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Meeting Abstract: 534

The effect of total obstruction of blood flow on traumatically induced vasospasm was studied in the central arteries of rabbits' ears. All side branches were ligated along a 7 cm segment of the artery. Obstruction of blood flow was achieved by ligation of the central artery distal to this segment. The inner diameter of the artery was measured microscopically after transillumination. A standardised injury was induced with a clip applying forceps. The duration, intensity (reduction of diameter) and severity (integrated change in diameter over time) of the resulting spasm were assessed. Spasm induced after cessation of blood flow lasted significantly less time (mean (SEM), 6.0 (2.0) minutes compared with 18.1 (2.5) min) and was less severe than spasm induced when the blood flow was intact (1.6 (0.6) mm/min compared with 6.2 (0.6) mm/min). The results may be explained by local accumulation of vasodilating substances in the injured segment of the vessel in the absence of blood flow.

The effects of partial denervation, partial denervation with additional nervous blockade with bupivacaine, and total denervation achieved by amputation and replantation of the ear on traumatic vasospasm were studied in the rabbit. The central ear artery was exposed and compressed in a standardized fashion. The inner diameter was determined by in vivo microscopy using transillumination with cold light. The resulting spasm was assessed in terms of its duration, intensity (reduction of initial diameter), and severity (integrated change in diameter over time). None of the types of denervation had any influence on the vasospasm. The results suggest that the vasospasm is a local phenomenon of the vascular smooth muscle and is not modified by the nervous system.

The effect of topical administration of 2 or 20% lidocaine and of 3% pentobarbital on traumatic vasospasm was studied in the central ear artery of the rabbit. The inner diameter of the artery was measured by in vivo microscopy. Vasospasm was induced by a standardised pinch of a 3.2 mm long arterial segment and lasted for 10-20 min. The drugs were given locally at maximal spasm, 1 min after spasm induction. All treatments caused prompt resolution of the vasospasm. This was followed by a plateau phase when the vessel diameter was reduced to about 60% of the initial pre-spasm value as a result of drug-induced vasoconstriction. The vasoconstriction lasted between 40 min and 24 h, depending on the treatment. Twenty per cent lidocaine was most effective, but caused thrombosis in microvessels surrounding the central ear artery. It is concluded that topical lidocaine and pentobarbital are both effective in resolving traumatic vasospasm but should only be used after careful consideration, since they also cause a general decrease in vascular diameter.

The effect of bleeding (20% of total blood volume) and of hypervolaemic haemodilution with dextran infusion (20% of total blood volume) on traumatic vasospasm was studied in the central ear arteries of 10 rabbits. The blood pressure dropped significantly after bleeding and the packed cell volume was significantly lower after dextran infusion. Neither treatment had any effect on the duration, intensity or severity of the vasospasm. The results suggest that moderate changes in blood volume do not influence traumatic vasospasm.

The effect of hypothermia on traumatically induced vasospasm was studied in an in vivo model of the rabbit ear artery. Spasm was induced by standardized compression of a 3.2 mm segment of the artery for 3 s. The internal diameter was continuously measured with the aid of an operating microscope during transillumination of the artery. Measurements were begun before spasm induction and continued until the spasm was completely resolved. Spasm was first induced at normothermia and then after reduction of the body temperature by 1.0 degrees C and 1.75 degrees C. The spasm was evaluated in terms of its duration, intensity (% reduction of initial diameter) and severity (area under the curve where diameter was plotted against time). The results were compared with those in a control group which was kept normothermic. Reduction of the body temperature caused a significant increase in the duration of the spasm and increased its severity, but did not influence its intensity.

A study was undertaken to develop a model for investigations of traumatically induced vasospasm. The left ear of the rabbit was denervated under short anesthesia. With the animal under light sedation, spasm of the central ear artery was repeatedly induced with a clip applying forceps. To evaluate the vasospasm, the vessel was transilluminated with cold light, and the internal diameter was continuously measured. The spasm was assessed in terms of its duration, intensity (reduction of initial diameter) and severity (integrated change in diameter over time). Repetitive application of the forceps on the same vessel segment shortened the spasm duration. With prolonged pinch duration, the spasm duration was lengthened. The preparation was stable for at least 3 hours. This model was effective for manipulating small vessels and producing spasm and is of potential value for studying the treatment of vasospasm by topical local intra-arterial and systemic methods.