Effects of intracoronary calcium chloride on regional oxygen balance and mechanical function in normal and stunned myocardium in dogs.

BACKGROUND: Brief myocardial ischaemia has been demonstrated to result in mechanical and coronary endothelial dysfunction, in which calcium may play a role. We examined whether the mechanical and vascular responses to calcium are altered in postischaemic, reperfused myocardium. METHODS: Regional myocardial oxygen consumption (MVO2), mechanical function and coronary blood flow (CBF) in response to calcium chloride (0.10, 0.25, 0.50 and 0.75 mg ml(-1) of CBF) directly infused into the left anterior descending (LAD) artery were determined before (normal) and 30 min after a 15-min-period of LAD occlusion (stunned) in an open-chest canine model. Percentage segment shortening (%SS) and percentage postsystolic shortening (%PSS) in the LAD territory were determined using ultrasonic crystals and CBF using a Doppler transducer. Myocardial extraction of oxygen (EO2) and lactate (Elac) was calculated. RESULTS: The infusion of calcium chloride resulted in dose-dependent increases in %SS and MVO2 but did not affect %PSS in normal myocardium. These changes were accompanied by parallel increases in CBF, resulting in no change in EO2. In stunned myocardium, the responses to calcium chloride were not significantly altered, with the exception of a reduction in %PSS. However, ischaemia and reperfusion itself significantly reduced %SS and Elac and increased %PSS. CONCLUSIONS: These data suggest that calcium chloride improves regional systolic and diastolic function both in normal and stunned myocardium. Calcium chloride is unlikely to cause direct coronary vasoconstriction or to deteriorate regional mechanical function in postischaemic myocardium.

Hemodynamic and catecholamine responses to laryngoscopy and tracheal intubation in patients with complete spinal cord injuries.

BACKGROUND: Endotracheal intubation in patients undergoing general anesthesia often causes hypertension and tachycardia, which may be altered when the efferent sympathetic fiber to the cardiovascular system is interrupted. The aim of the current study was to investigate the effects of different levels of spinal cord injury on the cardiovascular responses to intubation. METHODS: Fifty-four patients with traumatic complete cord injuries requiring tracheal intubation were grouped into quadriplegics (above C7; n = 22), high paraplegics (T1-T4, n = 8), and low paraplegics (below T5, n = 24) according to the level of injury. Twenty patients without spinal injury served as controls. Arterial pressure, heart rate, and rhythm were recorded at intervals for up to 5 min after intubation. Plasma concentrations of catecholamines were also measured. RESULTS: The intubation increased the systolic blood pressure similarly in control, high-paraplegic, and low-paraplegic groups (P < 0.05), whereas it did not alter the blood pressure in the quadriplegic group. Heart rate was significantly increased in all groups; however, the magnitude was more pronounced in the high-paraplegic group (67%) than in the control (38%) and quadriplegic (33%) groups. Plasma concentrations of norepinephrine were significantly increased after intubation in all groups; however, values were lower in the quadriplegic group and higher in the low-paraplegic group compared with those in the control group. Incidence of arrhythmias did not differ among groups. CONCLUSIONS: The cardiovascular and plasma catecholamine changes associated with endotracheal intubation may differ according to the affected level in patients with complete spinal cord injuries.

Intracoronary propofol attenuates myocardial but not coronary endothelial dysfunction after brief ischaemia and reperfusion in dogs.

We have investigated the effects of propofol on recovery of regional mechanical and coronary endothelial function and on lipid peroxidation in post-ischaemic myocardium in dogs. The animals were assessed for 180 min during reperfusion after 15-min of occlusion of the left anterior descending coronary artery (LAD). They were treated with intracoronary (i.c.) propofol 5 or 20 micrograms/ml of coronary flow or vehicle (control group) for 60 min, beginning 30 min before LAD occlusion. Propofol significantly enhanced recovery of regional contractile function (70% and 81% of baseline segment shortening in the propofol 5 and 20 micrograms ml-1 groups, respectively, compared with 51% in controls at 3 h of reperfusion). However, LAD flow responses to i.c. acetylcholine were similarly attenuated regardless of treatment with propofol throughout reperfusion. The increase in malondialdehyde induced by ischaemia-reperfusion was significantly suppressed by both doses of propofol. These results demonstrated that in vivo, propofol ameliorated dysfunction of the myocardium but not of the coronary endothelium resulting from brief ischaemia and reperfusion; the protection may be related, at least in part, to its ability to reduce lipid peroxidation.