Biomedical subjects
Publications and source records attributed to S Goldman.
Rhabdomyomas of the heart occur as multiple lesions in 90% of patients so affected, and 80% of the patients die in the first year of life. A 21-month-old child presented with a large isolated right atrial rhabdomyoma causing a supraventricular tachyarrhythmia. Surgical excision cured the arrhythmia.
A patient with severe pulmonary hypertension secondary to the CREST syndrome variant of scleroderma is described. Acute reductions in both pulmonary artery pressure and total pulmonary resistance were seen with nifedipine and oxygen administration. Reductions in resistance were maintained for over one month with this combination. These results raise the possibility that some of the pulmonary hypertension seen in this condition is reversible.
Plain chest x-rays, twelve-lead electrocardiograms, and M-mode echocardiograms were analyzed in 50 control patients and 79 consecutive patients with pulmonary hypertension documented at cardiac catheterization in order to determine the relative values of these noninvasive techniques as screening tests in detecting pulmonary hypertension. The sensitivity and specificity of selected findings previously described as being associated with pulmonary hypertension were calculated for each test. All test results were found to have sensitivities too low to function as satisfactory noninvasive screening techniques. Most findings were highly specific for pulmonary hypertension when present. Patients with pulmonary vascular disease were detected more frequently than those with pulmonary hypertension due to pulmonary venous congestion.
Pathogenic strains of Bordetella pertussis undergo spontaneous phase variation and become non-pathogenic upon culturing in vitro. Spontaneous variants of the Tohama and #165 pathogenic strains of B. pertussis were selected by their ability to grow on synthetic and semi-synthetic solid media. The frequency of these variants was between 10(-6) and 10(-7). About 250 variant strains were screened for the presence of virulence-associated traits, such as production of hemolysin, pertussis toxin and filamentous hemagglutinin (FHA). Only four different combinations of the traits were found: 7-11% of the variants displayed all traits, 17% of the variants carried the toxin and FHA, 5-11% carried FHA only and 66% were devoid of all virulence traits. The strains which had at least one virulence trait also demonstrated some adenylate cyclase activity. The disappearance of hemolysin quantitatively affected the other traits. These results suggest that phase variation in B. pertussis is a non-random process, involving multistep disappearance of virulence factors in the following order: hemolysin, pertussis toxin and FHA. In contrast, all 300 variants of strain #18323 of B. pertussis, which were able to grow on the selective solid media, carried all the virulence traits. This is in accordance with the strain's unique intracerebral growth capability.
The velocity of contraction has been reported to be more rapid in left atrium (LA) than left ventricle (LV), but the mechanics of contraction in these two chambers have not been compared under physiological conditions. Accordingly, sonomicrometer crystals and solid state pressure transducers were used to measure LV and LA systolic function simultaneously in seven conscious dogs. Two sets of crystals (LA-1, LA-2) were placed perpendicularly across the LA. Phenylephrine was infused at increasing doses from 0.4 to 1.2 microgram . kg-1 . min-1 to increase LV and LA afterloads. Constant heart rates were maintained by atrial pacing. The results indicated that LA motion was virtually identical in both diameters. LA fractional shortening (0.07 +/- 0.01) and ejection time (0.057 +/- 0.002 s) were much smaller than the ventricular values (0.21 +/- 0.01 and 0.18 +/- 0.01 s, respectively). The velocity of circumferential fibre shortening (Vcf) for the LV (1.16 +/- 0.05 cir . s-1) was not significantly different from LA-1 Vcf (1.19 +/- 0.09 cir . s-1) or LA-2 Vcf (1.22 +/- 0.08 cir . s-1). During phenylephrine infusions, LV systolic pressure increased from 120.0 +/- 3.4 to 190.8 +/- 15.5 mmHg and LV end-diastolic pressure increased from 3.6 +/- 0.3 to 27.7 +/- 2.7 mmHg. When Vcf for each chamber was plotted against the peak systolic pressure in that chamber, the curve of the LA was located upward and to the right of the LV curve.(ABSTRACT TRUNCATED AT 250 WORDS)
A 65-year-old man showed naloxone-reversible unconsciousness followed by downward gaze paralysis. CT scan suggested an ischaemic lesion in the mesodiencephalic region. This observation represents the first case of naloxone-reversible coma related to brainstem ischaemia.
The contribution of peripheral vascular factors to the high output state in thyrotoxicosis was examined in 11 calves treated with daily intramuscular injections of L-thyroxine (200 micrograms/kg) for 12-14 d. Thyroxine treatment increased cardiac output from 14.1 +/- 1.4 to 24.7 +/- 1.4 liters/min (P less than 0.001) and decreased systemic vascular resistance from 562 +/- 65 to 386 +/- 30 dyn-s/cm5 (P less than 0.01). Blood volume was increased from 65 +/- 4 ml/kg in the euthyroid state to 81 +/- 6 ml/kg when the animals were thyrotoxic (P less than 0.05). The role of low peripheral vascular resistance in maintenance of the high output state was evaluated by infusion of phenylephrine at two dosages (2.5 and 4.0 micrograms/kg per min). In the euthyroid state, no significant decrease in cardiac output was observed at either level of pressor infusion. In the thyrotoxic state, the higher dosage of phenylephrine increased peripheral resistance to the euthyroid control level and caused a small (6%) decrease in cardiac output (P less than 0.05). This small decrease in cardiac output probably could be attributed to the marked increase in left ventricular afterload caused by the pressor infusion as assessed from measurements of intraventricular pressure and dimensions. Changes in the venous circulation were evaluated by measurement of mean circulatory filling pressure and the pressure gradient for venous return in six animals during cardiac arrest induced by injection of acetylcholine into the pulmonary artery. Mean circulatory filling pressure increased from 10 +/- 1 mmHg in the euthyroid state to 16 +/- 2 mmHg (P less than 0.01) during thyrotoxicosis, while pressure gradient for venous return increased from 10 +/- 1 to 14 +/- 2 mmHg (P less than 0.02). These changes in venous return curves were not affected significantly by ganglionic blockade with trimethapan (2.0 mg/kg per min) before cardiac arrest. Thus, the high output state associated with thyrotoxicosis is not dependent upon a low systemic vascular resistance, but is associated with increases in blood volume, mean circulatory filling pressure, and pressure gradient for venous return.
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The epidemiological data collected suggest increasing occurrence of bronchial carcinoma throughout the world. The trend in mortality, and incidence if the latter is explored, reveal, with rare exceptions, a still increasing tendency. Separate evidence is presented from epidemiological surveys which suggest rising risk factor prevalence, above all smoking and occupational exposures. Descriptive and analytical epidemiology may considerably contribute to the fight against cancer, in particular to its prevention. Unfortunately, in many European countries no cancer records are maintained even for the most diseminated malignancy, i.e. bronchial carcinoma.
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The effect of propranolol on global and segmental left ventricular function at rest and after postextrasystolic potentiation was studied in 12 patients with chest pain. Heart rate was controlled with atrial pacing, and left ventricular cineangiograms were performed before and after 0.15 mg/kg of propranolol. During each ventriculogram a premature ventricular stimulus was introduced by means of a programmed stimulator. Propranolol decreased global left ventricular ejection fraction from 64 +/- 4.5 to 58 +/- 4.6 (p less than 0.03). Postextrasystolic potentiated global ejection fraction was not affected by propranolol (78 +/- 3.5 vs 73.6 +/- 3.4; p = NS). The area ejection fraction of the anteroapical region was decreased after propranolol (64 +/- 4.8 vs 52 +/- 6.5; p less than 0.01); however, the postextrasystolic potentiated area ejection fraction was not affected by propranolol (78 +/- 2.6 vs 71 +/- 4.6; p = NS). Frame by frame analysis of the ventriculograms demonstrated that propranolol depressed global and segmental left ventricular function by affecting the second one-third ejection fraction without influencing the first or third one-third ejection fraction. Propranolol has a small depressant effect on global and segmental left ventricular function in patients with coronary artery disease. Postextrasystolic potentiated global and segmental left ventricular function and early systolic ejection phase indices are not altered by propranolol and therefore may be useful in assessing left ventricular function in patients with coronary artery disease who are taking propranolol.
Regional myocardial perfusion was measured in 32 patients with the xenon-133 washout technique at rest and after 5 mg of intracoronary papaverine. Areas of decreased perfusion and/or decreased vasodilation were identified visually from computer-generated functional images. The locations of arteries and stenoses, obtained from identically positioned cineangiograms, were overlaid on the functional images. Perfusion rates for 62 myocardial regions were calculated and correlated with the percentage of stenosis. There was no association between degree of stenosis and perfusion at rest. Regional myocardial perfusion increased after papaverine in regions supplied by coronary arteries without stenoses (0% to 25%), 88.6 +/- 4.7 ml/min/100 gm. This increase was significantly greater (p less than 0.001) than the increase in regions supplied by 51% to 75% stenoses (23.7 +/- 6.3 ml/min/100 gm), or 76% to 99% stenoses (12.9 +/- 6.3 ml/min/100 gm), or 100% stenoses (2.5 +/- 3.8 ml/min/100 gm). Thus there was an inverse relationship between the increase in myocardial perfusion stimulated by papaverine and the degree of coronary artery stenosis measured angiographically. In regions supplied by two stenoses in series, vasodilation produced less of an increase than a single stenosis of a similar degree.
The net transport of glucose from blood to the cerebrospinal fluid compartment of cats was measured by ventriculocisternal perfusion to determine over a large range of serum glucose concentrations the influence of serum glucose levels and their changes on the net transport rate. Changes in serum glucose levels were followed within minutes by corresponding changes in cerebroventricular effluent fluid glucose concentration. At mean values of serum glucose concentration of 6.2 mM and cerebrospinal fluid formation rate of 24.3 microliter/min, the net glucose influx rate was 1.6 mmol/min. The effluent fluid-to-serum glucose concentration ratio was 0.25 and decreased when serum glucose was greater than 11.1 mM. The rate of glucose transport from blood to effluent fluid during ventricular perfusion was saturable, and approached a maximum of 3.5 mumol/min at serum glucose levels above 22 mM. From the cerebrospinal fluid formation and net glucose influx rates the calculated glucose concentration of nascent cerebrospinal fluid was 6.5 mM and higher than the corresponding serum glucose of 5.6 mM. It is concluded that during perfusion over a wide range of serum glucose concentrations, a saturable mediated glucose transport mechanism can be demonstrated. Changes in serum glucose are rapidly reflected in corresponding effluent fluid glucose levels. From effluent fluid-to-serum glucose concentration ratios and calculations of the glucose in newly formed cerebrospinal fluid, the technique, however, overestimates the glucose influx rates at normal serum glucose levels.