Dr Kevin Stewart
For several years Dr Kevin Stewart from Wintec has been conducting research in collaboration with a team at the University of Auckland using an ex-vivo isolated perfused rat lung system in a laboratory at the Wintec City Campus in Hamilton. This system enables lungs to be studied in detail while alive and breathing normally for several hours after being removed from an anaesthetised laboratory rat.
A model of ventilator-induced lung injury (VILI) which produces oedema and a decline in lung function over three hours was established. Experiments have been performed that demonstrate that our experimental drugs can prevent the onset of pulmonary oedema formation and maintain tidal volumes.
These results are very exciting and provide strong support to rapidly move towards gathering more evidence to support a human clinical trial. To do that, we need to transition from ex-vivo to an in-vivo system. To undertake this important translational research, we urgently need to investigate the drug activity in an in-vivo rodent model of lung damage while the animals are anaesthetised on a ventilator that mimics a patient in intensive care. This ventilator system must mimic the settings of a human ventilator, enable drug delivery and collect information on lung mechanical function at a very detailed level. Standard rodent ventilators are not able to do any of these things.
The only option on the market with the level of sophistication required for our purposes is the flexiVent FX System – a state-of-the-art research ventilator.
The device will reside in my Hamilton Wintec lab. It is expected that the purchase of this equipment will help to establish an advanced respiratory research facility at Wintec that will facilitate and enhance research at Wintec for the benefit of staff and students. In addition, the purchase of this system will pave the way to develop new collaborations with investigators at different research institutes, as there are no flexiVent systems currently in any New Zealand institutions. Furthermore, the ongoing research has the potential to benefit the patients and members of the general public in the Waikato as it will contribute to understanding the mechanisms involved in the deterioration of lung function in patients on ventilators with conditions such as COVID-19.
Dr Kevin Stewart is a senior lecturer in the Centre for Health & Social Practice at Wintec. He is working on a collaborative project with researchers at the University of Auckland to undertake critical research into protecting the lungs of patients with severe diseases like COVID-19.
Mechanical ventilation is used when the patient’s lungs fail to adequately oxygenate their blood. However, the act of mechanical ventilation itself frequently causes damage to the lungs. If this damage becomes significant, it can worsen patient outcomes. This is termed “ventilator-induced lung injury” (VILI). Various degrees of VILI are common in patients connected to a ventilator, but currently, there are no effective treatments available beyond adjusting the ventilator settings.
He currently has a study underway at Wintec to evaluate a range of therapies for the prevention of VILI.
This research funding is for a grant in aid contribution that will enable the purchase of a sophisticated research grade mechanical ventilator system that is required to make the necessary measurements and enable Kevin to carry out these experiments in his Wintec laboratory.
There is a real prospect that this research will lead to clinical trials for a completely new drug approach that may offer a potential preventative drug therapy to attenuate the severity of VILI. This would be the first drug treatment to successfully target the underlying pathogenesis of VILI. It has high relevance to many critically ill patients on ventilators including the COVID-19 patients.
This will be the first truly targeted drug directed at protecting the underlying lung from damage due to mechanical ventilation and also blocking the mediators that cause the lung inflammation as well as the mediators that transfer some of the mechanical signals into tissue inflammation. This has the potential to completely transform the management of VILI by providing a damage-preventing drug that complements the current mechanical initiatives.
The modulation of lung inflammation by these targeted drugs will also present a new platform for exploring the drugs’ efficacy in a wider set of lung injury settings that share features of VILI.