Search

To test the effect on the handling properties of a two component fibrin glue, the viscosity was increased with sodium hyaluronate and the glue was applied to a microvascular anastomosis in rats. The femoral artery of each rat was anastomosed with three conventional sutures and then sealed with fibrin glue. Three glues with different viscosities were tested: original Tisseel fibrin glue (Immuno AG, Vienna); Tisseel with 0.9% sodium chloride added to the fibrinogen component; and Tisseel with a high molecular weight sodium hyaluronate (10 mg/ml, Healon, Pharmacia, Sweden) added to the fibrinogen component. The increased viscosity of the fibrin glue to which hyaluronate had been added resulted in a significantly higher patency rate 20 minutes after completion of the anastomosis (p < 0.01), and reduced the amount of fibrin that entered the vessels.

Sodium hyaluronate (HA) is known to modulate wound healing and interact with inflammatory reactions. High concentrations of extracellular HA are for example correlated to scarless wound healing. Topical treatment with HA has, however, limited effect due to the rapid clearance of HA in the tissue. In an effort to prolong the dissolution rate and enhance the effect of topically administered HA, HA was incorporated in a cross linked fibrin clot and placed in NaCl. The concentration of HA in the NaCl solution was analysed after 30', 60', 4h, 8h, and 24h. It was found that the dissolution rate of HA incorporated in cross linked fibrin was dramatically decreased in vitro, especially when the HA-fibrin mixture was put at rest and not exposed to a mechanical stress. The findings indicate a new possibility for slow release of HA after topical administration.

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 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 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.

Closure of the abdomen after surgery has been performed in a multitude of fashions and the literature is flooded with differently tailored studies of this matter. In this paper the available literature in the field has been reviewed with special emphasis on the advantages and disadvantages of continuous or interrupted, mass or layered closure, and on the choice of monofilament or multifilament, resorbable or non-resorbable suture material. After weighing up all the aspects, the authors recommend that the abdomen should be closed with a continuous mass closure technique, using a monofilament suture. No firm conclusion can be drawn from the literature as to whether resorbable or non-resorbable suture should be chosen.

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.

An experimental model was developed for investigations of traumatically induced vasospasm (TVS) in the central ear artery (CEA) of the awake rabbit. Spasm was induced by a 3-second long pinch with a clip applying forceps exerting a standardized compression force between its claws. The vessel was transilluminated with cold light and inspected from above with an operating microscope equipped with a video camera. The internal diameter was continuously measured. TVS was assessed in terms of its duration, intensity (reduction of initial diameter) and severity (integrated change in diameter over time). The spasm lasted about 10-20 minutes and the inner diameter decreased to about 15-20% of the pretrauma values. The preparation was stable for at least 3 hours and repetitive pinches in different segments of the vessel caused reproducible spasms. TVS was more pronounced when the duration of trauma was prolonged and weakened when the same vessel segment was traumatized repeatedly. The nervous influence was studied after partial denervation of the ear, after partial denervation with additional nervous blockade, and after total denervation achieved by amputation and replantation of the ear. It was found that denervation had no influence on the TVS. Ice cooling was used to decrease the body temperature by 1.0 degree and 1.75 degree C. This caused a significant increase in duration and severity, but not in intensity of TVS. Bleeding by 20% of the total blood volume or hypervolaemic haemodilution with dextran infusion, 20% of total blood volume, did not affect the spasm. Blood flow of CEA was totally obstructed by ligation of the side branches along a 7 cm long segment and subsequent ligation of CEA distal to the segment. This resulted in decreased duration and severity of TVS. Topical application of 2 or 20% lidocaine or of 3% pentobarbital one minute after vessel trauma, when the vessel was maximally constricted, caused prompt resolution of the TVS. The rapid resolution was followed by drug-induced vasoconstriction to about 60% of the initial pre-spasm values. During this vasoconstriction the vessels were refractory to trauma. The results strongly suggest that TVS is a locally elicited phenomenon of vascular smooth muscle, and can be influenced by local application of lidocaine or pentobarbital.

Multiple vascular access failure is a frequent problem and we report our experience with 32 Hemasite devices implanted in 28 patients with end-stage renal disease. All of the patients were on maintenance haemodialysis or haemofiltration with a range of treatment of 1-17 years. Their mean age was 58 +/- 14 years (range 28-72 years). The main indication for using this device as an alternative vascular access was the presence of high-risk patients with a high incidence of previous access failure (1-8 accesses per patient). The majority of the patients were considered as high risk, due either to old age (more than 60 years) (60%) or to the presence of diabetes mellitus (29%). The results of 5 years' experience and follow-up showed that the Hemasite device could be successfully used as a secondary vascular access in high-risk patients who have problems of multiple access failures. The 1-year cumulative survival of the device (55%) was affected by complications such as thrombosis and infection (47% and 16%) which were noted mostly among patients with diabetes mellitus. These complications are the major ones endangering the longevity of the Hemasite implant and were important causes of implant loss (31% and 6% respectively). Being needleless and painless, the Hemasite was well-accepted by the patients and it functioned well, with adequate blood flow. We conclude that the Hemasite device is a valuable alternative when vascular access becomes a problem in haemodialysis patients.

The immune response of lymphocytes to subcutaneously administered pneumococcal vaccine was studied in five patients without spleens and in five healthy subjects. Seven days after immunisation circulating B cells synthesising IgG antipneumococcal capsular polysaccharides (anti-PCP) appeared in both groups. Twenty one days after vaccination this B cell population had disappeared and a B cell subset which secreted IgM and IgG anti-PCP in the presence of pokeweed mitogen was detected in the normal but not in the splenectomised subjects. In the splenectomised group polyclonal IgM synthesis induced by pokeweed mitogen was defective. It was concluded that the early events of the immune response to PCP may be mediated by lymph nodes but that, later, the spleen acquires a central role in producing lymphocyte subsets capable of synthesising specific antibodies and that this might explain the increased sensitivity of splenectomised subjects to pneumococcal infection.