CD36 autoantibodies and thrombotic diathesis, thrombocytopenia and repeated early fetal losses.

Background And Objectives: Autoantibodies to CD36, a platelet glycoprotein, have been found in patients with thrombotic thrombocytopenic purpura, and in those with lupus-like anticoagulant with thrombotic complications.

Materials And Methods: Conventional hematologic and laboratory methods were used. The patient was a pregnant woman, who had had two early fetal losses separated by a normal offspring.

Primary thrombocythemia and pregnancy: treatment and outcome in fifteen cases.

Pregnancy in patients with primary thrombocythemia (PT) is reported to be often complicated by recurrent abortion and fetal growth retardation. Fifteen pregnancies in nine patients with PT are reported. Nine pregnancies had a good outcome, with the birth of a healthy infant.

The heart rate after inhibition of nitric oxide release in the anaesthetized dog.

1. The effect of nitric oxide (NO) inhibition on heart rate was studied in anaesthetized vagotomized dogs. 2.

Myocardial, neural and vascular aspects of ischemic preconditioning.

Ischemic preconditioning can be obtained with brief coronary occlusions. It has been studied in different animal species including dogs, pigs, rabbits and rats. The suggested duration of the occlusions ranges from four periods of 5 min, separated from each other by 5 min of reperfusion, to one period of 2.

The role of nitric oxide in the initiation and in the duration of some vasodilator responses in the coronary circulation.

In the coronary bed vasodilation can be mediated by several mechanisms including endothelium-produced nitric oxide. To examine the contribution of nitric oxide, three different techniques to cause vasodilation in the coronary vessels were used in the anaesthetized dog: intracoronary injection of 1 microgram acetylcholine, sudden reduction of the aortic blood pressure inducing a myogenic response and transient occlusion followed by release of the left circumflex coronary artery causing reactive hyperaemia. Each manoeuvre was performed before and after intracoronary administration of 100 mg N-nitro-L-arginine, an inhibitor of the synthesis of nitric oxide.

Properties of the myocardium affecting the coronary circulation.

The mean coronary blood flow increases in response to an increase in myocardial oxygen consumption. Conversely, an increase in coronary perfusion is itself reported to induce an increase in myocardial oxygen consumption. Such an effect can be explained by stretching of the myocardial fibers surrounding the vessels, which become more distended with an increase in perfusion.

Heart rate decrease after inhibition of nitric oxide release in the anaesthetized dog.

In 5 anaesthetized vagotomized dogs the administration of an inhibitor of the synthesis of nitric oxide (NO) was seen to reduce the heart rate, although the arterial pressure was prevented from increasing. Such a finding suggests that the inhibition of nitric oxide release can produce bradycardia without the involvement of baroreceptor reflexes. Since NO inhibition is known to increase the concentration of adenosine in the myocardium, in 3 additional dogs, dipyridamole, which also potentiates the effect of adenosine, was infused: a reduction in heart rate was observed also in these animals.

Control of coronary blood flow by endothelial release of nitric oxide.

1. Nitric oxide (NO) is released from vascular endothelium following conversion of L-arginine to L-citrulline by calcium-calmodulin-dependent 'constitutive' NO-synthase. 2.

Transient effects of quick changes in myocardial metabolism and perfusion pressure on coronary vasomotor responses.

The effects of transient changes in coronary transmural pressure on the coronary vasomotor tone were studied in 23 anesthetized dogs. Increases and decreases of the coronary transmural pressure were obtained by constrictions of various duration (2 to 20 s) of the descending thoracic aorta. The maneuvers were performed in animals with intact cardiac innervation, with the vagi sectioned and with vagal section together with beta-blockade.

Increases in coronary intravascular pressure during maximal coronary vasodilatation in the anaesthetized dog.

The present study was planned to investigate whether or not, after complete suppression of vasomotor tone, increases in intravascular blood pressure distend the coronary vasculature causing passive decreases in the resistance to the coronary arterial inflow during the diastole. In anaesthetized dogs, aortic and left ventricular pressures and flow in the left circumflex coronary artery were recorded. Coronary flow was derived using an electromagnetic flowmeter.

The effect of the inhibition of the endothelial release of nitric oxide on coronary reactive hyperaemia in the anaesthetized dog.

The effect of the inhibition of the endothelial release of nitric oxide (NO) on the hyperaemia which follows a 10 s coronary occlusion was studied in anaesthetized dogs. Aortic blood pressure was kept constant during the experiments using an arterial reservoir connected with the femoral arteries. The blood flow in the left circumflex coronary artery was recorded with an electromagnetic flow probe.

Ventricular distension and diastolic coronary blood flow in the anaesthetized dog.

There appears to be no agreement as to whether or not an increase in diastolic left ventricular pressure and/or volume can cause a decrease in diastolic coronary blood flow. We investigated the problem in the anaesthetized dog using a flaccid freely distensible latex balloon inserted into the left ventricle with the animal on extracorporeal circulation and the coronary perfusion pressure constant at about 45 mm Hg. Maximal vasodilatation and suppression of autoregulation in coronary vasculature was obtained by the intracoronary infusion of dipyridamole (10-40 mg/h).

Endothelium and coronary reactive hyperaemia.

The effect of the inhibition of the endothelial release of nitric oxide (NO) on the hyperaemia which follows a 10 s coronary occlusion was studied in 5 anaesthetized dogs, keeping aortic blood pressure constant. The left circumflex coronary artery was occluded before and after the intracoronary infusion of an inhibitor of NO (LNNA). After LNNA, the peak amplitude of the hyperaemia was the same but the duration was reduced almost to a half of the control value; it is suggested that a myogenic vasodilatation is involved in the amplitude of the reactive hyperaemia, while the reduction in the duration of the hyperaemia after the inhibitor could result from the shear stress being less effective in causing the release of NO during the first part of the hyperaemia.

[The effect of maximal vasodilation on the distensibility of the coronary vascular bed].

This study aimed at investigating the changes in coronary vascular resistance induced by sudden increases in transmural pressure in the presence of a maximally vasodilated coronary bed. In anaesthetized open-chest dogs under artificial ventilation, aortic blood pressure, left ventricular pressure and the flow in the left circumflex coronary artery were recorded. The flow was derived by means of an electromagnetic flowmeter.

Energetics of best performances in middle-distance running.

Oxygen consumption (VO2) and blood lactate concentration were determined during constant-speed track running on 16 runners of intermediate level competing in middle distances (0.8-5.0 km).

The effect of pure right ventricular ischemia on right and left ventricular performance in the anesthetized dog.

This study was planned to investigate the effect of ischemic dysfunction of the free wall of the right ventricle on right and left ventricular performance in the presence of a normally contracting interventricular septum. The experiments were performed in 6 anesthetized dogs in which echocardiogram, electrocardiogram, aortic blood pressure and left and right ventricular pressure were recorded. In the dog, the contractility of the septum is not affected by the occlusion of the right coronary artery which does not perfuse this part of the myocardium.

"Resistance" to left ventricular outflow studied in anesthetized dogs.

A simple method is proposed to determine resistance to left ventricular output from the evaluation of a parameter Z, given by the ratio of peak systolic pressure and the corresponding instantaneous blood flow. The method, derived from the basic equation of the Windkessel model, is applied to analyze pressure and flow data measured in the ascending aorta of anesthetized dogs. The Z values obtained in this way are found to be closely related to resistance calculated from the ratio of mean aortic pressure and mean flow over the cardiac cycle.

Coronary flow and left ventricular pressure during diastole in the anaesthetized dog.

There is controversy about the effect of left ventricular pressure on resistance of the intramyocardial coronary vessels. In anaesthetized dogs the effect of left ventricular pressure on coronary flow during diastole was studied using an extracorporeal circulation and allowing the heart to contract and relax isovolumically. At constant coronary perfusion pressure of about 45 mmHg with maximal coronary vasodilatation, produced by dipyridamole, increases in diastolic left ventricular pressure to 22 mmHg, producing a volume of 50 ml, did not affect diastolic coronary flow.

[Ventricular volume and coronary flow].

This study aimed at investigating the role of ventricular volume (VV), left ventricular pressure (LVP) and myocardial contractility in causing changes in coronary flow (CF), in the absence of autoregulation. Changes in VV and, consequently, in LVP and myocardial contractility were induced in 5 anesthetized dogs using an extracorporeal circulation including a heart-lung machine. Left VV was changed in steps of 10 ml, from a lowest value of 10 ml to a maximum value of 70 ml and back, by introducing and subtracting different volumes of water in and from a latex balloon placed in the left ventricle.

The mechanical effects of rhinoceros horned viper (Bitis nasicornis) venom on the isolated perfused guinea-pig heart.

In the guinea-pig Langendorff heart preparation, addition of 0.1 mg Bitis nasicornis venom to the perfusion solution caused transient increases in heart rate (HR) and left ventricular systolic pressure (LVSP) with peak increases at 2 min. With higher doses (0.

The haemodynamic effect of Bitis nasicornis (rhinoceros horned viper) venom.

1. Intravenous venom (0.0625 mg/kg) in the dog caused an immediate increase in coronary blood flow due to a fall in coronary vascular resistance (CVR).

The mechanical and electrical effects of rhinoceros viper (Bitis nasicornis) venom on the isolated perfused guinea pig heart and atrial preparations.

The mechanical and electrical effects of the venom of Bitis nasicornis were studied on the guinea-pig Langendorff and left atrial myocardium preparations. While Langendorff preparations were treated with individual doses of 0.1, 0.

Acidotic effect of gaboon viper (Bitis gabonica) venom in the urethane-anaesthetized rat.

1. Intravenous venom (4 mg/kg) caused a non-compensated metabolic acidosis. 2.

Flow cytometric analysis of leukocytes eluted from haemodialysers.

The cellular immune system is impaired in uraemic and haemodialysed patients. We describe a method of studying leukocytes eluted from dialysers at the end of the dialysis session, and we have studied five haemodialysers: cuprophane (CU), cellulose acetate (CA), polymethylemethacrylate (PMMA), polyacrylonitrile (PN), and polysulphone (PS). The analysis was performed by flow cytofluorimetry using monoclonal antibodies.