Improved neuroprotective effect of methylene blue with hypothermia after porcine cardiac arrest.

BACKGROUND: Induced mild hypothermia and administration of methylene blue (MB) have proved to have neuroprotective effects in cardiopulmonary resuscitation (CPR); however, induction of hypothermia takes time. We set out to determine if MB administered during CPR could add to the histologic neuroprotective effect of hypothermia. METHODS: A piglet model of extended cardiac arrest (12 min of untreated cardiac arrest and 8 min of CPR) was used to assess possible additional neuroprotective effects of MB when administered during CPR before mild therapeutic hypothermia induced 30 min after restoration of spontaneous circulation (ROSC). Three groups were compared: C group (n = 8) received standard CPR; PH group (n = 8) received standard CPR but 30 min after ROSC these piglets were cooled to 34°C; the PH+MB group (n = 8) received an MB infusion 1 min after commencement of CPR and the same cooling protocol as the PH group. Three hours later, the animals were killed. Immediately after death, the brains were harvested pending histological and immunohistological analysis. RESULTS: Circulatory variables were similar in the groups except that cardiac output was greater in the PH+MB group 2-3 h after ROSC. Cerebral cortical neuronal injury and blood-brain barrier disruption was greatest in the C group and least in the MB group. The neuroprotective effect of MB and hypothermia was significantly greater than that of delayed hypothermia alone. CONCLUSION: Administration of MB during CPR added to the short term neuroprotective effects of induced mild hypothermia induced 30 min after ROSC.

Nitric oxide and pain: 'Something old, something new'.

Challenges have emerged following the revival of nitric oxide (NO) from 'something old', a simple gas derived from nitrogen and oxygen with a role in the early stages of evolution, into 'something new', an endogenously formed biological mediator regulating a wide variety of physiological functions. Although pain is a common sensation, it encompasses multiple neurobiologic components, of which NO is only one. In pain research, the study of NO is complicated by convoluted problems related mostly to the effects of NO, which are pro- or anti-nociceptive depending on the circumstances. This dual function reflects the multi-faceted roles of the NO molecule described in physiology. This review covers current information about NO and its implications in pain mechanisms. In addition, it follows the pain pathways, demonstrating the role of NO in peripheral nociceptive transmission as well in central sensitization. This knowledge may provide the scientific basis for developing new drugs that are indicated for different types of pain, drugs that may be related to the chemical links of NO. A comprehensive approach to understanding the effects of NO will help clinicians identify novel agents that combine the pharmacological profile of native drugs with a controllable manner of NO release. Inhibitors of NO synthesis may have analgesic effects and would be of interest for treating inflammatory and neuropathic pain. Unfortunately, only a few of these compounds have reached the stage of clinical pain trials.

The effects of propofol on laryngeal reactivity and the haemodynamic response to laryngeal mask insertion.

The ease of the insertion of laryngeal mask and the haemodynamic response were assessed 2 min after induction of anaesthesia with either propofol 2.5 mg kg-1 or thiopentone 4.0 mg kg-1 in 38 ASA I premedicated patients. The inserting conditions scored as excellent, good, poor and unable to insert were significantly better with propofol than with thiopentone (P < 0.001). Insertion of the laryngeal mask was followed by a transient but significant increase in both systolic (P < 0.05) and diastolic (P < 0.01) arterial pressure in the thiopentone group; there was no comparable response in the propofol group. The heart rate varied little from baseline in both groups.