Hypoxic ventilatory sensitivity in men is not reduced  by prolonged hyperoxia (Predictive Studies V and VI)

Gelfand, R., C. J. Lambertsen, J. M. Clark, and E. Hopkin.Hypoxic ventilatory sensitivity in men is not reduced by prolonged hyperoxia (Predictive Studies V and VI). J. Appl. Physiol. 84(1): 292–302, 1998.—Potential adverse effects on the O2-sensing function of the carotid body when its cells are exposed to toxic O2 pressures were assessed during investigations of human organ tolerance to prolonged continuous and intermittent hyperoxia (Predictive Studies V and VI). Isocapnic hypoxic ventilatory responses (HVR) were determined at 1.0 ATA before and after severe hyperoxic exposures: 1) continuous O2 breathing at 1.5, 2.0, and 2.5 ATA for 17.7, 9.0, and 5.7 h and 2) intermittent O2 breathing at 2.0 ATA (30 min O2-30 min normoxia) for 14.3 O2 h within 30-h total time. Postexposure curvature of HVR hyperbolas was not reduced compared with preexposure controls. The hyperbolas were temporarily elevated to higher ventilations than controls due to increments in respiratory frequency that were proportional to O2 exposure time, not O2 pressure. In humans, prolonged hyperoxia does not attenuate the hypoxia-sensing function of the peripheral chemoreceptors, even after exposures that approach limits of human pulmonary and central nervous system O2 tolerance. Current applications of hyperoxia in hyperbaric O2therapy and in subsea- and aerospace-related operations are guided by and are well within these exposure limits.

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Effects of estrogen and progesterone on carotid body neural output responsiveness to hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.5.1909 ◽

1990 ◽

Vol 68 (5) ◽

pp. 1909-1916 ◽

Cited By ~ 81

Author(s):

B. Hannhart ◽

C. K. Pickett ◽

L. G. Moore

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Carotid Body ◽

Shape Parameter ◽

Estrogen Treatment ◽

Progesterone Treatment ◽

Before And After ◽

Progressive Hypoxia ◽

End Tidal ◽

Sites Of Action

Pregnancy increases ventilatory and carotid body neural output (CBNO) responsiveness to hypoxia in cats (J. Appl. Physiol. 67: 797-803, 1989). To determine whether progesterone and estrogen stimulated hypoxic ventilatory and CBNO responsiveness, we studied 24 castrated male cats before and after 1 wk of placebo, estrogen, progesterone, or estrogen plus progesterone treatment. Estrogen plus progesterone treatment decreased end-tidal PCO2 (-3.8 +/- 0.8 Torr) and increased hypoxic ventilatory responsiveness, whereas estrogen or progesterone alone had no effect. Animals receiving progesterone alone or in combination with estrogen had higher CBNO responsiveness than placebo or estrogen-treated animals (shape parameter A = 45 +/- 7 vs. 27 +/- 4, P less than 0.05). However, the group treated with estrogen plus progesterone did not have greater CBNO responsiveness to hypoxia than the group receiving progesterone alone. The cross plot of the simultaneously measured CBNO and ventilation during progressive hypoxia revealed a greater slope in the estrogen-treated than in the placebo animals, suggesting that estrogen treatment increased central nervous system transduction of CBNO into ventilation. Thus the data taken together suggested that progesterone and estrogen had a combination of peripheral (carotid body) and central sites of action such that the administration of both hormones together had a more consistent stimulatory effect on hypoxic ventilatory responsiveness than either hormone alone.

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Role of endogenous female hormones in hypoxic chemosensitivity

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.5.1706 ◽

1997 ◽

Vol 83 (5) ◽

pp. 1706-1710 ◽

Cited By ~ 67

Author(s):

Koichiro Tatsumi ◽

Cheryl K. Pickett ◽

Christopher R. Jacoby ◽

John V. Weil ◽

Lorna G. Moore

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Shape Parameter ◽

Ovarian Hormones ◽

Serum Progesterone ◽

Ventilatory Responses ◽

Female Hormones ◽

Before And After ◽

End Tidal

Tatsumi, Koichiro, Cheryl K. Pickett, Christopher R. Jacoby, John V. Weil, and Lorna G. Moore. Role of endogenous female hormones in hypoxic chemosensitivity. J. Appl. Physiol. 83(5): 1706–1710, 1997.—Effective alveolar ventilation and hypoxic ventilatory response (HVR) are higher in females than in males and after endogenous or exogenous elevation of progesterone and estrogen. The contribution of normal physiological levels of ovarian hormones to resting ventilation and ventilatory control and whether their site(s) of action is central and/or peripheral are unclear. Accordingly, we examined resting ventilation, HVR, and hypercapnic ventilatory responses (HCVR) before and 3 wk after ovariectomy in five female cats. We also compared carotid sinus nerve (CSN) and central nervous system translation responses to hypoxia in 6 ovariectomized and 24 intact female animals. Ovariectomy decreased serum progesterone but did not change resting ventilation, end-tidal[Formula: see text], or HCVR (all P = NS). Ovariectomy reduced the HVR shape parameter A in the awake (38.9 ± 5.5 and 21.2 ± 3.0 before and after ovariectomy, respectively, P < 0.05) and anesthetized conditions. The CSN response to hypoxia was lower in ovariectomized than in intact animals (shape parameter A = 22.6 ± 2.5 and 54.3 ± 3.5 in ovariectomized and intact animals, respectively, P < 0.05), but central nervous system translation of CSN activity into ventilation was similar in ovariectomized and intact animals. We concluded that ovariectomy decreased ventilatory and CSN responsiveness to hypoxia, suggesting that the presence of physiological levels of ovarian hormones influences hypoxic chemosensitivity by acting primarily at peripheral sites.

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Anti-programmed cell death-1 (PD-1) monoclonal antibodies involve reversible cranial dura matter

Oxford Medical Case Reports ◽

10.1093/omcr/omab077 ◽

2021 ◽

Vol 2021 (9) ◽

Author(s):

Hiroshi Kataoka ◽

Daisuke Shimada ◽

Hitoki Nanaura ◽

Kazuma Sugie

Keyword(s):

Central Nervous System ◽

Cell Death ◽

Nervous System ◽

Monoclonal Antibodies ◽

Programmed Cell Death ◽

Adverse Effects ◽

Neuromuscular Disorders ◽

Neurological Complications ◽

Programmed Cell Death 1 ◽

The Central Nervous System

ABSTRACT This case is the first document to describe a patient receiving anti-programmed cell death 1 (PD-1) antibodies which showed cranial dura matter involvement. According to the increasing use of anti-PD-1 monoclonal antibodies, adverse effects can occur in several organs since its ligand PD-L1 and PD-L2 are expressed in a wide variety of tissues. The estimated rate of neurological complications is 1–4.2% of patients, and neuromuscular disorders are the most common. Adverse effects on the central nervous system including encephalitis are less frequent. Here, a patient receiving anti-PD-1 antibodies showed cranial dura matter involvement, and the dura enhancement on MRI was resolved by withdrawal of the treatment with anti-PD-1 antibodies only.

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Probable Encephalopathy and Spasticity in a Multiple Sclerosis Patient Following Carbapenem Administration: A Case Report and Brief Literature Review

Journal of Pharmacy Practice ◽

10.1177/08971900211063277 ◽

2021 ◽

pp. 089719002110632

Author(s):

Claire V Klimko ◽

James M Sanders ◽

Meagan L Johns

Keyword(s):

Risk Factors ◽

Multiple Sclerosis ◽

Adverse Effect ◽

Central Nervous System ◽

Nervous System ◽

Case Report ◽

Adverse Effects ◽

Multiple Sclerosis Patient ◽

Specific Patient ◽

Appropriate Treatment

Purpose: The purpose of this case report is to describe spasticity and encephalopathy that developed in a multiple sclerosis patient following carbapenem administration. Summary: A 55-year-old female with multiple sclerosis developed spasticity and encephalopathy within 24 hours of meropenem and ertapenem administration. This was the second time that she had developed encephalopathy following carbapenem administration. The patient gradually recovered over four days following discontinuation of carbapenem therapy. Conclusion: Carbapenem neurotoxicity, a well-documented adverse effect, has been linked to several risk factors, including central nervous system lesions. Despite this, there is little evidence describing the risk of neurotoxicity in patients with multiple sclerosis. It is important to understand the potential adverse effects of carbapenems in specific patient populations to help guide appropriate treatment of infections.

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Prediction of central nervous system oxygen toxicity in rats

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.4.1903 ◽

1994 ◽

Vol 77 (4) ◽

pp. 1903-1906 ◽

Cited By ~ 12

Author(s):

R. Arieli ◽

G. Hershko

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Exposure Time ◽

Electrical Discharge ◽

Oxygen Toxicity ◽

Threshold Value ◽

Power Equation ◽

The Mean

Cumulative O2 toxicity (K) can be calculated using the expression K = t2 x PO2c, where t is exposure time and the power c is to be determined; the phenomenon is liable to occur when K reaches Kc, the threshold value of K at which a symptom is manifested. Six rats were each exposed six times to 6 ATA O2 at 2-day intervals until the first electrical discharge (FED) was noted in an electroencephalogram. There was no difference in latency to FED in the series of six exposures. Thirteen rats were exposed to O2 until FED was noted in an electroencephalogram. They were exposed to four constant PO2's of 5, 6, 7, and 8 ATA and to two combined profiles of 1) 5 min at 7 ATA followed by 5 ATA and 2) 15 min at 5 ATA followed by 7 ATA. The solution of the equation for each rat was used to predict its latency to FED on the combined profile. The correlation of predicted to measured latency was significant (P < 0.0001), and the slope was not different from 1. Solving for these parameters using the combination of all the data, we obtained Kc = 5.71 x 10(6) and c = 5.39, which correctly predicted the mean latency but failed to predict individual latency. It is preferable to use each rat as its own control. The significance of the correlation supports the validity of the power equation for calculating K.

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Effects of hypercapnia and hypoxia on inspiratory and expiratory diaphragmatic activity in conscious cats

Journal of Applied Physiology ◽

10.1152/jappl.1994.77.4.1644 ◽

1994 ◽

Vol 77 (4) ◽

pp. 1644-1652 ◽

Cited By ~ 7

Author(s):

M. Bonora ◽

M. Boule

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Steady State ◽

Electromyographic Activity ◽

Large Reduction ◽

Before And After ◽

The Central Nervous System ◽

State Changes ◽

Chemical Stimuli ◽

Adult Cats

The influence of steady-state changes in chemical stimuli on ventilation and electromyographic activity of the diaphragm during both inspiration (total DI) and expiration (total DE) was studied in unanesthetized intact adult cats before and after carotid denervation. In intact animals, during hypercapnia (2 4, and 6% CO2), tidal volume (VT) and total DI increase, whereas total DE did not consistently change. During ambient hypocapnic hypoxia (14, 12, and 10% O2), VT increased only at 10% O2, whereas total DI increased at all levels studied. Total DE increased substantially at 14% O2, persisting up to the end of expiration with 12 and 10% O2. This effect was markedly attenuated during normocapnic hypoxia. During CO hypoxemia (1,700 ppm in air), VT as well as total DI and total DE decreased because of a large reduction in inspiratory and expiratory time elicited by tachypneic breathing. The effects of hypercapnia and hypoxia persisted after carotid denervation. Therefore, 1) in contrast to hypercapnia, hypoxia markedly enhances the expiratory diaphragmatic activity, 1) this expiratory braking mechanism depends on the severity of hypoxia and is partly due to hypocapnia secondary to hypoxia; and 3) because this effect was observed after carotid denervation and during CO hypoxemia, it may arise in the central nervous system, possibly in bulbopontine structures.

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Control Points To Reduce Movement of Central Nervous System Tissue during Beef Slaughter

Journal of Food Protection ◽

10.4315/0362-028x.jfp-16-302 ◽

2017 ◽

Vol 80 (2) ◽

pp. 355-360

Author(s):

J. L. Aalhus ◽

R. D. Thacker ◽

I. L. Larsen ◽

J. C. Roberts ◽

M. A. Price ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Cold Water ◽

Effective Means ◽

Hot Water ◽

Spongiform Encephalopathy ◽

Cross Contamination ◽

Central Nervous System Tissue ◽

Before And After ◽

Disease Variant

ABSTRACT Consumption of central nervous system tissue (CNST) from cattle with bovine spongiform encephalopathy (BSE) is thought to cause the human neurological disease, variant Creutzfeldt-Jacob disease. To identify points of cross-contamination of beef carcasses with CNST, 55 young beef cattle were slaughtered and processed through a federally inspected multispecies abattoir. The objectives of this study were to evaluate CNST spread following the placement of a plug in the penetration site of the skull after captive bolt stunning, to evaluate cross-contamination of carcasses before and after splitting, to compare the effects of hot water pasteurization (84°C for 10 s) versus cold water wash (10°C for 30 s) for reducing CNST on the carcass, and to examine other possible sources of cross-contamination in the abattoir. Results indicated that the use of a plastic plug reduced CNST contamination near the bolt penetration site. This study also confirmed that carcass splitting resulted in an increase in CNST contamination at various areas of the carcass. Hot water pasteurization appeared to be an effective means of removing CNST contamination from carcasses in most of the areas sampled.

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