ABSTRACT
Systemic complement activation has been noted in a variety of shock states, and there is growing evidence that, in addition to being proinflammatory effectors, products of complement activation contribute directly to generalized manifestations of shock, such as hypotension and acidosis. To study the effects of complement activation, we examined responses in rats to systemic activation of complement with cobra venom factor (CVF), including blood pressure, metabolic acidosis, changes in vascular permeability, and lung function. High doses of CVF produced circulatory collapse (mean arterial pressure = 110 +/- 16 and 35 +/- 9 mmHg in control and with CVF, respectively, P < 0.05), metabolic acidosis (HCO concentration = 27.8 +/- 1.7 and 9.6 +/- 3.4 meq/l in control and with CVF, respectively, P < 0.05), extravasation of albumin into the lung and gut, and modest arterial hypoxemia (PO2 = 486 +/- 51 and 201 +/- 36 Torr in control and during 100% O2 breathing, respectively, P < 0.05). Prior depletion of complement protected against these abnormalities. Other interventions, including neutrophil depletion and cyclooxygenase inhibition, prevented lung injury but had much less effect on systemic hemodynamics or gut permeability, suggesting that complement activation products induce injury by neutrophil- and cyclooxygenase-dependent pathways in the lung but not in the gut. These studies underscore the significant systemic abnormalities developing after systemic activation of complement.
Subject(s)
Complement Activation/physiology , Hemodynamics/physiology , Lung/physiology , Acidosis/metabolism , Animals , Blood Pressure/physiology , Capillary Permeability/drug effects , Complement Inactivator Proteins/pharmacology , Cyclooxygenase 2 , Cyclooxygenase 2 Inhibitors , Cyclooxygenase Inhibitors/pharmacology , Elapid Venoms/pharmacology , Enzyme Inhibitors/pharmacology , Hemodynamics/drug effects , Intestine, Small/pathology , Isoenzymes/metabolism , Lung/pathology , Lysine Carboxypeptidase/antagonists & inhibitors , Myocardium/pathology , Neutrophils/physiology , Oxygen/blood , Phospholipases A/antagonists & inhibitors , Prostaglandin-Endoperoxide Synthases/metabolism , Rats , Respiratory Function TestsABSTRACT
STUDY OBJECTIVE: To determine if acquired long QT syndrome following right or left, radical or modified, neck dissections result in malignant arrhythmias or deaths. DESIGN: Prospective study. SETTING: Inpatient head and neck service of the Massachusetts Eye and Ear Infirmary. PATIENTS: 69 patients who underwent extensive neck surgery, without congenital long QT syndrome, medications known to prolong the QT interval, preoperative ventricular arrhythmias, or electrolyte abnormalities. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Preoperative and postoperative electrolytes were evaluated. Preoperative and postoperative electrocardiograms and QT intervals were evaluated. Continuous intraoperative and 10- to 12-hour postoperative monitoring of lead II or V5 were evaluated. Twenty-six patients (Group 1) underwent either right radical neck dissection or modified right radical neck dissection, 25 patients (Group 2) underwent either left radical neck dissection or modified left neck dissection, and 18 patients (Group 3) underwent extensive neck surgery without radical or modified neck dissection. Postoperatively, 38 patients (19 Group 1, 11 Group 2, and 8 Group 3 patients) developed a QT interval corrected for heart rate (QTc) of greater than 440 milliseconds. Repeated measures analysis of variance, comparing preoperative and postoperative QTc showed a statistically significant preoperative to postoperative change, but no significant difference among the three groups. No malignant arrhythmias or deaths were recorded in any of the three groups. CONCLUSIONS: Acquired long QT syndrome following radical neck dissection, without congenital, metabolic, or pharmacologic disturbance, is unlikely to trigger malignant arrhythmias, as previously reported for right radical neck dissection.
