Unexplained deaths in pulmonary tuberculosis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Smith.
Explore the source record for details and available documents.
Coronary vascular reserve was studied in 11 patients with severe chronic aortic regurgitation (AR). Nineteen patients with the chest pain syndrome and normal findings on cardiac catheterization served as control subjects. Resting coronary sinus flow and contrast-agent-induced hyperemia were measured by continuous thermodilution. Left ventricular (LV) dimensions and mass were obtained echocardiographically. All patients had normal coronary arteries. Resting coronary flow was increased and coronary reserve was decreased in patients with AR compared with the control subjects: 310 +/- 38 versus 121 +/- 13 ml/min and 56 +/- 9 versus 86 +/- 7.5%, respectively. The decrease in coronary vascular reserve correlated with the increase in LV mass (r = -0.86, p = 0.001) and LV wall thickness (r = -0.83, p = 0.002) and with the decrease in LV volume/mass ratio (r = 0.761, p = 0.007). There was no significant correlation between the decrease in coronary vascular reserve and LV volume (r = 0.255), LV peak wall stress (r = 0.292), LV systolic pressure (r = -0.495), aortic or LV diastolic pressure (r = 0.322 and -0.318, respectively), or aortic-LV diastolic gradient, nor with the voltage on the electrocardiogram (limb leads r = -0.60, precordial leads r = -0.118). Thus, coronary vascular reserve is decreased in proportion to the degree of left ventricular hypertrophy in patients with chronic AR. Patients with angina pectoris tended to have a lower coronary vascular reserve than those without angina (median 26 versus 76%, difference not significant). LV wall thickness and not LV volume is the critical component of left ventricular mass related to coronary reserve. No significant correlation between the decrease in coronary vascular reserve and the presence of angina pectoris was demonstrated.
Many patients with coronary artery disease (CAD) in whom ventricular tachycardia (VT) develops have transmural scars or frank aneurysms. However, only a minority of patients with ventricular aneurysms go on to develop VT. To determine which factors are associated with the development of VT in patients with aneurysms, we retrospectively reviewed the records of 154 patients with CAD and segments of akinesia or dyskinesia, or both, on left ventriculography. Of the 154 patients, 85 had 24-hour Holter monitoring or 48 consecutive hours of continuous electrocardiographic monitoring in an intensive care unit within 6 months of catheterization. VT occurring at least 10 days after myocardial infarction (MI) or in the chronic phase was recorded in 19 patients (Group I); the remaining 66 patients did not have VT (Group II). The clinical, hemodynamic, and angiographic characteristics of these 2 groups showed no significant difference with respect to age, time from first transmural MI to catheterization, congestive heart failure (CHF), ejection fraction, or presence of dyskinesia. Patients with VT had significantly larger aneurysms and a higher prevalence of septal akinesia or dyskinesia. However, stepwise discriminant analysis revealed septal akinesia or dyskinesia to be the only independently significant variable distinguishing the 2 groups. Thus, septal involvement appears to be a major determinant of VT in patients with CAD and ventricular aneurysm.
A procedure is described for carrying out repetitive bronchopulmonary lavage in the rat, in which a given volume of lavage fluid is introduced into the lungs from a reservoir and then withdrawn from the lungs back into the reservoir, the process being repeated a number of times. During this procedure there is a net release of endogenous surfactant and macrophages from the lungs. [14C] pulmonary surfactant was prepared from rats previously injected intravenously with [1-14C] palmitate, and pulmonary macrophages labelled with 85Sr were prepared from rats which had received by intratracheal injection a suspension of fused clay particles labelled with 85Sr. It was shown by carrying out repetitive bronchopulmonary lavage with 0.15M-NaCl containing either exogenous [14C]-surfactant or [85Sr]-macrophages that the release of endogenous surfactant and macrophages from the lung into the lavage fluid occurred concomitantly with the retention within the lung of radioactive exogenous surfactant and macrophages from the lavage fluid. It is concluded that the process of surfactant and macrophage detachment during bronchopulmonary lavage is reversible and that the exchange processes are of substantial magnitude.
Pregnant ferrets were inoculated intra-cardially on day 30 of gestation with influenza virus. The animals were sacrificed on days 5 to 11 after inoculation and the products of conception including the uterus were examined virologically and histopathologically. The results indicate that the initial site of infection of the conceptus is the haemophagous organ and that spread occurs from this site to the endometrium, placental labyrinth and fetus. Lesions in the fetus are confined to the liver and respiratory tract. In the liver they may represent either a viral hepatitis or a secondary response to placental damage resulting in the stimulation of erythropoiesis. In the respiratory tract they first occur in the nasal sinuses and upper airways suggesting that infection is via the amniotic fluid rather than via the blood stream. The relevance of these findings to human pregnancy is discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We and others have demonstrated a high prevalence of total coronary occlusion during the acute phase of myocardial infarction (MI). This study reports the angiographic appearance of the infarct-related artery (IRA) in 130 patients with a history of MI, who underwent cardiac catheterization 2 weeks to more than 12 months afterwards. The IRA was the left anterior descending in 47%, the right coronary artery in 50%, and the circumflex in 3% of cases. Total coronary occlusion was found in 80% of patients studied 2 to 4 weeks after MI, and decreased gradually reaching 40% of those studied after 12 months of MI. In those patients with a patent IRA, severe stenosis remained: 99% obstruction at 2 to 4 weeks, decreasing to 85.9% obstruction after 12 months (p less than 0.005). The prevalence of total coronary occlusion (TCO) and the severity of stenosis in those without TCO was similar in those with transmural or nontransmural MI and in those with one-, two- or three-vessel disease. This study suggests that endogenous lysis is probably a slow process, and that severe coronary narrowing persists in those with recanalization.
The myocardium from 44 patients undergoing open cardiac surgery was studied to determine if alterations demonstrable with the electron microscope could be related to prognosis. Planimetric methods were used to evaluate myofibrils, Golgi, mitochondria, myelin figures, other organelles, and intracellular space in order to achieve as objective a measurement as possible. Morphologic changes were graded and correlated with clinical findings and results after long-term follow-up. Factors evaluated in terms of survival included patient age, degree and extent of valvular disease, the presence of coronary artery disease, and degenerative changes of the myocardium as demonstrated ultrastructurally. Patients dying, of cardiac causes, within the first 5 years, had a higher ultrastructural grade than those surviving for more than 10 years. Statistical analysis, using stepwise regression methods, demonstrated a highly significant correlation (P less than 0.001) between cardiac ultrastructural integrity and prognosis. The addition of age to the prediction model was also significant (P less than 0.04), using the two variable models, EM grade and age were, similarly, highly significant (P less than 0.001).
Explore the source record for details and available documents.
The effects of chronic smoking on the coronary circulation were studied by evaluating the coronary vascular reserve in 12 chronic smokers (group 1) and 10 nonsmokers (group 2). All patients were referred to cardiac catheterization for evaluation of chest pain and were found to have normal coronary and left ventricular angiograms. Coronary vascular reserve was measured by analyzing the hyperemic response to selective coronary injection of contrast agent. There was no statistically significant difference between groups 1 and 2 with regard to age, baseline electrocardiogram or response to treadmill or thallium-201 exercise tests. The mean coronary reserve (+/- standard deviation) was 74.1 +/- 20.1% in the smokers versus 117.1 +/- 45.1% in the nonsmokers (p less than 0.02). In patients who smoked 1 pack a day or less and in those who smoked more than 1 pack a day, the mean coronary reserve was 89.5 and 64.9%, respectively (p less than 0.05). Additionally, of 20 patients followed up for an average of 20 months, 7 of 10 smokers and 1 of 10 nonsmokers continued to have chest pain (p less than 0.03). The cause for the chest pain has not been established in these patients. These results suggest that coronary vascular reserve is significantly less in chronic smokers than in nonsmokers, and that this decrease is more pronounced in heavy smokers.
A series of the little compounds was prepared by cyclization of the appropriate 5-(aryloxy)-v-triazole-4-carboxylic acids and evaluated for antiallergic activity by the rat passive cutaneous anaphylaxis (PCA) screen. The most potent compounds were 6-(mesyloxy)-9-oxo-1H,9H-benzopyrano[2,3-d]-v-triazole and its 5-methyl homologue, which were some tenfold more potent than disodium cromoglycate. Dialkyl derivatives, especially those substituted at C-5 and C-6 or C-6 and C-7, and 6-methoxy compounds were also among the more potent compounds. One compound, 6,7-dimethyl-9-oxo-1H,9H-benzopyrano[2,3-d]-v-triazole, was further evaluated and shown to be a potent inhibitor of rat PCA when given orally.
A short series of the title compounds was prepared and evaluated for antiallergic activity in the rat passive cutaneous anaphylaxis screen. All but the two N-methylated derivatives were active in this screen by the intravenous route, the most potent being the symmetrical dimethyl compound, 4,9-dihydro-6,7-dimethyl-4,9-dioxo-1H-naphtho[2,3-d]-v-triazole, and its 5-nitro derivative. The latter two compounds were noticeably more potent than disodium cromoglycate, and one of these, the unnitrated material, was selected for further evaluation as a potential antiasthmatic drug.
Adherence of Candida albicans to human buccal epithelial cells varied with the composition of the culture medium used to grow the fungus and the donor of epithelial cells, and even from day to day with the same fungal growth conditions and cell donor. Small differences in adherence were detected between four laboratory strains of C. albicans that differed in virulence for mice, and between three pairs of minimally subcultured isolates from cases of oral thrush and from the mouths of healthy donors. However the differences were not only small but did not consistently show that the adherence capacities of the strains virulent for mice or obtained recently from oral thrush were greater than those of the other strains.
Explore the source record for details and available documents.
This study in human volunteers was designed to compare the retention of diethylenetriaminepentaacetic acid (DTPA) in the body after intravenous (i.v.) injection with that following inhalation by using a 14C labelled tracer. After i.v. injection retention in the blood could be described by three exponential components with half-times of about 1.4 min (approximately 60%) 14.3 min (approximately 20%) and 95 min (approximately 20%). By 24 hr more than 99% of the 14C-DTPA had been excreted in the urine and less than 0.5% remained in the plasma. After inhalation of 14C-DTPA retention in the lungs could be represented by a single component with a half time of about 75 min. As a consequence the length of time that a therapeutically useful amount of DTPA is retained in the body is approximately twice that following intravenous injection.
Neutropenia often accompanies septicemia in burned patients. This paradox suggests a defect in the regulation of granulopoiesis. Colony stimulating factor (CSF) produced by the monocyte-macrophage system is an important regulator of granulocyte production. We followed serial serum CSF levels and peripheral blood leukocyte differential counts in 22 patients with greater than 30% burns. Six patients (mean burn, 58%) developed Gram-negative septicemia and died (Group I). Sixteen patients (mean burn, 38%) had no fatal septicemias (Group II). Nonsurvivors had initially low levels of CSF and developed persistent monocytopenia. Survivors, in contrast, had prompt rises in CSF and developed monocytosis. The presence of monocytopenia and low CSF levels in Group I suggests an abnormality in the stimulatory arm regulating granulopoiesis. Such a defect may play a role in the development of fatal septicemia following severe thermal injury.
Using fluorescent antibody techniques, a semi-quantitative survey has been made of the distribution of influenza virus antigen in the trachea, main bronchi, and three zones (hilar, intermediate and alveolar) of all four lung lobes of ferrets following intranasal inoculation of a virulent clone (7a) of the recombinant influenza virus A/PR/8/34-A/England/939/69 (H3N2). The results confirm the indications from our previous quantitative surveys of infectious virus and histological damage in these areas, namely that infection is confined largely to airway epithelium and is rare in the alveoli. Furthermore, in the lung zones, viral antigen resided mainly in the bronchial rather than bronchiolar epithelium. In attempts to identify the reasons for lack of alveolar involvement organ cultures of alveolar tissue, from which all major airways had been removed, produced levels of virus similar to cultures of bronchus and trachea and the hilar and intermediate lung zones which contain airway and alveolar tissue. Hence, the lack of alveolar infection in vivo must be due to factors which prevent virus attack of susceptible alveolar cells. However, these organ culture experiments showed that a contributing factor could be very poor release of virus from any alveolar cells that do become infected. In contrast, although cultures of bronchi produced less virus than those of nasal turbinates (the most susceptible tissue in vivo) they released a high proportion of their yield and this ease of release may contribute to spread of infection in vivo.