SummaryFifteen haemostasis parameters have been measured in 48 normal persons, 36 diabetics without and 44 with complications and 27 with peripheral arterial disease. Since the patients groups are older than normals, part of the differences are due to age. However, the differences are significant between normals and patients. They become highly significant for the diabetics with complications and nephropathy (Table 7). In diabetics without complications factor VIII functions, fibrinogen and thrombin time are related to age whereas there is a negative correlation for the fibrinolytic activity and antithrombin III. The diabetic complications shade off the correlations, which subsist only for VIIIR: CoF, VIIIR: Ag, ATIII and lysis before stasis. With Hbalc as dependent variable VIIIR:CoF is the only significant predictor variable in diabetics (Table 9).

SummaryWe have studied 155 subjects, 48 normals, 36 diabetics without complications, 44 with complications and 27 patients with macroangiopathy. β-Thromboglobulin (β-TG) and platelet factor 4 (PF4) are elevated in the patients groups. There is no correlation between the plasma levels of β-TG and the stages of either retinopathy or macroangiopathy or nephropathy. The difference is more marked between normals and diabetics with neuropathy (p = 0.026). The aggregation response to ADP and platelet activating factor (PAF) is enhanced at lower stimulator concentration. Using the β-TG, PF4 and aggregation values the discriminant analysis allows a distinction of several subgroups especially with nephropathy and neuropathy (Table 6).

SummaryThe contact phase has been studied in diabetics and patients with macroangiopathy. Factor XII and high molecular weight kininogen (HMWK) are normal. C1-inhibitor and also α2-macroglobulin are significantly elevated in diabetics with complications, for α1-macroglobulin especially in patients with nephropathy, 137.5% ± 36.0 (p <0.001). C1-inhibitor is also increased in vasculopathy without diabetes 113.2 ± 22.1 (p <0.01).Prekallikrein (PK) is increased in all patients’ groups (Table 2) as compared to normals. PK is particularly high (134% ± 32) in 5 diabetics without macroangiopathy but with sensomotor neuropathy. This difference is remarkable because of the older age of diabetics and the negative correlation of PK with age in normals.

SummaryIn 306 subjects, 217 without and 89 with peripheral arterial disease (PAD), VIIIR:Ag and α2-antiplasmin are significantly higher in PAD (p < 0.01). In the PAD negative group the ratio α2-antiplasmin/antithrombin III activity is significantly higher 1.11 ± 0.3 in the patients with an abnormal exercise ECG typical of coronary disease than in normal subjects 1.02 ± 0.2 (p < 0.05). In the PAD positive group antithrombin III concentration is higher in patients with a normal exercise ECG than in patients with abnormal exercise ECG (p < 0.05). The same is true for α2- antiplasmin but not for the antithrombin III activity. Fibrinogen and VIIIR:Ag are higher in patients with a previous myocardial infarction, however, the age is also significantly different as compared to the group without previous myocardial infarction. Disturbance of the cerebral arterial circulation is characterized by an elevation of VIIIR:Ag and of α2-antiplasmin as comapred to the values obtained in patients without this complication. There is a general tendency towards higher α2-antiplasmin values with the extension of the arterial disease.

This study was designed to assess effects of acute apelin administration on cardiac and coronary performance in anesthetized, open‐chest swine. Systemic intravenous administration of pyr‐apelin 13 (3nM to 1μM) did not significantly affect coronary blood flow (0.37 + 0.07 to 0.29 + 0.06 mL/min/g; p=0.93) or myocardial oxygen consumption (46.47 + 8.64 to 36.84 + 5.93 μL O2/min/g; p=0.91). However, pyr‐apelin 13 elicited a dose‐dependent peripheral dilator response as mean aortic pressure was decreased by 12 + 4 mmHg at 1μM pyr‐apelin 13 (p=0.001). Left ventricular pressure volume relationships were assessed to establish the potential inotropic effects of pyr‐apelin 13. No changes in cardiac output (2074 + 347 to 2052 + 185 mL/min; p= 0.96), stroke volume (35 + 2 to 33 + 1 mL; p=0.34) or end systolic pressure volume relationship (Ees 10.55 + 3.78 to 18.23 + 3.84; p = 0.20) were noted in response to pyr‐apelin 13 (3nm to 1μM). Mass spectroscopic analyses of plasma samples at each dose confirmed a ~700 fold increase in plasma apelin concentrations (0.39 + 0.14 to 287.55 + 43.58 ng/mL; p<0.001) with treatment. Taken together, these data support that acute systemic administration of pyr‐apelin 13 dose‐dependently decreases arterial pressure via reductions in systemic vascular resistance, independent of alterations in cardiac inotropic function.