Mediastinal Vascular Anomalies Causing Tracheal and Esophageal Compression and Obstruction in Childhood

Over an 11-year period, 22 children have been operated upon at the Hospital for Sick Children, Toronto, for vascular compression of the trachea and esophagus. Thirteen had a double aortic arch; three, a right aortic arch and left ligamentum arteriosum; three, an anomalous innominate artery; and one, an aberrant right subclavian artery. An unusual case of right aortic arch, aberrant left subclavian artery and left ligamentum arteriosum is reported for the first time. One child with an anomalous left pulmonary artery producing emphysema of the right lung is also described. One death occurred during the process of intubation, and three patients died postoperatively despite tracheotomy. These children were in serious condition, and the importance of rigid preoperative and postoperative care, avoiding tracheotomy if possible, is emphasized.     

Surgical complications of endoscopic sphincterotomy

Endoscopic sphincterotomy (papillotomy) was performed in 289 patients for choledocholithiasis (250, of whom 223 had undergone cholecystectomy previously), papillary stenosis or spasm (32) and ampullary neoplasm (7). The complications encountered in 39 patients were hemorrhage (15 patients), perforation (4), hemorrhage and perforation (1), cholangitis (5), pancreatitis (11), impaction (1) and others (2). Laparotomy was required in seven of these patients for hemorrhage (two), perforation (two), hemorrhage and perforation (one), pancreatitis (one) and impaction (one). Bleeding required duodenotomy with an extension of the sphincterotomy incision to control hemorrhage, and a formal sutured sphincteroplasty. Perforation occurred at the junction of the distal bile duct and duodenum and was managed by mobilization of the duodenum, with T-tube drainage through the perforation, and sutured closure. A pancreatic abscess following pancreatitis required surgical drainage. An impacted Dormia basket with entrapped stone in the bile duct required duodenotomy for its removal. There was a high risk of perforation in those patients who did not have choledocholithiasis or who had had a previous Billroth II gastrectomy. There were two deaths but the overall complication rate of 2.4% is considered low, because many of the patients were elderly or debilitated.     

Effect of the concentration of Ca2+ in the suspending medium on the responses of human and rabbit platelets to aggregating agents

The effect of the concentration of Ca2+ in the suspending medium of human and rabbit platelets on aggregation, release of 14C-serotonin, and TXB2 formation in response to ADP, thrombin, 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (PAF), collagen and arachidonic acid was studied in either platelet-rich plasma anticoagulated with D-phenylalanyl-prolyl-arginyl chloromethylketone (PPACK) or citrate, or suspensions of washed platelets in modified Tyrode-albumin solutions containing 1 mM Mg2+ and concentrations of added Ca2+ ranging from 0 to 5 mM. In response to ADP, thrombin, or PAF, human platelets were stimulated to form TXA2 by close platelet contact in a low-Ca2+ medium; at physiological concentrations of Ca2+, TXB2 formation was much less and declined progressively as the concentration of Ca2+ was raised. When the formation of TXA2 was blocked with aspirin or indomethacin, aggregation and release by human platelets were strongest at physiological concentrations of Ca2+. Rabbit platelet responses differed markedly from those of human platelets because close contact of rabbit platelets in a low-Ca2+ medium did not promote TXA2 formation. Rabbit platelet responses were more strongly inhibited by the lack of added Ca2+ in the medium than the responses of human platelets, possibly because rabbit platelets do not contain releasable Ca2+. In all studies of human platelets in media with low concentrations of Ca2+, the additional contribution to platelet responses of TXA2 formed because of close platelet contact should be considered because TXA2 formation is not usually stimulated in this way at physiological concentrations of Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral hemorrhage following heart surgery.

The authors report a study of the problem of intracranial hemorrhage in 16 children following cardiac surgery, four studied clinically, and 12 by postmortem pathological review. Eleven children sustained subdural hematomas of varying sizes, one had a massive extradural clot, and four had intracerebral clots. The pre-, intra-, and postoperative data of these 16 patients are presented, but the specific factors causing the intracranial hemorrhage remain unexplained. The neurological course was similar to that of patients with an intracranial space-occupying lesion, and fundamental neurosurgical management principles for the treatment of this potentially reversible process should be observed.     

Serotonin transport and storage in rabbit blood platelets—The effects of reserpine and imipramine

Serotonin transport and storage in suspensions of washed rabbit platelets were investigated by following the exchange of platelet-bound [³H]serotonin and [¹⁴C]serotonin added to the suspending medium. Assuming a three-compartment system (suspending medium, platelet cytoplasm and platelet storage organelles), the transfer rates between the different compartments were calculated from the exchange data by statistical analysis. Reserpine reduced the storage organelle serotonin content by inhibiting the transfer of serotonin from the cytoplasm into the amine storage organelles. It also reduced the fraction of serotonin in the cytoplasm transferred per unit of time into the suspending medium. Imipramine (20 μM) inhibited the uptake of serotonin across the platelet plasma membrane into the cytoplasm and reduced the fraction of cytoplasmic serotonin transferred per unit of time into the suspending medium. At this concentration it had no effect on serotonin transport across the amine storage organelle membrane in either direction. The method used allows the serotonin transfer rates across the platelet plasma membrane to be distinguished from those across the amine storage organelle membrane in intact cells, and permits these transfer rates to be estimated simultaneously. The method may be used for determining the effects of drugs that interfere with transport and storage of biogenic amines and in defining the defects in diseases with abnormal transport or storage of biogenic amines.     

Platelet interactions with the endothelium and the subendothelium: the role of thrombin and prostacyclin.

The adherence of 51Cr-labeled platelets to rabbit aortae everted on probes rotated in platelet-red cell suspensions has been measured. Platelet adherence to the subendothelium exposed by passage of a balloon catheter before everting the aortae was inhibited by compounds that increase platelet cyclic AMP levels (PGE1, PGI2 or dipyridamole). These agents, however, did not abolish platelet adherence to the subendothelium. Aspirin treatment of the vessel wall was used to block PGI2 production; platelet adherence to the surface of the 'undamaged' aorta and the subendothelium was studied following this treatment. Since aspirin treatment of the 'undamaged' vessel wall did not cause platelets to adhere to it, it seems unlikely that PGI2 formation by the vessel wall is the mechanism that prevents platelet adherence to normal endothelium. In addition, PGI2 formation by the vessel wall does not appear to influence platelet adherence to the subendothelium, since adherence was not increased by aspirin treatment of the damaged wall. Thrombin treatment of the 'undamaged' vessel wall increased platelet adherence to the surface, but the adherent platelets were seen to be adherent only to small areas where the endothelium was lost or damaged. Heparin reversed the effect of thrombin. Similar results were found when the subendothelium was exposed to thrombin or thrombin and heparin.     

Effects of reserpine and serotonin on adenine nucleotide metabolism and glucose oxidation of washed rabbit platelets

Reserpine inhibits the transfer of ATP from the metabolically active pool into the releasable pool (amine storage organelles) of washed rabbit platelets. Since reserpine is known to interfere with oxidative phosphorylation of isolated mitochondria, possible effects of reserpine on the energy metabolism of intact platelets were examined with the aim of determining whether or not such effects could explain the reduced transfer of metabolic ATP into the releasable pool of ATP. Reserpine caused a small increase in [¹⁴C]hypoxanthine and [¹⁴C]inosine accumulation in a suspension of washed rabbit platelets prelabeled with [¹⁴C]adenosine or [¹⁴C]adenine. Reserpine also caused increased oxidation of [¹⁴C]glucose. Serotonin mimicked these effects of reserpine, and imipramine inhibited the serotonin-induced as well as the reserpine-induced increases in [¹⁴C]hypoxanthine and [¹⁴C]inosine formation and glucose oxidation. However, imipramine did not prevent the reserpine-induced inhibition of [¹⁴C]ATP transfer from the metabolically active pool into the releasable pool. It is concluded, that the effects of reserpine on energy metabolism are at least partially attributable to the increased demand for energy for the uptake of serotonin, liberated from the platelets during incubation with reserpine, and not to uncoupling of oxidative phosphorylation. Furthermore, the small decrease of the metabolically active ATP pool upon incubation of platelets with reserpine cannot explain the reduced transfer of ATP from the metabolic pool into the amine storage granule pool.     

Epinephrine-induced aggregation of rabbit platelets refractory to ADP

The mechanisms involved in platelet aggregation induced by epinephrine are unclear. Although epinephrine does not aggregate washed rabbit platelets, platelets made refractory to ADP will aggregate in response to epinephrine in the presence of ADP. We have examined whether the mechanism(s) by which epinephrine induces aggregation of refractory platelets involves fibrinogen binding and Ca2+ association. With normal platelets, ADP causes aggregation, fibrinogen binding and Ca2+ association in a medium containing 0.2 mM 45Ca2+. After 3 min of incubation with ADP, fibrinogen dissociates from platelets, but 45Ca2+ does not. Epinephrine alone does not cause aggregation, fibrinogen binding or 45Ca2+ association. Platelets that are refractory to ADP do not aggregate and bind fibrinogen upon addition of ADP, but aggregate and bind fibrinogen in response to epinephrine, provided ADP is still present. These effects of epinephrine are mediated by the alpha-adrenergic receptor since they are blocked by phentolamine or verapamil and potentiated by propranolol. However, epinephrine-induced aggregation of platelets refractory to ADP does not involve further detectable increase in the amount of 45Ca2+ associated with the platelets.