The Effects of Components of Vagotomy on the Lung and the Effects of Anesthesia on Vagotomy Induced Lung Change

Shanklin, Douglas R.; Sotelo‐Avila, Cirilo

doi:10.1159/000240055

Cited by 7 publications

(19 citation statements)

References 23 publications

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“…Semi-log 10 plot of survival of 225 newborn rabbits after bilateral cervical vagotomy: 36 after pre-BCV thyroxine at age 3 hours, 63 after pre-BCV thyrotropin at 3 hours, and 126 air controls after BCV only. The control curve shows the typical result of such experiments, a sharp loss of animals by 10 hours post-BCV (Phase A), an extended Phase B to about 45 hours, and an accelerated final Phase C. By contrast thyroxine pretreatment greatly shortened Phase A with a similar length of Phase B and a sharper final Phase C. The thyrotropin effect on Phase A was along the control plot until about 4 hours when an extremely protracted Phase B set in , about twice as long as that of either of the two other subsets, and then a moderately sharp final Phase C. These survival plots are conguent with the interpretation of Shanklin and Sotelo-Avila (1967) which concluded Phase A was likely the result of partial laryngeal constriction because bilateral cervical vagotomy also interrupts the recurrent larnygeal nerve. From this, then, thyroxine and thyrotropin may act against the loss of that motor nerve action but the mode or manner of this remains unknown.…”

Section: Page 16supporting

confidence: 55%

“…They were maintained there until 24 hours of age without caloric supplementation. At 24 hours all animals were subjected to bilateral cervical vagotomy as previously described (Shanklin and Berman, 1964;Shanklin and Sotelo-Avila, 1967). Almost all vagotomies took less than one minute to complete, including positioning and restraining the subject for the procedure.…”

Section: Methodsmentioning

confidence: 99%

“…Almost all vagotomies took less than one minute to complete, including positioning and restraining the subject for the procedure. A few drops of dilute local anesthetic were used in all cases (Shanklin and Berman, 1964;Shanklin and Sotelo-Avila, 1967).…”

Section: Methodsmentioning

confidence: 99%

“…Animals were removed after death and were autopsied according to the methods and procedures previously reported (Shanklin and Berman, 1964;Shanklin and Sotelo-Avila, 1967;Shanklin, 1969). In brief, the extent of lesion was determined by a grid approximation .formula on the pleural surface of the lungs, with each of the four principal lobes considered separately.…”

Section: Methodsmentioning

confidence: 99%

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On the pulmonary toxicity of oxygen. 4. The thyroid arena

Shanklin

2012

Experimental and Molecular Pathology

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Section: Page 16supporting

confidence: 55%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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On the pulmonary toxicity of oxygen. 4. The thyroid arena

Shanklin

2012

Experimental and Molecular Pathology

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“…When the technique of Farber was replicated in newborn rabbits the complete profile of clinical distress and the gross appearance and the histopathology of HMD was produced on a varied scale of extent which was dependent in part on time of survival, sex of the animal, and birth weight (Shanklin and Berman, 1964;Shanklin and Sotelo-Avila, 1967). This model served to elucidate two major attributes of oxygen as the initiating etiological agent of HMD.…”

Section: Methodsmentioning

confidence: 99%

On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen

Shanklin

2012

Experimental and Molecular Pathology

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Oxygen uptake by the pulmonary circulation is a chemical reaction. The physicochemical attributes of oxygen are critical when studying pulmonary oxygen toxicity. Extent of lung injury depends on the percentage of oxygen in an oxygen:nitrogen mix in polybaric circumstances . Further change in extent of lesion follows when other gases are used in the inhalant mix instead of nitrogen (Shanklin and Lester, 1972), with oxygen at 21-100% of the mix. Comparative subatmospheric oxygen levels down to 3% in hydrogen, helium, nitrogen, argon, or sulfur hexafluoride, were run with and without ventilatory distress by the Farber (1937) model, bilateral cervical vagotomy (BCV). This yielded coherent results indicating a need to consider molecular characteristics at the atomic level. Molecular mass and size, gas viscosity, and thermal conductivity yielded no obvious correlates to lung injury. Saturation of the outer electron shells of the diluents fit the empiric data, prospectively an interaction between oxygen and nitrogen from their electronegativity and closely approximate molecular mass, size, and shape. The lesion is essentially eliminated at 7% oxygen in nitrogen. At 3% oxygen, the least lesion is found with N 2 , H 2 , and SF 6 , all gases with incomplete outer electron shells, allowing for transient, possibly polarized, covalent bonding with oxygen as the significant minority component in the mix. Argon and helium do not interfere with oxygen. With 3% oxygen in argon without BCV, the experiments ran so long (>70 hours) they were terminated once the point had been made. 3% oxygen in argon after BCV yielded a mean survival more than twice that of BCV in air, indicating a remarkable degree of nitrogen interference with oxygen in the respiratory medium of terrestrial animal life. Argon displayed other advantages for the lung compared to nitrogen. Hydrogen, nitrogen, and oxygen are diatomic molecules, a feature which does relate to the extent of lung injury, but only oxygen is paramagnetic.Magnetic effects on lesion formation were tested: [1] with ventilatory distress induced in newborn rabbits, and [2] in young adult female white mice exposed to 100% oxygen without added mechanical distress. A noninvasive model for ventilatory distress, thoracic restraint (TR), with longer mean survivals of 40-50 hours, was employed rather than the Farber model. Parallel runs with TR, one subset receiving 100% oxygen in a plastic chamber resting on six strong ring magnets with measured fields up to +1200 gauss, the other plain 100% oxygen, were performed. Both subsets developed moderate metabolic acidosis with average weight losses circa 25%, but over different time courses, 82.89 ± 4.91 hours in magnetized oxygen, 55.4 per cent longer than the 53.34 ± 9.82 hours in plain oxygen ( p <0.001). The longer survival in magnetized oxygen meant extensive lung injury (99.57 ± 0.42% pleural surface, versus 83.86 ± 14.03%), but the rate of lesion formation was 30.89 per cent faster in plain oxygen (1.5722% per hour) than in magnetized oxygen...

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Pulmonary Oxygen Toxicity

Huber¹,

Drath²

1981

Topics in Environmental Physiology and Medicine

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The Effects of Components of Vagotomy on the Lung and the Effects of Anesthesia on Vagotomy Induced Lung Change

Cited by 7 publications

References 23 publications

On the pulmonary toxicity of oxygen. 4. The thyroid arena

On the pulmonary toxicity of oxygen. 4. The thyroid arena

On the pulmonary toxicity of oxygen. 5. Electronic structure and the paramagnetic property of oxygen

Pulmonary Oxygen Toxicity

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