SummaryDuring body cooling, a progressive thrombocytopenia is observed, with platelet sequestration mainly in the liver. Platelets return progressively to the circulation during re warming. In this work the presence of platelet clumps is demonstrated by electron microscopy inside the hepatic sinusoids of dogs cooled to 20° C by immersion in iced water. Such clumps were not found either before cooling or after body rewarming. Similar platelet clumps in the hepatic microcirculation were found in two other groups of dogs cooled and rewarmed as before, but previously treated with the antiaggregants sulphinpyrazone or ticlopidine. Another group of dogs was cooled and rewarmed by intra-abdominal circulation of physiological saline respectively at 4° C and 40° C. In these animals a similar decrease of circulating platelets was observed. However, just after re warming was started, with the body temperature still at 22° C, sequestered platelets came back abruptly to circulation. We conclude that hepatic platelet sequestration induced by hypothermia appears mainly due to local haemodynamic conditions.
After injection of 51Cr-labelled platelets, dogs were cooled down to 20 °C and rewarmed to 36 °C. Radioactivity increased over the hepatic area during cooling, to decrease again during rewarming. It increased continuously during the observation period over the splenic area. The inverse symmetry of the curves representing the radioactivity measured over the liver and in the peripheral blood together with the fact that splenectomy did not alter significantly the thrombocytopenia observed, strongly suggests that in the dog the liver is the main organ responsible for platelet sequestration during hypothermia.
Two groups of patients were submitted to electric coiivulsive therapy, one without pre-treatment (ECT) and the other after administration of thiopentone and succinylcholine (modified ECT). After ECT, there was a large increase in the blood level of catecholamines (noradrenaline -+ adrenaline), of factor VIII and of plasminogen activator. After modified ECT, the release of catecholamines and of factor VIII was significantly reduced, but hyperfibrinolysis took place as in ECT. These results suggest that while catecholamines are-probably not responsible for plasminogen activator release during stress, adrenergic mediation of the concomitant increase in factor VIII is highly probable.An increase in factor-VIII activity has been described after therapeutic electroshock (Mannucci et al, 1971) and other conditions of stress, such as muscular exercise (Rizza, 1961; Goudemand et al, 1962;Egeberg, 1963;Cohen et al, 1968) and haemorrhagic shock (Pina-Cabral, 1967). Concomitantly, a large increase in the blood level of plasminogen activator (
SummaryAfter the injection of DDAVP in 39 non-anaesthezised dogs (0.4 μg/kg) factor VIII: C activity rose to 145% of baseline values (p <0.0001) and the fibrinolytic potential of euglobulin precipitate rose to 196% (p <0.0001). The injection of DDAVP was repeated three times in each dog of a group of good responder animals at weekly intervals, but after: A) Pentobarbital anesthesia (30 mg/kg) - the increase of factor VIII: C was reduced from 164% to 116% (n = 11; p <0.0005) and the increase in fibrinolytic activity was reduced from 270% to 192% (n = 11; p <0.05). B) Injection of propranolol (1 mg/kg) - the increase of factor VIII :C was reduced from 167% to 110% (n = 13; p <0.0005) and there was no significant decrease of fibrinolytic activity (n = 13; n.s.). C) Splenectomy - the increase of factor VIII: C was reduced from 166% to 122% (n = 10; p <0.0005) and fibrinolytic activity was not significantly changed from 196% to 256% (n = 9; n.s.). There were no statistically significant differences in the increases of factor VIII :C and fibrinolytic potential of euglobulin precipitate after repeating only the injection of DDAVP three times in the same animal at weekly intervals (n = 5; n.s.). We conclude that the increases in factor VIII: C and fibrinolytic activities observed after DDAVP infusion in the dog are due to different mechanisms of action. Pentobarbital anesthesia reduced the increase of factor VIII: C and fibrinolytic activity, but on the other hand, beta-blockade and splenectomy influenced differently the behaviour of both biological activities.Injection of the synthetic analogue of vasopressin 1-deamino-8-d-arginine vasopressin (DDAVP) increases the plasma levels of factor VIII procoagulant activity (factor VIII: C) and plasminogen activator both in man and dog (1, 2, 3, 4).The mechanism of action of DDAVP in determining these responses is not well known. In this work, after having confirmed that DDAVP increases factor VIII: C and fibrinolytic activity in the blood of the unanaesthezised dog, and in order to clarify the mechanisms involved in these pharmacological effects, we repeated the DDAVP injection in animals previously submitted to propranolol, pentobarbital anesthesia and splenectomy.
SummaryA new case of congenital hypoprothrombinemia is described, in which the level of factor II in the propositus has been consistently near 1 per cent. Several specific assays of this factor have been used, including an immunochemical assay that rules out the presence of an abnormal molecule of prothrombin. The normal levels found for the other known coagulation factors, the lack of response to vit. K1 administration and the absence of a specific inhibitor, are all reasons to discard a secondary cause for this hypoprothrombinemia. Thromboplastin generation test was not only deficient, but it was also delayed. Serum composition was found responsible for this abnormality. The family pedigree of the propositus was compatible with autosomal recessive transmission of the disease.
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