The termination package that just didn't register.
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Biomedical subjects
Publications and source records attributed to J F Daly.
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OBJECTIVE: Preconditioning the heart with 5 min of ischaemia followed by reperfusion renders the myocardium resistant to infarction from subsequent ischaemia. This protection lasts for about 1 h. The aim of this study was to test whether the protection could be reinstated with a second episode of preconditioning after protection from an initial episode had worn off. METHODS: To induce infarction animals experienced 30 min of coronary artery occlusion and then 3 h reperfusion. Ischaemic preconditioning was accomplished with 5 min of coronary branch occlusion. In one group of rabbits the subsequent reperfusion period was prolonged to 2 h to permit protection to wear off before the 30 min coronary occlusion was initiated. In another group a second 5 min coronary occlusion was performed at the end of the 2 h reperfusion. After 10 min of reperfusion the 30 min ischaemic period began. Control animals experienced only the 30 min ischaemia and 3 h reperfusion. Infarct volume was measured with tetrazolium and expressed as a percentage of the ischaemic zone volume. RESULTS: Average infarct size in seven control rabbits [36.0 (SEM 2.0)% of the ischaemic zone] was not significantly different from that in eight rabbits with the prolonged coronary occlusion occurring 2 h after the preconditioning stimulus [28.6 (2.9)% infarction]. In contrast infarcts were significantly smaller in the re-preconditioned group of seven rabbits [8.3 (4.2)%] and comparable to those previously seen with a single preconditioning stimulus followed 10 min later by the 30 min occlusion [6.1 (1.8)%]. CONCLUSIONS: The rabbit heart can be protected with a second preconditioning stimulus after protection from an initial period of preconditioning has subsided.
The role of catecholamines in ischemic preconditioning is unclear. Accordingly, the effects of tyramine-induced norepinephrine release and alpha 1-receptor blockade were examined. Ischemic preconditioning with a 5-minute coronary occlusion 10 minutes before a 30-minute ischemic interval resulted in only 7.7 +/- 3.1% infarction of the risk area, significantly less than that in control rabbits with isolated 30-minute coronary occlusions (34.4 +/- 3.2%, P < .01). Intravenous infusion of tyramine 10 minutes before 30 minutes of ischemia also protected the heart from infarction to an extent similar to that seen with ischemic preconditioning (6.9 +/- 2.4% infarction). This protection observed with tyramine infusion was eliminated by alpha 1-receptor blockade with BE 2254 (36.8 +/- 2.6% infarction) but was unaffected by beta-blockade with propranolol (10.5 +/- 2.4% infarction). Furthermore, the protection was unaffected when the tyramine-induced hypertension was attenuated by allowing blood to flow into a volume reservoir (3.9 +/- 0.8% infarction, P < .01 vs control value). The nonselective adenosine-receptor blocker PD 115,199 also eliminated tyramine-induced protection (40.2 +/- 5.6% infarction), indicating that adenosine is involved in adrenergic-mediated protection. BE 2254 could not block ischemic preconditioning (3.9 +/- 1.1% infarction, P < .01 vs control value). Therefore, catecholamine release before prolonged ischemia can protect the heart from infarction via the alpha 1-receptor, but adenosine receptor stimulation is also involved. alpha-Adrenergic stimulation does not appear to be critical to the protection observed after ischemic preconditioning.
Bilateral lesions which appeared clinically to be branchial cleft sinuses were removed from a patient's neck. One was indeed a branchial cleft sinus, with elements of salivary tissue, but the other proved to be pure salivary tissue with a duct characteristic of a salivary gland. The embryology and clinical characteristics of heterotopic salivary glands are discussed. The occurrence of a heterotopic gland together with a branchial cleft sinus supports the contention that the heterotopic glands arise through errors of development in the branchial apparatus.
The campomelic syndrome is characterized by dwarfism, craniofacial anomalies, bowing of the tibiae and femora, cutaneous dimpling overlying the tibial bend, respiratory distress, and early death. Otolaryngologic manifestations include flat facies with a broad nasal bridge, low-set ears, cleft palate, mandibular hypoplasia, and tracheobronchial malacia. The underlying pathologic feature appears to be disturbance in cartilage growth involving the affected bones and the respiratory tract cartilage. The cause is unknown. We report clinical and histopathologic features in two cases of this syndrome. The endochondral layer of the otic capsule contained no cartilage cells. The cochlea was short and flattened, presenting a scala communis. The vestibule and the canals were deformed by bone invasion. Defective endochondral ossification of the petrooccipital synchondroses possibly explains the shortened skull base seen in this syndrome. The tracheobronchial malacia significantly contributes to respiratory distress and neonatal death.
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Cephalexin monohydrate suspension was used in the treatment of 97 children with otitis media. Pretreatment middle-ear exudate specimens in pure or mixed culture yielded Diplococcus pneumoniae in 47 cases, Haemophilus influenzae in 26, Neisseria catarrhalis in 20, group A beta-hemolytic streptococci in 13, and Staphylococcus aureus in one. The usual dosage was 100 mg/kg/day given orally in divided doses for 10 to 12 days. After 48 hours of treatment, follow-up cultures showed that therapy had been successful in 90 children; 81 remained clinically and bacteriologically free of disease for at least three weeks following therapy. Of the seven children for whom therapy failed, H influenzae persisted in five and D pneumoniae in two. Acceptance of the drug was entirely satisfactory with no important side effects encountered.
Laryngofissure and cordectomy is one of the first of the successful surgical procedures for the cure of cancer limited to the vocal cord. When the lesion is confined to the membranous cord and the motion of the cord is not impaired, cure rates ranging from 85 to 98 percent have been reported. Decline in the use of the procedure is due to the success of radiation therapy in achieving comparable cure rates while preserving normal voice quality. Hemilaryngectomy procedures are now done where laryngofissure and cordectomy had previously been indicated. The more extensive procedure gives greater security due to wider margins of resection and increase applicability, particularly when the lesion involves the anterior commissure. Although the indications for laryngofissure have diminished, the surgeon may use it when a simple, less extensive procedure is called for.
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