The dominance of scientific English. One language or two?
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Biomedical subjects
Publications and source records attributed to R M Robertson.
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The organization and functional properties of interneurons in the flight system of the locust, Locusta migratoria, were investigated by using intracellular recording and staining techniques. Interneurons were found to be distributed within the three thoracic and the first three abdominal ganglia, and they could be subdivided into three organizational categories: (1) members of one of two serially homologous groups controlling either the forewing or the hindwing, (2) unique individuals with no known homologues in other ganglia, and (3) members of a set of serial homologous in the metathoracic and first three abdominal ganglia. Interneurons in the last two categories influenced both forewing and hindwing motoneurons in a similar manner. Thus interneuronal organization is not characterized by two distinct homologous groups of interneurons for the separate control of forewing and hindwing motor activity. Flight interneurons may also form two separate functional categories: (1) those making short latency connections to motoneurons (premotor interneurons), and (2) those which reset the flight rhythm when depolarized by brief current pulses (pattern generator interneurons). None of the ten premotor interneurons we identified influenced the flight rhythm when depolarized and none of the three groups of pattern generator interneurons were found to form short latency connections with motoneurons. This separation of function may allow phase-shifts in motor output for flight control without changes in wingbeat frequency. Pattern generator interneurons influence motor output to both forewings and hindwings. Thus we conclude that the flight rhythm is generated in a distributed neuronal oscillator driving both the pairs of wings. The organization of flight interneurons is considerably more complex than predicted from existing models of the flight system, or anticipated from the relative simplicity of the motor output. Our finding of homologous sets of interneurons in the abdominal ganglia supports the notion that insect flight evoked from a behavior using appendages distributed along the thorax and the abdomen. Thus the organization of flight interneurons may reflect an interneuronal system which controlled the behavior from which flight evolved.
Cardiac applications for digital subtraction angiography appear promising, but few correlative studies with contrast ventriculography have been done. Left ventricular volume, ejection fraction, and regional wall motion by digital subtraction angiography were evaluated after intravenous injection of 40 ml of iodinated contrast medium and after left ventricular injection of 5 to 10 ml of contrast medium. A film-based system of the authors' own design was used. Results were compared with those after direct left ventricular injection of 40 ml of contrast medium. The ventriculograms after intravenous injection were of diagnostic quality in 9 of 12 studies, and there were close correlations between intravenous and direct-injection studies for left ventricular ejection fraction (r = 0.89, n = 9, and p = 0.001) and for left ventricular volume (r = 0.91, n = 18, and p less than 0.001). Regional wall motion scores showed close correspondence in 83% of sectors. After small-volume left ventricular injections, the ventricular image was enhanced considerably by digital subtraction. Correlations between small- and large-volume ventriculograms were close for left ventricular ejection fraction (r = 0.91, n = 8, and p = 0.002) and for left ventricular volume (r = 0.96, n = 16, and p less than 0.001). There was close correspondence of wall motion scores in 87% of sectors. Thus, digital subtraction angiography improves the visibility of the left ventricle after either intravenous or small-volume direct left ventricular injection. Digital images produce excellent estimates of left ventricular volume and should have considerable usefulness for the study of cardiac performance and anatomy.
Twenty-four quantitative cineangiographic studies were performed in 19 patients with congenitally corrected transposition of the great arteries to assess right and left ventricular size and function. Ages ranged from 7 days to 44 years and associated lesions included ventricular septal defect (13 of 19), pulmonary stenosis (9 of 19), and systemic (tricuspid) valvular insufficiency (7 of 19). Systemic (anatomically right) ventricular end-diastolic volume was within normal limits in most patients and averaged 119% of predicted normal. Pulmonary (anatomically left) ventricular end-diastolic volume also was normal in most patients, averaged 112% of predicted, and was not different from systemic (right) ventricular end-diastolic volume. Systemic ventricular ejection fraction (RVEF) averaged 0.61 +/- 0.02 and was not different from pulmonary ventricular ejection fraction (LVEF) (0.65 +/- 0.02), but important differences were apparent when age was considered. With exclusion of 2 patients with hypoplastic systemic ventricles and 2 studies performed less than 6 months after open heart surgery, all 12 patients aged less than 10 years had a normal RVEF, whereas 2 of 5 patients aged greater than 17 years had a definitely low RVEF and 1 of 5 had a value at the lower limit of normal. In children, systemic and pulmonary ventricular pump function is usually normal in congenitally corrected transposition of the great arteries and any deviation from normal should suggest ventricular hypoplasia or an increase in afterload. After childhood, systemic ventricular dysfunction is more common and may reflect the inability of the anatomic right ventricle to function as the systemic pumping chamber over a normal lifetime in most patients with congenitally corrected transposition of the great arteries.
We studied plasma catecholamine levels in 10 patients with frequent spontaneous episodes of coronary artery spasm to evaluate the role of the sympathetic nervous system. Peripheral venous norepinephrine in supine and upright postures, urinary excretion of catecholamines, and functional testing of the sympathetic nervous system did not differ from the same measurements in control subjects. Arterial and coronary sinus levels of norepinephrine and epinephrine drawn early in ischemia were not elevated over baseline; coronary sinus norepinephrine levels were higher than those in arterial samples and rose from 315 +/- 32 (pg/ml +/- SE) at the onset of ST elevation to 490 +/- 49 pg/ml late in ischemia (p less than 0.05). Plasma epinephrine levels, higher in arterial than coronary sinus samples, also rose significantly only late in ischemia, from 44 +/- 14 pg/ml to 148 +/- 35 pg/ml (p less than 0.05) in arterial blood and from 33 +/- 10 pg/ml to 108 +/- 29 pg/ml in coronary sinus samples (p less than 0.05). Generalized sympathetic nervous system activation is not likely to be the sole cause of coronary artery spasm.
The hemodynamic effects of clonidine were studied in four patients with sever idiopathic orthostatic hypotension and one patient with baroreceptor dysfunction. No depressor response to clonidine was observed in any patient with idiopathic orthostatic hypotension at any dosage. Rather, two patients responded to 0.4 mg of oral clonidine with a 40 mm Hg increment in systolic blood pressure lasting several hours. Each has been receiving clonidine, 0.4 mg twice daily, for one year with greatly increased functional capacity. The other two patients with idiopathic orthostatic hypotension had an even greater pressor response to 0.8 mg of oral clonidine, but adverse effects prevented continued therapeutic use. In marked contrast, the patient with baroreceptor dysfunction had a profound depressor response to 0.2 mg of clonidine. In the treatment of idiopathic orthostatic hypotension, the major advantage of clonidine over other pressor agents is its longer duration of action. The major adverse effects of the drug in these patients are sedation, dry mouth, altered mentation, and excessive hypertension. The drug should not be given to patients with mild idiopathic orthostatic hypotension or selective baroreceptor dysfunction, since severe hypotension may result.
To clarify the possible role of the alpha 1-adrenergic receptor in angina due to coronary artery spasm, a double-blind, randomized, placebo-controlled trial of the specific alpha 1-antagonist, prazosin, was performed. Six patients with vasotonic angina were studied, with efficacy measured by continuous electrocardiographic recording and the tabulation of chest pain and nitroglycerin usage. Despite plasma prazosin levels adequate to produce a six-fold shift in the response to phenylephrine, there was no significant difference in the number of ischemic episodes while taking prazosin (9.8 +/- 6.3 episodes/24 h) compared with placebo (10.5 +/- 6.9). There was also no difference in the length of ischemic episodes, which averaged 231 +/- 35 seconds with placebo and 231 +/- 33 with prazosin. Chest pain and nitroglycerin usage were not altered by prazosin. These data suggest that coronary artery spasm is not primarily caused by an effect on or an abnormality of the coronary vascular alpha 1-receptor.
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Using a double-blind protocol, we investigated the use of propranolol in patients with coronary artery spasm as assessed by subjective and objective variables. Both low-dose (40 mg every 6 hours) and high-dose (160 mg every 6 hours) propranolol were administered. At both doses, the duration of angina attacks was significantly prolonged but the frequency was not. We conclude that propranolol at doses up to 160 mg every 6 hours as single therapy is frequently detrimental in angina pectoris due to coronary artery spasm and should not be used as the sole treatment of this disorder.
Myocardial thallium scintigraphy was performed in four subjects with variant angina and in one subject with isolated, fixed coronary obstruction. Three subjects with variant angina had short episodes of ischemic ST-segment elevation that lasted 20--100 seconds. Thallium scintigrams demonstrated excess uptake in regions judged to be ischemic by angiographic and electrocardiographic criteria. Two subjects, one with variant angina and the other with a fixed coronary lesion, had prolonged episodes of ischemia that lasted 390--900 seconds. Both had reduced thallium uptake in the ischemic regions. We conclude that myocardial reactive hyperemia is the cause of excess thallium uptake in patients with variant angina who have short episodes of myocardial ischemia.
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Landing signal officers (LSOs), exposed to high noise levels during carrier operations, do not routinely wear hearing protectors. Noise exposure data obtained during carrier qualifications on the USS Lexington and the USS Forrestal suggested a clear risk for hearing damage. Moreover, a comparison of the hearing of LSO and non-LSO pilots matched for age and number of flight hours, indicated a trend for LSOs to have poorer hearing. Questionnaire data from 225 LSOs indicate they need full access to aircraft auditory cues, which is not attainable with current off-the-shelf hearing protectors. It is recommended that a hearing protector be developed for the LSO which would permit passage of critical auditory cues and, at the same time, provide hearing protection. There should be a redesign or elimination of the UHF handset. If eliminated, a boom-type noise-cancelling microphone in conjunction with earphones integral to the hearing protector should be considered. Additional hearing studies of LSO and non-LSO pilots should be undertaken.
An identified interneuron in the lobster commissural ganglia fires spikes only between membrane potential values of -60 and -30 millivolts. The membrane potential of this neuron can also oscillate, and interaction between these two properties has important implications in determining the firing pattern of the neuron itself and the modalities of driving of a distant postsynaptic neuron.
Thromboxane A2 (TxA2), an arachidonic acid metabolite causing vasoconstriction and platelet aggregation, is a putative mediator of coronary-artery vasospasm. To determine whether platelet-released TxA2 causes coronary arterial vasospasm, we measured plasma thromboxane B2 (TxB2, the inactive hydration product of TxA2) in the radial-artery and coronary-sinus blood of seven patients and performed therapeutic trials of antiplatelet agents in nine. Although coronary-sinus TxB2 levels rose from the base line approximately fivefold with spontaneous ischemia, samples drawn early in ischemia showed no rise over base-line values. Although a 150 mg dose of aspirin reduced urinary dinor-TxB2 levels by over 75 per cent, it had no effect on the course of the chronic recurrent form of angina pectoris due to vasospasm ("vasotonic angina"). Similarly, indomethacin had no effect on the frequency or duration of ischemia. TxA2 is unlikely to cause vasotonic angina, but it may be released during coronary vasospasm.
In Homarus, the central pattern generators for the rhythmic motor activities of the gastric teeth and the pyloric chamber are located in the stomatogastric ganglion. It is shown that independent gastric and pyloric oscillators are also contained in higher nervous centres (the commissural ganglia) and provide a phasic rhythmic input to the stomatogastric pattern generators. This demonstrates that rhythmic behaviour can be organized by a hierarchy of linked oscillators each capable of producing the rhythm.
A patient with a 5-year history of nonexertional episodic chest discomfort terminating in nausea presented with recurrent periods of marked ST elevations. Each observed episode terminated in the triad of bradycardia, hypotension, and nausea. ST elevation normalized almost immediately when this triad supervened. It is hypothesized that this represented activation of the Bezold-Jarisch reflex. Resolution may have been due to reflexly mediated parasympathetic coronary vasodilation. An episode of ST elevation occurred 24 h after admission which did not result in activation of the Bezold-Jarisch reflex. Following this latter episode, Q waves and enzymatic evidence of myocardial infarction were documented.
The effect of food ingestion of supine blood pressure was assessed during 25 studies in 10 subjects with autonomic dysfunction. Profound decreases in both systolic and diastolic pressure occurred. The mean (+/- standard error of the mean) maximal reduction in systolic blood pressure for the entire group was 49 +/- 6 mm Hg (range 22 to 98). The response also occurred in hypertensive subject after surgical sympathectomy and during alpha adrenergic blockade and hence appears to be a general phenomenon when sympathetic vasoconstrictor function is impaired. The depressor effect of food ingestion was enhanced by propranolol, attenuated by indomethacin and unaffected by diphenhydramine and cimetidine. The phenomenon is thus not explained by histamine release, and can only partly be accounted for by release of arachidonic acid metabolites. Evidence that insulin may play a role in the phenomenon is discussed. Manipulation of diet may prove to be an important adjunct in the management of patients with autonomic dysfunction.