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The object of the paper is to analyze changes in modal and port allocation of general cargo flows in Sweden's foreign trade between 1960 and 1976. It summarizes some results of a forthcoming report on the project ‘Tendencies in Liner Shipping’ financed by the ‘Transport Research Delegation’, Stockholm.

The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitroin whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2and the rate of SPA (measured as a percentage of changes in free platelet number in whole blood) were higher (p<0.01) in MI than PC. The de-aggregatory effect of PGI2in whole blood was higher (p<0.05) on the first day of MI than on day 14 following MI. The highest de-aggregatory effect of PGI2was found in whole blood of patients with MI complicated by ventricular fibrillation. In neither of the groups did the de-aggregatory effect of PGI2correlate with patients' age, haematocrit, erythrocyte and leucocyte counts, triglycerides, HDL, LDL or total cholesterol levels. In the MI group, de-aggregatory effect of PGI2was correlated with free platelet concentration (r-0.59, p<0.05), elevation of glutamic oxalacetic transaminase (r0.53, p<0.05) and creatinine Phosphokinase (r0.69, p<0.001). The de-aggregatory effect of PGI2in blood of patients with evolving MI did not differ from that in PC. It is concluded that the increased rate of SPA and formation of PGI2-sensitive platelet aggregates in vitroin whole blood of MI patients are secondary to myocardial necrosis.

The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitro in whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2 and the rate of SPA (measured as a percentage of changes in free platelet number in whole blood) were higher (p<0.01) in MI than PC. The de-aggregatory effect of PGI2 in whole blood was higher (p<0.05) on the first day of MI than on day 14 following MI. The highest de-aggregatory effect of PGI2 was found in whole blood of patients with MI complicated by ventricular fibrillation. In neither of the groups did the de-aggregatory effect of PGI2 correlate with patients' age, haematocrit, erythrocyte and leucocyte counts, triglycerides, HDL, LDL or total cholesterol levels. In the MI group, de-aggregatory effect of PGI2 was correlated with free platelet concentration (r=-0.59, p<0.05), elevation of glutamic oxalacetic transaminase (r=0.53, p<0.05) and creatinine Phosphokinase (r=0.69, p<0.001). The de-aggregatory effect of PGI2 in blood of patients with evolving MI did not differ from that in PC. It is concluded that the increased rate of SPA and formation of PGI2-sensitive platelet aggregates in vitro in whole blood of MI patients are secondary to myocardial necrosis.

M-mode echocardiography and indirect blood pressure measurements were used to examine nemodynamics in three groups of pregnant patients: 19 who were preeclamptic, nine who had essential hypertension, and 19 who were normotensive. The preeclamptic patients had significantly lower heart rate (68.4 versus 74.7 beats/min, p < 0.05), stroke volume (89 versus 101 ml; p < 0.02), and cardiac index (5.9 versus 7.5 L/min/sq m; p < 0.001) than those of control patients matched for age, parity, and gestational age. The mean values for heart rate, stroke volume, and cardiac index in patients with essential hypertension were not significantly different from those in the control group; however, the former had widely varying individual hemodynamic patterns. The significant inverse correlation was found between cardiac index and mean blood pressure (r = −0.602) in preeclamptic patients. There was a positive correlation between maternal cardiac index and infant birth weight (r = 0.813) and also an inverse relationship between systemic vascular resistance and infant birth weight (r = −0.890) in this group. Possible explanations for these findings are discussed.

The hemodynamic profile of 26 patients with gestational hypertension (GH) was compared to that of 47 matched for gestational age normotensive pregnant women (NP). The patients with GK studied at 32 - 36 weeks of gestation had significantly higher cardiac index (CI) (4.81 versus 4.35 L/min/sqm, p < 0.01) than control patients. CI in GH group studied at 37 - 41 weeks of gestation was also higher than in their control counterparts (4.69 vs. 4.14 L/min/sqm, p < 0.02). The heart rate averaged 80.9 beats) min in this GH group, compared with 7 2.8 beats/min in a group of normotensive controls (p < 0.01). The calculated systemic vascular resistance did not differ between GH and NP groups, despite significant differences in arterial pressure. The fetal outcome in GH group was uneventful and it seems to be accounted for by normal values of vascular resistance in these patients. The hyper kinetic circulatory state in women with GH resembles the pattern described in early forms of essential hypertension in nonpregnant patients. It is concluded that hemodynamic observations in GH patients supports previous suggestions that this condition may represent a latent essential hypertension.

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