Infective endocarditis: prudent treatment for a lethal disease.
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Biomedical subjects
Publications and source records attributed to J D Rutherford.
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The effects of aminophylline were examined in 19 conscious dogs subjected to coronary arterial occlusion. Measurements were made of left ventricular pressure and its first derivative (dP/dt), segment length and the velocity of segment length shortening in normal an severely ischemic zones. Regional blood flow was measured in these zones using the radioactive microsphere technique. Coronary occlusion increased heart rate, mean arterial pressure and left ventricular end-diastolic pressure but did not change left ventricular systolic pressure or dP/dt significantly. It also resulted in increased end-diastolic segment length and reduced segment length shortening (114 +/- 6 percent, that is, paradoxical bulging) associated with marked reduction of blood flow to ischemic myocardium. Aminophylline, 1 mg/kg per min for 9 to 15 minutes administered after occlusion, increased heart rate 6 +/- 2 beats/min, mean arterial pressure 5 +/- 1 mm Hg, left ventricular systolic pressure 9 +/- 2 mm Hg and left ventricular dP/dt 670 +/- 50 mm Hg/s while reducing left ventricular end-diastolic pressure by 3.4 +/- 0.3 mm Hg. In severely ischemic zones aminophylline increased transmural blood flow by 21 +/- 8.0 percent (p less than 0.02), reduced end-diastolic segment length by 0.23 +2- 0.05 mm (p less than 0.01) and reduced paradoxical bulging by 0.15 +/- 0.06 mm (p less than 0.02). Thus, in the presence of coronary arterial occlusion, aminophylline increased mean arterial pressure, left ventricular dP/dt and heart rate while reducing left ventricular end-diastolic pressure. In severely ischemic myocardium aminophylline appeared to exert a salutary effect and improved both regional perfusion and function.
The effects of aminophylline, 1 mg/kg/min infused intravenously for 10 minutes, were examined on left ventricular (LV) diameter, pressure, an indexes of myocardial contractility, as well as systemic, coronary and regional hemodynamics in conscious dogs. Aminophylline increased mean arterial pressure 12 +/- 2%, LV systolic pressure 8 +/- 1%, LV dP/dt 20 +/- 2%, velocity of myocardial fiber shortening 13 +/- 2% and heart rate 5 +/- 2%, and reduced LV end-diastolic diameter 2 +/- 0.5%. Vascular resistance rose in the systemic bed 13 +/- 5%, the coronary bed 26 +/- 3%, the mesenteric bed 26 +/- 5% and the iliac bed 36 +/- 4%, but did not rise in the renal bed. Both beta-adrenergic receptor blockade with propranolol and chronic treatment with reserpine attentuated but did not abolish the positive inotropic response induced by aminophylline. Alpha-adrenergic receptor blockade with phentolamine prevented aminophylline-induced vasoconstriction in the systemic, coronary, mesenteric and iliac beds. In contrast to the vasoconstriction with i.v. aminophylline, when the drug was infused directly into the iliac artery, it elicited marked iliac vasodilation. Thus, in the intact conscious dog, i.v. aminophylline, in a dose that had little effect on heart rate, increased LV contractility and reduced preload. The increase in contractility was dependent in part on intact beta-adrenergic nervous activity and endogenous catecholamine stores. The increase in systemic, coronary, iliac and mesenteric resistances involved alpha-adrenergic mechanisms. These actions appear to involve autonomic mechanisms, because the only direct effect of aminophylline on the iliac artery was marked vasodilation.
The interaction of carotid chemoreceptor and pulmonary inflation reflex control of peripheral and coronary vasoactivity and myocardial contractility was examined in conscious dogs. Stimulation of carotid chemoreceptors resulted in an increase in rate and depth of respiration, an increase in myocardial contractility, and more intense vasoconstriction in the iliac than in the mesenteric, renal, or cerebral beds. The coronary bed responded primarily with vasodilation. The increase in rate and depth of respiration stimulated pulmonary inflation reflexes, which in turn were partially responsible for the coronary vasodilation, but also attenuated the positive inotropic response and even reversed the initial peripheral vasoconstriction to a period of significant vasodilation.
The effects of carotid chemoreceptor reflex stimulation (intracarotid injection of nicotine 0.2 microgram/kg) were examined in conscious dogs on the cerebral circulation, using the radioactive microsphere technique to measure cerebral blood flow. In intact dogs (n = 18) with ventilation controlled, carotid chemoreceptor reflex stimulation increased (P less than 0.01) mean arterial pressure by 36 +/- 5% (SE) and calculated cerebral vascular resistance by 58 +/- 13%, whereas cerebral blood flow fell by 7 +/- 6% (NS). After bilateral cervical sympathectomy (n = 9), carotid chemoreceptor reflex stimulation induced significantly different (P less than 0.01) effects on cerebral blood flow, which rose by 42 +/- 8%, and cerebral vascular resistance, which did not change. To determine whether the difference in effect was due to the sympathectomy or merely to the repetition of the stimulus, another group of dogs (sham; n = 6) that had intact sympathetic nerves were studied a second time. In "sham" dogs, the repeat response to carotid chemoreceptor stimulation also induced significantly different effects from those in dogs with sympathectomy. After general anesthesia with sodium pentobarbital, or after section of the ipsilateral carotid sinus nerve, carotid chemoreceptor stimulation with nicotine, 0.2 microgram/kg, failed to induce a detectable hemodynamic effect. Thus, in the conscious dog, stimulation of the carotid chemoreceptor reflex elicits significant sympathetically mediated vasoconstriction in cerebral vessels.
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The effects of intravenous infusion of nitroglycerin (NTG), 8 and 32 microgram/kg.min for 7 min, and of sublingual NTG, 1.2 mg, were examined on direct and continuous measurements of systemic, coronary, and regional hemodynamics, left ventricular (LV) dimensions, pressures, and myocardial contractility in conscious dogs. NTG induced sustained reductions in LV dimensions and transient increases in heart rate and dP/dt, and decreases in mean arterial pressure. Initially NTG increased cardiac output and flows to the coronary, mesenteric, renal, and iliac beds, while systemic and regional vascular resistances fell. Later, cardiac output, cardiac work, and mesenteric and iliac flows fell significantly below control, and significant vasoconstriction in the systemic as well as mesenteric, iliac, and coronary beds was observed at a time when LV end-diastolic dimensions were still significantly reduced. Peripheral vasoconstriction was not observed with systemic NTG in deafferented dogs or when NTG, 1 microgram/kg.min, was infused intra-arterially into the iliac bed. Thus, systemic NTG induces a biphasic response consisting of initial arteriolar vasodilation followed by vasoconstriction in the mesenteric, iliac, coronary and systemic beds, which is presumably due to longer lasting effects on preload and to secondary reflex responses to the drug.
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The effects of carotid chemoreceptor stimulation with intracarotid injections of either nicotine, 0.2 mug/kg, or cyanide, 2 mug/kg, were compared with the effects of bilateral carotid occlusion on left ventricular (LV) pressure, dP/dt, and diameter in conscious dogs instrumented with ultrasonic diameter gauges and miniature pressure gauges. With heart rate maintained constant, carotid chemoreceptor stimulation increased mean arterial pressure by 27+/-3%, LV and diastolic diameter by 4+/-0.9% and LV dP/dt by 21+/-2%. With ventilation controlled during succinylcholine infusion, carotid chemoreceptor stimulation increased mean arterial pressure by 43+/-2% and dP/dt by 37+/-5%, values significantly greater, P < 0.01, than were observed in dogs with spontaneous ventilation. Similarly, in dogs with spontaneous ventilation after vagotomy, carotid chemoreceptor stimulation also increased dP/dt by a greater amount, i.e., by 48+/-9%. The increases in LV end diastolic diameter were not affected significantly by either cholinergic blockade with atropine or beta adrenergic blockade with propranolol. Although cholinergic blockade did not affect the inotropic or pressor responses significantly, beta adrenergic blockade attenuated the pressor response and essentially abolished the inotropic response. Bilateral carotid occlusion increased mean arterial pressure and LV end diastolic diameter by similar amounts to those observed with chemoreceptor stimulation, but increased dP/dt significantly less, P < 0.02, i.e., by 13+/-2%. As was observed with chemoreceptor stimulation, inotropic responses were not affected significantly by cholinergic blockade, but were essentially abolished by beta adrenergic blockade. Thus, in the conscious dog with heart rate constant, carotid chemoreceptor stimulation induces a clear positive inotropic effect, which is greater in the absence of the attenuating influences of pulmonary inflation reflexes, and for an equal elevation in arterial pressure appears to exert a greater increase in myocardial contractility than does carotid baro-receptor unloading.
Serum digoxin levels were measured in 53 neonates and infants receiving 18-22 microgram/kg/day (high dose) oral maintenance digoxin, and 44 neonates, infants and children receiving less than 18 microgram/kg/day (low dose) oral maintenance digoxin. In both groups, patients under four months of age had significantly higher serum digoxin levels than older patients, in the high dose group 2.6 ng/ml compared with 1.4 ng/ml and in the low dose group 2.2 ng/ml compared with 1.0 ng/ml. Correlation between digoxin dosage and serum level was weak and unaffected by blood urea level. Only two patients in the entire series showed toxic manifestations. Sixteen patients had serum digoxin levels measured before and after corrective cardiac surgery while receiving comparable dosages of digoxin. Despite lower serum digoxin levels postoperatively pulse rates fell significantly, illustrating the influence of changing haemodynamic status on the inter-relationships of digoxin dosage, serum levels and clinical response. Recommended dosage regimens are outlined.
Myocardial infarction (MI) occurring during pregnancy is a rare but potentially lethal event for both mother and fetus, particularly when it occurs in the third trimester or peripartum period. The authors report two cases of MI occurring in the third trimester of pregnancy and review the literature. Management of the acute infarct and the medical, obstetric, and anesthetic considerations in such patients during labor and delivery are discussed. Successful use of percutaneous transluminal coronary angioplasty is described in a patient with evolving MI and ongoing pain. The preferred method of delivery in the pregnant MI patient is addressed, with emphasis on the need for individualization of care and coordination between the cardiac, obstetric, and anesthetic teams. Finally, the authors review the risks of subsequent pregnancy in this patient population.
1. Plasma levels of propranolol were measured fluorometrically in patients with angina pectoris and in patients admitted to the Coronary Care Unit with acute myocardial infarction. 2. In thirty patients with stable angina pectoris, plasma propranolol levels varied almost linearly with doses between 10 and 120 mg during 6-hourly chronic oral administration. Plasma levels greater than 100 ng/ml produced 70-80% reduction in the tachycardia induced by strenous exercise on a treadmill. 3. In nineteen patients with acute myocardial infarction given oral propranolol, 20 mg 6-hourly, peak as well as trough plasma levels of the drug increased progressively but remained below 100 ng/ml in all except two patients during the first 24 h after their admission to the Coronary Care Unit. 4. The data suggest that the use of low and fixed doses of propranolol may not produce adequate plasma levels or significant beta-adrenoceptor blockade in the early stages of acute myocardial infarction in man.
A 29-year-old woman was found to have diabetic ketoacidosis associated with classic findings of pheochromocytoma, an association previously undescribed. The patient also had a significant insulin requirement that resolved after tumor excision. Pheochromocytoma with associated hyperglycemia and glycosuria has been reported since 1912, but ketoacidosis has been thought not to occur with pheochromocytoma. The findings in this case are described, and glucose metabolism in pheochromocytoma is reviewed.