Use of a novel acellular dermal matrix allograft to treat complex trauma wound: a case study.

OBJECTIVE: To report the novel use of acellular dermal matrix allograft to treat a complex open fracture of the arm. METHODS: Case report outlining the steps taken to treat the fracture and soft tissue trauma. RESULTS: The complexity of the wound required multiple types of treatments that ultimately resulted in a healed fracture and full wound closure. CONCLUSIONS: Acellular dermal matrix has shown promise in closing the wound of a complex open fracture within the limitations of a single patient case study.

Lidocaine/tetracaine patch (Rapydan) for topical anaesthesia before arterial access: a double-blind, randomized trial.

BACKGROUND: Arterial catheterization is painful and is associated with patient stress and anxiety. Analgesia is usually provided by subcutaneous injection of local anaesthetic. An alternative is topical anaesthesia, such as Rapydan which is a novel topical anaesthetic patch containing 70 mg each of lidocaine and tetracaine. We therefore tested the hypothesis that Rapydan patch analgesia is non-inferior to subcutaneous local anaesthetic. METHODS: Ninety patients undergoing elective major cardiac surgery were included in this prospective, double-blind clinical trial. Patients were randomly assigned to receive either a lidocaine/tetracaine patch, followed by subcutaneous injection 0.5 ml of normal saline solution, or placebo patch with subsequent subcutaneous injection of 0.5 ml of lidocaine 1%. Pain during arterial catheterization using 100-mm-long visual analogue scale (VAS) was the primary outcome. Other outcomes were pain during anaesthetic/saline injection and plasma tetracaine concentrations. RESULTS: VAS pain scores during arterial puncture were comparable in both groups and Rapydan was non-inferior to subcutaneous lidocaine. Pain scores at the time of subcutaneous injection were significantly lower (better) in patients assigned to the lidocaine/tetracaine patch than to lidocaine (P=0.001). Plasma tetracaine concentrations never exceeded the detection limit of 25 ng ml(-1) at any time in any patient. CONCLUSIONS: Both the lidocaine/tetracaine patch and subcutaneous injection of lidocaine provided comparable pain control during arterial catheter insertion. Subcutaneous lidocaine caused discomfort during injection, whereas the lidocaine/tetracaine patch required placement 20 min before the procedure. Given adequate time, the patch provided better overall analgesia by obviating the need for subcutaneous infiltration.

HEPES inhibits contractile responses of canine basilar artery.

N-2-hydroxyethylpiperazine-N'-2-ethanesulphonic acid (HEPES) is a commonly-used buffer. This study determined the effect of HEPES on contractility of the dog basilar artery and tested the hypothesis that HEPES inhibits vasoconstriction of isolated arterial segments by generating H2O2. Rings of dog basilar artery with or without endothelium were suspended under isometric tension and contracted with KCl, serotonin, or prostaglandin F2 alpha (PGF2 alpha) in bicarbonate or HEPES buffer. Addition of HEPES, 30 mmol l-1, before or after contraction with KCl, serotonin or PGF2 alpha significantly decreased maximal tension in rings with or without endothelium. Preincubation with HEPES buffer, 10 mmol l-1, significantly decreased maximal contractions to each agonist in rings with endothelium and to KCl and serotonin in rings without endothelium. HEPES, 30 mmol l-1, noncompetitively inhibited concentration-contraction curves to increasing concentrations of each agonist in rings with or without endothelium. Inhibition by HEPES was completely reversible with washing. The inhibitory effects of HEPES on responses to each agonist in rings with endothelium were significantly less in the dark or after coincubation with catalase. Unlike HEPES, effects of H2O2 were endothelium-dependent in that H2O2 caused contractions in rings with endothelium and relaxations in rings without endothelium. 5-(N,N'-dimethyl)-amiloride and 4,4'-diisothiocyanataostilbene-2,2'-disulfonic acid did not affect contractility in this preparation. These results show that HEPES exerts significant inhibitory effects on arterial smooth muscle contractility. The mechanism does not involve endothelium-dependent relaxation, effects on chloride channels or the sodium-hydrogen exchanger or generation of H2O2 by HEPES in the light.

Extracellular nucleotide-induced [Ca2+]i elevation in rat basilar smooth muscle cells.

BACKGROUND AND PURPOSE: Extracellular nucleotides play an important role in the regulation of vascular tone and may be involved in cerebral vasospasm after subarachnoid hemorrhage. The objective of this study was to investigate the receptor subtypes for nucleotides and their mechanisms of [Ca2+]i mobilization in cerebral vasculature. METHODS: Rat basilar smooth muscle cells were isolated by an enzymatic method. [Ca2+]i response, a large transient peak followed by a slowly decaying plateau. The potency of nucleotides to raise [Ca2+]i was ATP gamma S > or = UDP > or = ATP approximately UDP approximately TTP, indicating that P2u receptors were expressed in the rat basilar smooth muscle cells. The effect of UTP to release Ca2+ from internal stores was reduced by pertussis toxin, by the phospholipase C inhibitor 2-nitro-4-carboxyphenyl N,N-diphenylcarbamate, and by the Ca(2+)-pump inhibitor thapsigargin. The Ca2+ entry induced by UTP was partially attenuated by the receptor-operated Ca2+ channel blocker SK&F96365 and by the voltage-dependent Ca2+ channel blocker verapamil. P2 receptor antagonists suramin and, at higher concentrations, pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid reduced the effect of UTP. CONCLUSIONS: The results are the first demonstration that nucleotides activate G protein-coupled P2u receptors to mobilize [Ca2+]i in rat basilar smooth muscle cells.

Effect of P2-purinoceptor antagonists on hemolysate-induced and adenosine 5'-triphosphate-induced contractions of dog basilar artery in vitro.

OBJECTIVE: To test the hypothesis that the vasoactive effects of hemolysate of dog erythrocytes on dog basilar artery in vitro are caused by adenosine 5'-triphosphate (ATP). METHODS: Dog erythrocyte hemolysate was assayed for ATP by high-pressure liquid chromatography. Dog basilar arteries were cut into rings and studied under isometric tension to determine the effects of the P2-purinoceptor antagonists suramin, pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid, and reactive blue 2 on contractions induced by hemolysate, prostaglandin F2 alpha (PGF2 alpha), KCl, uridine 5'-triphosphate, and ATP. RESULTS: Dog erythrocyte hemolysate contained 34 mumol/L of ATP. Hemolysate produced concentration-dependent contractions of dog basilar artery. Suramin (100 mumol/L) significantly inhibited contractions to hemolysate, ATP, and uridine 5'-triphosphate but not to PGF2 alpha and KCl (P < 0.05). Pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid (100 mumol/L) caused a small but significant reduction of the contractions to hemolysate and did not affect contractions to PGF2 alpha and KCl. Reactive blue 2 (30 mumol/L) produced significant inhibition of contractions to hemolysate and PGF2 alpha but did not affect contractions to KCl. CONCLUSION: These findings suggest that ATP mediates a smooth muscle contractile response of hemolysate on dog basilar artery. Because erythrocyte cytosol is known to be important in the pathogenesis of vasospasm, these results suggest that ATP may contribute to the vasoconstriction that occurs in vasospasm.

Time course of changes in arterial relaxation following subarachnoid hemorrhage in dogs.

This experiment determined if the time course of inhibition of arterial relaxation correlates with angiographic vasospasm following subarachnoid hemorrhage (SAH) in dogs. Twenty-two dogs underwent cerebral angiography followed by SAH by 2 injections of blood into the cisterna magna. Dogs had repeated angiography and were sacrificed 4 (n = 5), 7 (n = 4), 10 (n = 4), 14 (n = 5), or 21 (n = 4) days later. Four dogs served as controls and underwent angiography only, followed by sacrifice. The basilar arteries were removed and studied under isometric tension to determine relaxations to acetylcholine and sodium nitroprusside. There was significant reduction in basilar artery diameter at each time after SAH (day 4: -52% +/- 10%, day 7: -37% +/- 10%, day 10: -54% +/- 10%, day 14: -37% +/- 10%, and day 21: -26% +/- 18%, p < 0.05, analysis of variance), although there were no pairwise differences in the degree of vasospasm over time. Relaxations to acetylcholine were significantly reduced at all times after SAH (p < 0.05, analysis of variance). Relaxations to sodium nitroprusside were significantly reduced 7 days after SAH. There was a significant linear correlation between increasing time after SAH and decreasing relaxation to acetylcholine. There was no correlation in univariate or multivariate analysis, between the time after SAH, the degree of vasospasm and the relaxation to acetylcholine or sodium nitroprusside. It is concluded that inhibition of arterial relaxation depends on the relaxant used and does not correlate with vasospasm. The lack of correlation between angiographic vasospasm and relaxation suggests that while the latter occurs after SAH, contractile processes may be more important in the pathogenesis of vasospasm.

Papaverine-sensitive vasospasm and arterial contractility and compliance after subarachnoid hemorrhage in dogs.

This study examined the relationship between papaverine-sensitive and -insensitive components of vasospasm, arterial contractility and compliance, and time after subarachnoid hemorrhage (SAH) in dogs. Eighteen dogs underwent angiography and then two intracisternal injections of blood. Angiography was repeated 4 (n = 5), 7 (n = 4), 10 (n = 4), or 14 (n = 5) days later. Papaverine, 100 to 200 mg, was infused into the basilar artery, and angiography was repeated. Four additional dogs had cerebral angiography only and served as controls. The basilar arteries were removed and studied pharmacologically. Significant vasospasm of the basilar artery was observed each time after SAH. Papaverine significantly reversed vasospasm at 4 and 7 days (88 +/- 6% and 63 +/- 11% of vasospasm reversed; analysis of variance, P < 0.05). The papaverine-insensitive component of vasospasm increased significantly with increasing time after SAH and with increasing severity of vasospasm. Arterial contractility and compliance decreased significantly with increasing time after SAH and were significantly related to the degree of papaverine-insensitive vasospasm but not to the severity of vasospasm. In conclusion, the majority of vasospasm early after SAH in dogs was caused by reversible vasoconstriction. The ability of papaverine to reverse vasospasm depended on the time after SAH and on the severity of vasospasm, a finding that may be important to the use of papaverine in humans. The pathological and biochemical basis for the association between papaverine-insensitive vasospasm and reduced arterial wall contractility and compliance remains to be determined.