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Biomedical subjects

J A Kennealy

Publications and source records attributed to J A Kennealy.

11 recordsLinked to original sources
PubMed1986

EEG and spectral analysis in acute hyperventilation.

Acute hypocapnia decreases CBF, increases hemoglobin affinity for oxygen and causes cerebral tissue hypoxia. This tissue hypoxia is reversed with inhalation of 100% O2 in dogs. EEG slowing produced by hyperventilation is considered a manifestation of cerebral hypoxia due to decreased CBF and is thought to be reversed with hyperoxia. This study evaluated the effects of 3 gas mixtures (16% O2, 21% O2, 100% O2) on posterior frequencies of the resting and hyperventilatory EEG in normal subjects aged 23-37. Hypocapnia was maintained to an end-tidal pCO2 of 21 mm Hg for 3 min. Respiratory measures, heart rate, saO2, minute ventilation and side effects were recorded. EEG was analyzed by visual inspection and by spectral analysis. Spectral analysis evaluated total amplitude, percentile frequencies, and peak frequencies. There were significant changes from eucapnia to hypocapnia for the group in all physiologic parameters, total amplitude by spectral analysis, and posterior frequencies by visual analysis. There were no significant differences among the gases. We conclude that the EEG changes of hyperventilation are independent of the concentration of inspired oxygen over the range studied in our subjects. Symptoms of hyperventilation are likewise independent of the inspired oxygen concentration for the range studied.

Acute Disease↗
PubMed1984

Acetazolamide and cerebral oxygenation in dogs.

Acetazolamide could theoretically impair oxygen delivery to cerebral tissue by inhibiting local acidification of capillary blood. There is considerable evidence, however, that acetazolamide improves cerebral oxygen tension. This experiment was designed to demonstrate increased deep cerebral oxygen tension after acetazolamide. Three groups of dogs were anesthetized with pentobarbital and ventilated with a respirator. A Teflon-coated stainless steel catheter was placed through a craniotomy into the parietal lobe and advanced into the corona radiata to monitor cerebral pO2 and pCO2 with a mass spectrometer. Group one dogs were normoxic and eucapneic. Group two dogs were hypoxemic, and Group three dogs were hypocapneic. After control cerebral and arterial gas tensions had been recorded, acetazolamide (30 mg kg-1) was injected intravenously. Cerebral gas tensions were monitored continuously and arterial gases were analyzed at 30, 60, 90 and 120 min. Cerebral oxygen tension was not decreased by acetazolamide in any of the dogs. Cerebral carbon dioxide tension was increased by acetazolamide in all dogs. We conclude that acetazolamide does not deplete cerebral oxygen tension even in the face of hypoxemia or acute hypocapnea.

Acetazolamide↗
PubMed1981

Respiratory failure in malignant histiocytosis.

A 29-yr-old man with a fever of several days duration developed rapidly progressive bilateral lung disease with respiratory failure. An open lung biopsy showed extensive acute lung injury with atypical cells, but was not diagnostic. Subsequent cervical lymph node biopsy was consistent with malignant histiocytosis. There was a brief response to chemotherapy, but respiratory failure progressed. He died 34 days after hospital admission. Autopsy revealed extensive neoplastic involvement of both lungs as well as the spleen, cervical, mediastinal, and upper abdominal lymph nodes. This is the first report, to our knowledge, of malignant histiocytosis presenting primarily in the lung and progressing rapidly to respiratory failure. The possibility that this represents a neoplasm of the pulmonary macrophages is discussed.

Adult↗
PubMed1980

Hyperventilation-induced cerebral hypoxia.

Acute respiratory alkalosis decreases cerebral blood flow, increases the affinity of hemoglobin for oxygen, and can result in cerebral hypoxia. This experiment was designed to study this phenomenon in dogs, and to demonstrate the effect of an increased concentration of inspired oxygen. Seven mongrel dogs were anesthetized with pentobarbital and ventilated with a constant volume respirator. A Telfon-coated stainless steel catheter was placed through a craniotomy into the parietal lobe and advanced through the corona radiata to monitor cerebral PO2 and PCO2 with a mass spectrometer. Steady state cerebral and arterial gas tensions were recorded during eucapnic ventilation with air, eucapnic ventilation with 100% oxygen, hypocapnic ventilation with air, and hypocapnic ventilation with 100% oxygen. Decreased cerebral tissue oxygen tension was demonstrated in hypocapnic dogs ventilated with air. When the concentration of inspired oxygen was increased, the relatively small increase in artrial oxygen content was associated with a marked increase in PO2 at the cerebral tissue level. This may be of clinical importance in therapeutic or centrally mediated hyperventilation.

Animals↗
PubMed1977

Serum myocardial enzymes after +Gz acceleration.

Circulating levels of lactate dehydrogenase, glutamate-oxaloacetate, glutamate-pyruvate transaminase, and creatine phosphokinase, as well as its isoenzymes, were measured to investigate the possibility of myocardial damage during acceleration to high +Gz. Serum samples were analyzed in 12 human volunteers before, 6 h after, and 24 h after several bouts of accleration to 6, 8, 9, and 10 G. No substantial elevations of enzyme activities were observed. However, multivariate analysis of variance and multiple comparisons of the data indicated a small but statistically significant (p less than 0.01) increase in creatine phosphokinase. The results were consistent with enhanced skeletal muscle cell permeability consequent to muscular exercise.

Acceleration↗
PubMed1977

Correlates of maximal oxygen consumption during treadmill exercise.

According to the Balke treadmill protocol, 39 healthy male USAF volunteers were subjected to maximal exercise. The subjects as a group passed the anaerobic threshold by the end of exercise since average venous lactate concentrations increased from 11.2 +/- 1.6 mg% (95% confidence limits) to 93.0 +/- 8.5 mg% (95% confidence limits), and the average gas exchange ratio (R) at the end of the exercise was greater than unity (p less than 0.0005). Tests for correlations showed weak but statistically significant (p less than 0.05) relationships between change in venous lactic acid concentrations and R (r = 0.44) and maximal heart rate (r = 0.34). Maximal oxygen consumption was correlated with time of exercise (r = 0.70) and subject weight (r = 0.33). Subject age and initial plasma lactate concentrations were not significantly correlated with any other variables. Multiple linear regression yielded an equation for prediction of maximal oxygen consumption which included terms for time of exercise and subject weight. Although the multiple correlation coefficent (r = 0.75) was statistically significant (p less than 0.05), it was considered insufficient for accurate prediction of maximal oxygen consumption.

Adult↗
PubMed1976

Bradycardia induced by negative acceleration.

Four volunteers were subjected to negative acceleration in a human centrifuge for the purpose of testing a standard lap belt. Three subjects developed a sinus bradycardia. The fourth developed a sinus arrest with a junctional rhythm at -2 G. With return to +1 G, the sinus mechanism recovered with a prolonged P-R interval. Within 2 h, the P-R interval returned to normal. Negative acceleration maneuvers, well within the capabilities of high-performance aircraft, can effect marked changes in the cardiac rhythm. This phenomenon appears to be vagally induced and is remarkably well tolerated.

Acceleration↗
PubMed1976

A chronic implant for intracerebral mass spectrometric gasometry in the rhesus monkey.

A cranial implant was developed to facilitate mass spectrometric gasometry in cerebral tissue of conscious primates. It is permanently fixed to the skull and allows repeated introduction of a Teflon diffusion membrane into the cerebrum. The implant is simple to manufacture and mount. It has been tolerated well with repeated introduction of the catheter for more than 6 mo in 10 rhesus monkeys. The preparation avoids the complication and artifacts of an acute surgical preparation for investigation of cerebral pO2 and CO2.

Animals↗
PubMed1976

Intracerebral oxygen and carbon dioxide tensions in the rhesus monkey.

Five rhesus monkeys (M. mulatta) were prepared by surgical placement of a stainless steel implant in the parietal area of the skull. The implant was designed to firmly hold a Teflon coated membrane of a medical mass spectrometer in an intracerebral position. Animals were consecutively exposed to varying ambient oxygen concentrations from 11% to 21%. Intracerebral PO2 and PCO2 and arterial PO2 were all stimultaneously recorded for computer analysis. Results indicate an almost linear relationship between cerebral PO2 and ambient PO2 as well as between cerebral PO2 and arterial PO2. With an ambient oxygen concentration of 21%, the cerebral Po2 and Pco2 were 13.5 +/- 3.5 mm Hg and 50.4 +/- 7.9 mm Hg, respectively. With an ambient oxygen concentration of 10.7%, these values decreased to 2.5 +/- 2.7 mm Hg and 38.0 +/- 5.6 mm Hg.

Animals↗