Propranolol Diminishes Extremity Blood Flow in Burned Patients
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Abstract:
Beta adrenergic blockade diminishes the catecholamine-mediated elevations in heart rate and myocardial contractility that characterize postburn hypermetabolism. To examine how these alterations in cardiac performance affect peripheral pcrfusion, indirect calorimetry and leg blood flow were measured before and then after a 2-hour intravenous propranolol infusion. Five severely burned patients (55% + 7% total burn surface area), given propranolol at 8 μg/kg/minute, had a significant reduction in cardiac index and heart rate with an increased leg vascular resistance resulting in a decrease in extremity perfusion. Four healthy volunteers were given propranolol at 5 μg/kg/minute, resulting in a comparable decrease in heart rate, yet there was no change in leg vascular resistance or extremity perfusion. In both patient groups, propranolol decreased the plasma lactate concentration. This suggests that in hypermetabolic patients, beta adrenergic blockade reduces peripheral perfusion and that peripheral perfusion is not a principal determinate of plasma lactate levels. Rather adrenergic blockade appears to decrease lactate concentration as a consequence of the inhibition of li-polysis.Keywords:
Hypermetabolism
The effects of nitroglycerin on systemic vascular resistance and cardiac output are highly debated. This study demonstrates that these effects depend on the initial haemodynamic condition, and explains the conflicting results previously reported. 31 patients presenting initially with a fairly wide spectrum of various haemodynamic parameters underwent cardiac catheterisation with measures of parameters before and after nitroglycerin infusion. Multifactorial statistical analysis by correspondence analysis identifies 3 types of haemodynamic responses and demonstrates the association of each response with a particular haemodynamic profile. It is demonstrated that systemic vascular resistance is decreased only when it is initially elevated and cardiac output is increased only when initial pulmonary wedge pressure and systemic vascular resistance are elevated and cardiac output is low. The effects of nitroglycerin on cardiac output, systemic vascular resistance, heart rate and arterial pressure differ significantly according to the presence or not of cardiac insufficiency and depend mainly on the initial value of three parameters: systemic vascular resistance, pulmonary wedge pressure and cardiac output.
Pulmonary wedge pressure
Cardiac catheterization
Haemodynamic response
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Invasive and noninvasive investigations suggest that the hemodynamics of pregnant hypertensive patients are heterogeneous. Nineteen pregnant patients were evaluated before changes in antihypertensive therapy. Cardiac output was measured by Doppler technique. Blood pressure was measured by automated cuff. Systemic vascular resistance was calculated. Two distinct groups were identified on the basis of differences in cardiac output (p < 0.0001) and systemic vascular resistance (p < 0.0001). Those with high resistances were treated with hydralazine. A modest antihypertensive effect was achieved (-6.9 mmHg, p = 0.01), but systemic vascular resistance was dramatically reduced, (-534 dyne·sec·cm-5, p < 0.0001) and was associated with a compensatory increase in cardiac output (2.0 liters/min, p < 0.0001). Those with a high cardiac output were treated with atenolol. An antihypertensive effect was achieved, (-17.0 mmHg, p = 0.008), which was associated with a reduction in cardiac output (-2.8 liters/min, p < 0.0001).
Hydralazine
Atenolol
Impedance cardiography
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Ten mongrel dogs were placed on 5 and 10 cm. H20 of CPPV. Cardiac output, pulmonary vascular resistance and pleural pressures were measured. At 5 cm. H20/CPPV there was no significant change in cardiac output or pulmonary vascular resistance. At 10 cm. H20 CPPV cardiac output significantly decreased and pulmonary vascular resistance increased. The physiologic basis for these changes is discussed and related to the clinical situation.
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The effect of the beta-adrenoblocker propranolol on adrenaline-stimulated lipolysis was studied in the adipose tissue of spontaneously hypertensive rats (SHR) and control rats. The lipolytic activity was estimated from the increase in glycerol concentration in the incubation medium in vitro. The adipose tissue of SHR responded to adrenaline similarly to that of control rats, but the concentration of adrenaline inducing the half-maximum response (KA) was 2 times less for SHR than KA for normotensive controls. Under propranolol effect this parameter was increased more significantly in SHR than in controls. These data indicate higher sensitivity of SHR adipose tissue to propranolol that may well be relative to alteration of the properties of beta-adrenergic receptors of adipose tissue in this form of hypertension.
Phentolamine
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The eicosanoid vasodilator prostacyclin (PGI2) reduces resistance to pulmonary blood flow and attenuates pulmonary hypertension in mammals. However, sparse information is available regarding the responsiveness of the avian pulmonary vasculature to PGI2. Accordingly, in 3 experiments we evaluated the pulmonary vascular responses to PGI2 in male broilers. In experiment 1, infusing PGI2 (10 microg/min) into clinically healthy broilers did not reduce their pulmonary vascular resistance (PVR) but did reduce their pulmonary arterial pressure (PAP) by lowering their cardiac output. Within 4 min after stopping the PGI2 infusion, the cardiac output and PAP returned to preinfusion levels. In experiment 2, the responses to PGI2 were evaluated after arachidonic acid (AA) had been infused to preconstrict the pulmonary vasculature. The AA infusion (400 microg/min) consistently triggered dramatic, sustained pulmonary vasoconstriction (increased PVR) and pulmonary hypertension (increased PAP). Concurrent PGI2 infusions did not reduce PVR but did reduce PAP by lowering cardiac output. Within 4 min after stopping the PGI2 infusion, PAP and cardiac output returned to their previous (hypertensive) levels attributable to the ongoing AA infusion. In experiment 3, PGI2 was infused (10 microg/min) into clinically healthy (PAP < or = 24 mmHg) or subclinically hypertensive (PAP > or = 27 mmHg) broilers. Throughout this experiment broilers in the hypertensive group had higher PAP values than broilers in the healthy group. The PGI2 infusion reduced PAP in both groups but did not reduce PVR. Instead, the pulmonary hypotensive response to PGI2 infusion was associated with a reduction in cardiac output in both groups. In all 3 experiments PGI2 reduced PAP by reducing cardiac output rather than by reducing PVR. There was no evidence that PGI2 acts as an effective pulmonary vasodilator in broilers regardless of whether their pulmonary vasculature was apparently normal (clinically healthy), had been pharmacologically preconstricted (AA infusion), or initially exhibited the vasoconstriction that is typical of the pathogenesis of pulmonary hypertension syndrome in broilers (PAP > or = 27 mmHg). The consistent failure of PGI2 to elicit pulmonary vasodilation in this study suggests fundamental differences in AA metabolism or the etiology of pulmonary hypertension may exist when broilers are compared with mammals.
Hypoxic pulmonary vasoconstriction
Iloprost
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A prospective study of cor pulmonale in 74 patients relates pulmonary haemodynamics to survival. Mean arterial oxygen tension (PaO2) was 7.2 +/- 0.14 kPa and mean arterial carbon dioxide tension (PaCO2) 6.6 +/- 0.12 kPa at entry. Pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), and cardiac output (CO) sitting and supine and where possible on exercise, were measured every one or two years by a floating catheter technique. Survivors showed very little change in pulmonary artery pressure, pulmonary vascular resistance or cardiac output. Those who did not survive, showed a steady increase of PAP and PVR, whether or not they had received continuous oxygen therapy at home. Cardiac output remained normal or slightly elevated despite increasing pulmonary artery pressure. The relationship between VO2 (minute oxygen consumption) and cardiac output remained within the normal or greater than normal range, even on exercise. Although a deteriorating clinical situation may be paralleled by changes in pulmonary haemodynamics, it is questioned whether such changes are causally implicated in mortality.
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Summary. Cardiac output, heart‐rate, stroke volume, pressures in the brachial artery, right ventricle and pulmonary artery, forearm blood flow and in addition arterial concentrations of lactate, glucose and free fatty acids were measured in eight healthy male volunteers during i.v. infusion of prostacyclin in doses corresponding to 2 ng, 6 ng and 12 ng min ‐1 kg ‐1 b.w. The highest dose almost doubled cardiac output and this was achieved by similar increases in stroke volume and heart‐rate. Arterial diastolic and mean pressures decreased slightly while systolic pressure was unaffected. The calculated total systemic vascular resistance decreased to half the initial level. However, forearm blood flow increased insignificantly and forearm vascular resistance was not significantly altered. Pulmonary artery pressure rose only minimally, which in the presence of a great increase in cardiac output indicates pulmonary vasodilatation. Arterial lactate and glucose concentrations were not significantly altered while free fatty acid concentration increased slowly during the infusion period to a similar degree as previously shown in fasting individuals undergoing catheterisation. It is concluded that prostacyclin decreases both pulmonary and total systemic vascular resistance but unlike the most potent vasodilator of the ‘classical’ prostaglandins, PGE 17 it has dissimilar vasoactive potency in different systemic vascular beds as evidenced by the insignificant decrease in forearm, simultaneous with the pronounced decrease in total systemic vascular resistance.
Brachial artery
Cardiac index
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Splanchnic Circulation
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Experiments were performed to determine whether different methods of increasing cardiac output would have similar effects on lung lymph flow, and to assess the contribution of the microvasculature (fluid-exchanging vessels) to the total calculated pulmonary vascular resistance. Yearling unanesthetized sheep with chronic vascular catheters and lung lymph fistulas underwent intravenous infusions of isoproterenol at 0.2 micrograms X kg-1. min-1 (n = 8) or were exercised on a treadmill (n = 16). Both isoproterenol and exercise increased cardiac output, lowered calculated total pulmonary and systemic vascular resistances, and had no effect on the calculated pulmonary microvascular pressure. Isoproterenol infusions did not affect lung lymph flow, whereas exercise increased lung lymph flow in proportion to the increase in cardiac output. We conclude that 1) the sheep has a different pulmonary hemodynamic response to exercise than dogs and man, 2) the microvasculature is recruited during exercise-induced but not isoproterenol-induced increases in cardiac output, and 3) the microvasculature represents only a small proportion of the total calculated pulmonary vascular resistance.
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