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Gerard Laden

Publications and source records attributed to Gerard Laden.

5 recordsLinked to original sources
PubMed2005

Pretreatment with hyperbaric oxygen and its effect on neuropsychometric dysfunction and systemic inflammatory response after cardiopulmonary bypass: a prospective randomized double-blind trial.

OBJECTIVE: Animal studies have shown that pretreatment with hyperbaric oxygen can induce central nervous system ischemic tolerance and also modulate the inflammatory response. We evaluated this therapy in patients undergoing cardiopulmonary bypass. METHODS: Sixty-four patients were prospectively randomized to group A (n = 31; atmospheric air, 1.5 atmospheres absolute) or group B (n = 33; hyperbaric oxygen, 2.4 atmospheres absolute) before on-pump coronary artery bypass grafting. Age, sex, body mass index, diabetes, hypertension, smoking, coronary disease severity, left ventricular function, Parsonnet score, Euroscore, bypass time, myocardial ischemia time, and number of grafts were comparable in both groups. Canadian Cardiovascular Society angina, New York Heart Association dyspnea, and previous myocardial infarction were significantly higher in group B. Inflammatory markers were analyzed before surgery and 2 and 24 hours after bypass. Neuropsychometric testing was performed 48 hours before surgery and 4 months after surgery and included trail making A and B, the Rey auditory verbal learning test, grooved peg board, information processing table A, and digit span forward and backward. Neuropsychometric dysfunction was defined as more than 1 SD deterioration in more than 2 neuropsychometric tests. Chi-square tests, Fisher tests, t tests, and analysis of variance were used as appropriate for statistical analysis. RESULTS: Group A had a significant postoperative increase in the inflammatory markers soluble E-selectin, CD18, and heat shock protein 70. This was not observed in group B. Neuropsychometric dysfunction was also significantly higher in group A compared with group B. There was no difference in any other early postoperative clinical outcome. CONCLUSIONS: Our results seem to indicate that pretreatment with hyperbaric oxygen can reduce neuropsychometric dysfunction and also modulate the inflammatory response after cardiopulmonary bypass. However, further multicenter randomized trials are needed to clinically evaluate this form of therapy.

Aged↗
PubMed2003

Gastric barotrauma in a scuba diver: report of a case.

Stomach rupture can occur as a consequence of the expansion of compressed air during rapid ascent after diving. We present the case of a middle-aged woman who suffered a gastric tear from surfacing too quickly after diving, and discuss the diagnosis and management of such patients by reviewing previously reported similar events. Gastric barotrauma should be suspected in divers who complain of abdominal pain, even in the absence of frank signs of peritoneal irritation. Although pneumoperitoneum is always present in these patients, it can also occur as a consequence of pulmonary barotrauma, making gastroscopy or radiological contrast studies, or both, essential for a definitive diagnosis. Surgical repair represents the treatment of choice for an active full-thickness tear and, if associated with arterial gas embolism or decompression sickness, should ideally be performed in a center where a category I (intensive care-capable) hyperbaric unit is available.

Barotrauma↗
PubMedDate not supplied

Hyperbaric oxygen: a novel technology for modulating myocardial schemia-reperfusion via a single drug.

Over the years, the anecdotal medical use of oxygen has demonstrated, in a non-evidence-based manner, that it may have wide-ranging clinical consequences. Although oxygen is a critical substrate in the alleviation of hypoxia, anoxia, and ischemia, paradoxically, it also functions as a deleterious metabolite during the reperfusion of previously ischemic tissues. In adding to this controversy, a spate of new pioneering work has identified hyperoxygenation (hyperoxia) and its metabolites as solely and purposefully demonstrating cellular and clinical benefit,particularly in the field of ischemic reperfusion injury (IRI). Furthermore, the beneficial effects of oxygen have been technologically augmented by administration at doses above atmospheric pressure and at higher concentrations. The novel technology that involves oxygen treatment at supra-atmospheric pressures in high concentrations is known as hyperbaric oxygen (HBO). Although the concept of hyperbaric oxygen has been around since the mid 20th century, it is only during the past decade or so that its therapeutic potential as a new technology-based drug has been exploited for the purposes of cellular tolerance and protection. HBO has recently been shown to be a useful adjunct in several models of IRI, including myocardial infarction. How it does this remains to be elucidated. This article attempts to bring into the spotlight some pertinent developments regarding HBO and myocardial IRI, while simultaneously stimulating intellect, thought, and discussion as to whether this novel technology--HBO--which consists of only a singular drug--oxygen--is a therapy that warrants further laboratory and clinical investigation as a therapeutic modality that may be safe and cost-effective, without producing significant adverse effects.

Animals↗
PubMedDate not supplied

Hyperbaric oxygen: a new drug in myocardial revascularization and protection?

Ischemia-reperfusion injury (IRI) occurs following coronary artery revascularization. Reactive oxygen species (ROS) were initially thought to play a role in the pathogenesis of this injury. However, the evidence for this is inconclusive. Recent studies involving ischemic preconditioning have identified ROS as potential mediators for the cardioprotective effects observed following this technique. Furthermore, cardiac studies involving IRI and the use of hyperbaric oxygen (HBO) have demonstrated the ability of HBO to induce cardioprotection and to attenuate IRI. This review suggests the possible role for HBO as a new drug in the arena of myocardial revascularization and cellular protection. While there is mounting clinical evidence for this, a methodological understanding of HBO's cellular mechanisms of actions appears to be lacking. As such, this article attempts to draw the similarity between HBO and other protective oxidative stress mechanisms and then to speculate in an evidence-based manner its possible cellular mechanistic role as a drug via the generation of ROS.

Animals↗