pressure in man might be initiated by cerebral artery occlusion or narrowing of sufficient severity and extent to prevent adequate compensatory vasodilation.

Comparative study of effects of levarterenol and methoxamine in shock associated with acute myocardial ischemia in dogs.

Coronary arterial injections of levarterenol in dogs in shock from acute experimental myocardial ischemia (by selective coronary embolization with lycopodium spores) directly increased myocardial contraction and resulted in a lowering of both atrial and pulmonary arterial pressures while at the same time raising systemic arterial pressure. Appropriate intravenous administration of the same drug had similar effects and produced a greater rise in systemic arterial pressure. Methoxamine, when administered intravenously, elevated the lowered systemic arterial pressure, but produced a further elevation in the already high atrial and pulmonary arterial pressures. These experiments demonstrate that during acute myocardial ischemia with arterial hypotension, and even in the presence of elevated atrial and pulmonary pressures, a more favorable effect, i.e., increased systemic pressure at lower atrial and pulmonary pressures, is achieved by employing a pressor amine with a direct cardiac stimulating action which increases myocardial contraction in addition to a peripheral vasoconstricting effect. By selective coronary arterial injections, levarterenol has been shown to have a direct cardiac stimulating effect, and therefore satisfies the above requirement, whereas methoxamine does not, since it fails to stimulate myocardial contraction, or actually depresses it, when given into the same site.

Hemodynamic and metabolic effects of angiotensin II during rest and exercise in normal healthy subjects

Ten normal male subjects were studied hemodynamically by cardiac catheterization during infusions of angiotensin II. Arterial levels of free fatty acid, lactate, pyruvate, and glucose were measured. Arterial pressure and the peripheral resistance index rose 31 and 68.8 per cent, respectively (p = < .001 for both). Cardiac index fell 23.5 per cent (p = < .02), and arteriovenous oxygen difference widened 25.3 per cent (p = < .01) in compensatory fashion, since oxygen consumption did not change. Stroke index fell 20.7 per cent (p = < .05), and augmented “central blood volume” (3 subjects) fell slightly. The temperature of the skin fell as pressure rose and returned to normal concurrent with a fall in pressure after angiotensin was discontinued. No change occurred in coronary blood flow (3 subjects) or metabolic substrate levels. Pressures in the right atrium and pulmonary artery rose gradually several minutes after the rise in systemic arterial pressure. During supine leg exercise with angiotensin II (3 subjects) the peripheral resistance index did not rise as high as it had during rest, which indicates that normal vasodilation of skeletal muscle still occurred in response to exercise. Reinfusion of angiotensin II was effective in one individual in the restoration of normal blood pressure after postinfusion hypotension.

Reflexogenic areas of the cardiovascular system.

After the discovery ofthe pulmonary circulation by Ibn-an-Nafis in the thirteenth century and by Servetus in the sixteenth century and the discovery of the systemic circulation of the blood by Harvey in 1628, arterial pressure was first measured by Stephen Hales in 1733 and then by Poiseuille in 1828 and Ludwig in 1847, wno recorded arterial blood pressure by means ofa glass tube or a mercury manometer connected with an artery. As a result of numerous observations, the physiologists concluded that the arterial pressure was subject to regulation and tried to clarify the mechanisms. In 1836 Astley Cooper observed that compression of both common carotid arteries, which induced a fall of arterial pressure in the head and brain, provoked acceleration of the heart rate and a rise in the systemic arterial pressure (1). This observation was confirmed by Magendie in 1838 (2). Experiments done between 1877 and 1926 by several workers (3-10) showed that a rise of blood pressure in the carotid-cephalic circulation induces bradycardia and a fall of the systemic arterial pressure, while a drop in the carotid-cephalic pressure provokes acceleration ofthe heart rate and a rise ofsystemic arterial pressure. All these experimental observations were considered to be a demonstration ofa direct sensitivity of the cardiovascular centers to blood pressure variations. The direct central regulation and homeostasis of arterial pressure by means of the action of blood pressure variations on the cardiovascular centers was thus generally accepted. But as early as 1900 Pagano (11) and Siciliano (12), of the laboratory of Spallitta in Palermo, published an interesting series of experiments. Siciliano showed that while clamping of both common carotid arteries induced tachycardia and a rise in the systemic arterial pressure, clamping of

Relative importance of venous and arterial resistances in controlling venous return and cardiac output.

In dogs with cardiovascular reflexes completely blocked by total spinal anesthesia, the total peripheral resistance was increased five- or more fold in two ways: first, by injecting small plastic microspheres into the arteries, thereby increasing the arterial resistance, and, second, by inflating pneumatic cuffs around the major veins, thereby increasing venous resistance. A small increase in venous resistance decreased cardiac output eight times as much as an increase in arterial resistance of similar magnitude. This difference was caused principally by a) a marked rise in systemic arterial pressure when arterial resistance was increased; this maintained the cardiac output at almost normal levels and b) a fall in systemic arterial pressure when venous resistance was increased; this promoted even more fall in cardiac output than increased total peripheral resistance alone would have caused.

The dynamics of mitral insufficiency

By using specially constructed models, the hydrodynamic factors affecting the degree of mitral regurgitation were analyzed. Forward flow into the aorta is enhanced by increases in atrial pressure, ventricular filling, viscosity of the blood, celerity of ventricular contraction, and by lateral pressure effects on the regurgitant orifice. The tendency to mitral regurgitation is heightened by a rise in systemic arterial pressure, an increase in the size of the regurgitant orifice, or a decrease in the celerity of ventricular contraction. The proximity of the aortic orifice to the mitral opening operates to reduce reflux because of competition of the two valve areas for streamlines of flow. The role of pipe competition is examined and discussed. The relative contributions of each of the foregoing factors are reviewed in terms of findings on an integrated model of the circulation. The significance of these findings in clinical mitral insufficiency is discussed.

The effect of the Valsalva maneuver on the circulation. III. The influence of heart disease on the expected poststraining overshoot.

The normal response following sustained straining, as in a Valsalva maneuver, is a rise in systemic arterial pressure and a reflex slowing of the heart rate. This response was found to be abolished in some patients with mitral stenosis, with organic heart disease, with pulmonary vascular disease (including kyphoscoliosis), or with congenital heart disease. It was abolished in all three instances of pericardial disease studied. The relationship of the presence or absence of a poststraining bradycardia to cardiovascular dynamics at rest and on exercise as determined by right heart catheterization is presented, and the suggestion is made that the Valsalva maneuver, when performed under electrocardiographic control, may be a simple, dynamic stress test of the circulation. This suggestion is waiting for further exploration.