Effects of intravenously administered propranolol on wall motion abnormalities

Although propranolol is frequently utilized as therapy for angina pectoris in patients with previous myocardial infarction, its effects on wall motion abnormalities in such patients have not been adequately defined. Accordingly, using external wall motion video tracking, we studied 18 patients with previous myocardial infarction and wall motion disorders and 5 normal subjects before and after administration of propranolol, 5 mg intravenously. Systolic time intervals, heart rate and left heart size (measured by the distance between the mid-line and left heart border in an X-ray film triggered at end-diastole after a standard inspiration) were also measured before and after administration of propranolol. In each instance propranolol produced a reduction in the amplitude and velocity of wall motion in areas of normal movement, hypokinesis and paradox, resulting in decreased outward bulging. In the normal subjects, the amplitude and velocity of wall motion also decreased. In the patients with previous myocardial infarction, propranolol increased the ratio of the preejection period to the left ventricular ejection time from a mean of 0.377 ± 0.03 (standard error of the mean) to 0.409 ± 0.03 (P <0.001); decreased heart rate by an average of 7.5 beats/min (P <0.001); and increased the distance from the mid-line to the left heart border from 94.3 ± 2.6 to 97.3 ± 2.6 mm (P <0.001). Similar changes occurred in the 5 normal subjects. We conclude that doses of propranolol sufficient to increase the ratio of the preejection period to left ventricular ejection time, decrease heart rate and increase heart size do not exaggerate preexisting paradoxical wall motion or accentuate latent areas of paradox in patients with previous myocardial infarction.     

Adaptation of the gastric mucosa to repeated administration of aspirin in the rat

The effects of single and repeated doses of aspirin on the gastric mucosa of the rat were compared to determine whether the mucosal response alters after repeated aspirin. Aspirin (120 mg/kg) was administered by esophageal intubation either as a single dose or daily for 3, 14, 28 and 56 days. Mucosal damage was present in all treated rats but, on histologic quantitation, there was a highly significant reduction in the numbers of acute erosions in the groups receiving repeated daily aspirin. This apparent adaptation did not persist when aspirin administration was interrupted for 3 days. Repeated aspirin administration was not associated with any reduction in aspirin absorption or excretion, nor was there any significant change in hydrochloric acid or pepsin secretion. The investigation has shown an adaptation to repeated aspirin in the rat which appears to result from an alteration in the gastric mucosa. The precise mechanism of the adaptation remains uncertain.Supported by the National Health and Medical Research Council and the Alfred Hospital.Presented, in part, to the Gastroenterological Society of Australia, May 1971.     

Sequelae of Haemophilus influenzae meningitis

Fourteen children who had had Haemophilus influenzae meningitis more than two years earlier have been compared with their siblings. WISC, Frostig and Bender psychological tests and neurological examination were performed so that subject/sibling differences could be analysed. On neurological examination, subjects overall performed worse than the controls, although no "hard" neurological signs were found. Prolonged fever during the meningitis was associated with poorer results in psychological tests. In the subjects, there was a significant increase in left lateral dominance which may have been due to brain damage by the meningitis. However, most subjects did not differ significantly from their siblings in the tests, suggesting that prompt and adequate treatment of bacterial meningitis can prevent sequelae.     

Effect of carbenoxolone sodium on aspirin-induced injury of the rat gastric mucosa

Investigations were performed in the rat to examine the effect of carbenoxolone sodium on aspirin-induced gastric mucosal injury. Mucosal damage was quantitated histologically in the body of the stomach (corpus) after a single dose of aspirin and after 2 weeks of daily aspirin. Over dosage ranges of 2–30 mg/kg/day of carbenoxolone and 10–120 mg/kg of aspirin, carbenoxolone treatment conferred no protection, despite evidence of a significant carbenoxolone effect on gastric mucus. This contrasts with the known protective action of carbenoxolone against injury by restraint stress and by corticosteroids. Much current evidence suggests that the mechanisms of erosion production by aspirin differ from those by restraint stress and corticosteroids, and it is likely that the present findings reflect such differences in pathogenesis.     

Recent advances in the treatment of ectopic tachycardias by electrical pacing

Cardiac pacing may be useful both prophytactically and therapeutically in the management of ectopic tachycardias. Ectopic tachycardias may be prevented by atrial or ventricular pacing for a sustained period at a rate faster than the spontaneous rate but slower than the rate of the tachycardia being suppressed.

Supraventricular tachycardias, except atrial fibrillation, may be terminated by atrial or ventricular pacing for a brief period in one of three ways: (1) delivery of a single stimulus or two serial stimuli in quick succession; (2) repetitive stimulation at a rate slower than the tachycardia; or (3) repetitive stimulation (atrial only) at a rate faster than the tachycardia.

Atrial pacing may slow the ventricular rate of supraventricular tachycardia resistant to all forms of therapy by (1) actually increasing the atrial rate which produces functional atrioventricular block and reduces the number of transmitted impulses to the ventricle, or (2) inducing stable atrial fibrillation with a slower average rate more easily controllable by digitalis.

Aside from its relative simplicity, pacing offers certain advantages over standard d-c cardioversion for the termination of tachyarrhythmias, particularly when the latter is contraindicated as in digitalis toxicity.     

Factors influencing the healing rate of chronic gastric ulcer

A retrospective survey was made of 99 patients with benign gastric ulcer admitted to hospital for medical treatment over a 3 1/2-year period. Healing rate was measured by use of profile surface area, obtained by air contrast radiography of the stomach every 21 days. Ulcer size was found to be greater in those who smoked cigarettes or gave a history of ingestion of salicylate-containing preparations. Healing rate was accelerated by admission to hospital but was uninfluenced by age or sex of the patient, a positive family history of gastric ulcer, duration of ulcer symptoms prior to admission, number of recurrences, therapy with frequent doses of potent antacids, or cessation of smoking. At the extremes of ulcer size, large ulcers healed more slowly than small ulcers.This work was partially supported by the Australian Tobacco Research Foundation.     

Patterns of cardiac output response to acute reduction of ventricular preload and afterload pressures

Venous return and therefore cardiac preload and afterload pressures were reduced by means of lower body decompression in two groups of patients. Group 1 consisted primarily of patients with valvular heart disease and Group 2 of patients with cardiomyopathy.

Patients in Group 1 with mitral or aortic stenosis had invariable decreases of cardiac output values irrespective of the height of the initial filling pressures. Patients in Group 2 (with cardiomyopathy) had reduced output values except when the left heart filling pressures were about 40 mm Hg. In patients in Group 1 with nonstenotic valvular disease, cardiac output decreased when initial right and left heart filling pressures were below 8 and 25 mm Hg, respectively, but increased by a small amount when the filling pressures exceeded these values.

From these results we have concluded that the cardiac output response to physical reduction of preload and afterload depends on both the type of heart disease and the height of the initial ventricular filling pressures. The small increases in cardiac output that occurred in patients with severely decompensated nonstenotic valvular disease suggested that a shallow descending limb to the cardiac function curve can occur in some types of heart disease. However, this probably resulted from changes in regurgitant fractions at the atrioventricular valves and not from an actual descending limb to a myocardial muscle function curve.