Effect of muscle relaxation and its reversal on the control of breathing

Effect of neuromuscular blockade and reversal by sugammadex versus neostigmine on breathing when hypoxic or hypercapnic in volunteers - BREATH

Status

Not yet recruiting

Phases

Phase 4

Study type

Interventional

Source

EU CTR

Registry ID

EUCTR2015-005222-19-NL

Enrollment

Unknown

Registered

2016-07-13

Start date

2016-07-14

Completion date

Unknown

Last updated

2016-08-08

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Postoperative ventilatory control MedDRA version: 19.0 Level: LLT Classification code 10038680 Term: Respiratory depression postoper System Organ Class: 100000004855

Interventions

Trade Name: Bridion Product Name: Sugammadex Product Code: EMEA/H/C/000885 Pharmaceutical Form: Solution for injection Pharmaceutical form of the placebo: Injection Route of administration of the plac

Eligibility

Sex/Gender

All

Inclusion criteria

Inclusion criteria: Healthy male volunteers aged 18 and older with a body mass index =65 years) no F.1.3.1 Number of subjects for this age range

Exclusion criteria

Exclusion criteria: Known or suspected neuromuscular disorders impairing neuromuscular function; allergies to muscle relaxants, anesthetics or narcotics; a (family) history of malignant hyperthermia or any other muscle disease; any medical, neurological or psychiatric illness (including a history of anxiety).

Design outcomes

Primary

Measure	Time frame
Main Objective: This trial is designed to assess the effect of reversal of neuromuscular blockade by sugammadex or neostigmine on ventilatory control in healthy volunteers. ;Secondary Objective: Not applicable;Primary end point(s): We will apply hypoxic and hypercapnic challenges and measure ventilation on a breath-to-breath basis using the Dynamic End-tidal Forcing (DEF) technique. This technique allows the manipulation of inspired gas concentrations to steer the end-tidal concentrations of O2 and CO2 independent of the ventilatory response or the concentrations of O2 and CO2 in mixed venous blood. The technique allows a reliable assessment of carotid body function (in this case hypoxia) without the confounding effects of variations in end-tidal CO2. Additioanlly we will obtained the ventilatory response to hypercapnia at hyperoxic conditions. This allows assessment of the response activity of the central chemoreceptors in the brainstem. HYPOXIA: Hypoxic responses will be obtained (1) prior to administration of rocuronium; (2) During administration of rocuronium at a TOF of 0.6; (3) at 5 min intervals following the end of the administration of rocuronium and the administration of the reversal agent. Hypoxia will be induced by lowering the end-tidal PO2 in a step-wise fashion from 14.5 kPa (110 mmHg) to 7 kPa (53 mmHg) for 2 min. Thereafter the end-tidal concentration will be returned to normoxic values. The target arterial oxygen saturation of this challenge is 80 ± 2%. This method allows assessment of the hypoxic ventilatory sensitivity (HVR) as defined by: HVR = [Delta ventilation from normoxia to hypoxia]/[Delta saturation from normoxia to hypoxia]. (Dahan et al., Anesthesiologu 1996) HYPERCAPNIA: We will apply two 7 min steps in end-tidal PCO2 at the background of a hyperoxic gas mixture. At the end-of each step a ventilation and arterial oxygen saturation will be obtained. This allows assessment of the hypercapnic ventilatory response slope (S) which is cal	—

Measure

Time frame

Main Objective: This trial is designed to assess the effect of reversal of neuromuscular blockade by sugammadex or neostigmine on ventilatory control in healthy volunteers. ;Secondary Objective: Not applicable;Primary end point(s): We will apply hypoxic and hypercapnic challenges and measure ventilation on a breath-to-breath basis using the Dynamic End-tidal Forcing (DEF) technique. This technique allows the manipulation of inspired gas concentrations to steer the end-tidal concentrations of O2 and CO2 independent of the ventilatory response or the concentrations of O2 and CO2 in mixed venous blood. The technique allows a reliable assessment of carotid body function (in this case hypoxia) without the confounding effects of variations in end-tidal CO2. Additioanlly we will obtained the ventilatory response to hypercapnia at hyperoxic conditions. This allows assessment of the response activity of the central chemoreceptors in the brainstem. HYPOXIA: Hypoxic responses will be obtained (1) prior to administration of rocuronium; (2) During administration of rocuronium at a TOF of 0.6; (3) at 5 min intervals following the end of the administration of rocuronium and the administration of the reversal agent. Hypoxia will be induced by lowering the end-tidal PO2 in a step-wise fashion from 14.5 kPa (110 mmHg) to 7 kPa (53 mmHg) for 2 min. Thereafter the end-tidal concentration will be returned to normoxic values. The target arterial oxygen saturation of this challenge is 80 ± 2%. This method allows assessment of the hypoxic ventilatory sensitivity (HVR) as defined by: HVR = [Delta ventilation from normoxia to hypoxia]/[Delta saturation from normoxia to hypoxia]. (Dahan et al., Anesthesiologu 1996) HYPERCAPNIA: We will apply two 7 min steps in end-tidal PCO2 at the background of a hyperoxic gas mixture. At the end-of each step a ventilation and arterial oxygen saturation will be obtained. This allows assessment of the hypercapnic ventilatory response slope (S) which is cal

—

Secondary

Measure	Time frame
Secondary end point(s): Not applicable;Timepoint(s) of evaluation of this end point: Not applicable	—

Countries

Netherlands

Contacts

Public ContactAlbert Dahan

LUMC

a.dahan@lumc.nl31715269111

Outcome results

None listed

Source: EU CTR (via WHO ICTRP) · Data processed: Feb 4, 2026