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Biomedical subjects

P Pagliaro

Publications and source records attributed to P Pagliaro.

At least 19 recordsLinked to original sources
PubMed1998

The energy cost of level walking before and after hydro-kinesi therapy in patients with spastic paresis.

In this study the energy cost of level walking was measured in 23 patients with stationary spastic paresis before and after a two-week treatment (45 min daily) of hydro-kinesi therapy, the latter consisting of passive and active movements in warm (32 degrees C) sea water, free swimming and water immersion walking. Among the subjects (80.2 +/- 13.2 kg body mass; 56.0 +/- 14.6 years of age; 10.7 +/- 6.6 years of duration of spasticity), 12 were affected by hemiparesis, 4 by multiple sclerosis and 7 by spinal cord injury. The energy cost of level walking (Cw) was measured before and after therapy from the ratio of the overall steady-state oxygen consumption to the effective speed of progression. The differences in Cw due to the treatment, at matched speeds, were found to be negligible at speeds higher than 0.75 m.s-1 (less than 5%) but to increase, with decreasing speed, up to about 17% at 0.1 m.s-1. The treatment was therefore effective in improving the gait characteristics of the subjects, through a decrease of their Cw, mainly at low speeds of progression.

Aged↗
PubMed1998

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility.

The present study was planned to investigate the effect of left ventricular pressure and inotropic state on coronary arterial inflow in systole in the anaesthetized dog. A wide range of left ventricular systolic pressures, including the physiological range, were studied. Experiments were done under conditions of maximal vasodilatation and low perfusion pressure in order to avoid vascular autoregulative interference and to keep the microvascular pressure within the normal range. In five anaesthetized dogs, perfused with extracorporeal circulation system, ventricular volume was changed from 20 to 50 ml in steps of 10 ml by filling an intraventricular latex balloon, and the related changes in left ventricular pressure and coronary flow were measured. The volume was then extended to 70 ml to obtain an overstretch which induced a transient decrease in cardiac contractility. During the period of low cardiac contractility the volume was brought back to 20 ml in steps of 10 ml. Systolic ventricular pressure changed with volume but was lower during the period of low contractility. For systolic pressures below 100 mmHg there was no significant relationship between pressure and coronary systolic flow, but the relationship shifted to higher flows during low contractility. For systolic pressures above 100 mmHg systolic coronary flow decreased significantly when systolic pressure increased. In this case the slopes of the relationships were not significantly different before and after the reduction in contractility. These findings suggest that for systolic pressures less than 100 mmHg (i.e. below the physiological range) the shielding effect of the contracting ventricle prevents the ventricular pressure from being transmitted in the myocardial wall. When systolic pressure exceeds 100 mmHg the shielding effect is overcome and the amplitude of the systolic flow reduction varies with ventricular pressure.

Acid-Base Equilibrium↗
PubMed1997

The Gaboon viper, Bitis gabonica: hemorrhagic, metabolic, cardiovascular and clinical effects of the venom.

The effects of Bitis gabonica venom have been studied in several animal species, including the monkey, dog, rabbit, rat and guinea pig. Further information has been provided by observations on the effects of snake bite in man. Bitis gabonica venom exerts a number of cytotoxic and cardiovascular effects: cytotoxic effects include widespread hemorrhage, caused by the presence of two hemorrhagic proteins. These hemorrhagins bring about separation of vascular endothelial cells and extravasation of blood into the tissue spaces. Metabolic alterations include decreased oxygen utilization by tissues and increased plasma glucose and lactate concentrations. Metabolic non-compensated acidosis has also been seen in the rat as a consequence of the cytotoxicity of the venom. Cardiovascular effects include disturbances in atrio-ventricular conduction and reduction in amplitude and duration of the action potential brought about by a decreased calcium membrane conductance. A progressive decrease in myocardial contractility can also be attributed to the decreased calcium conductance, which together with the severe acidosis may cause death in experimental animals. A severe, though reversible, vasodilatation was observed after envenomation due to unidentified compounds in the venom. In man, envenomation causes a variable clinical picture depending on the time course and severity of envenomation. Frequently seen effects include hypotension, hemorrhage at the site of the bite and elsewhere and disseminated intravascular coagulation. Envenomation can be satisfactorily treated with antivenom.

Animals↗
PubMed1997

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. Despite severe thrombocytopenia, she was asymptomatic. RESULTS: Serological investigations were strongly suggestive of CD36 autoantibodies. Neither clinical nor laboratory data were typical of those usually associated with cd36 autoantibodies, namely thrombotic thrombocytopenic purpura (TTP), systemic lupus erythematosis (SLE), or prothrombotic compliance. Prophylaxis with salicylates and prednisone was started at the 8th week of gestation, and an offspring with mild thrombocytopenia was delivered by cesarean section at the 32nd week of gestation because of abruptio placentae. CONCLUSIONS: There may be a cause-and-effect relationship between early fetal losses and CD36 autoantibodies.

Abortion, Habitual↗
PubMed1997

[Mechanisms of ischemic preconditioning: relation with ischemia-reperfusion injury].

If a coronary occlusion long enough to produce a myocardial infarction is preceded by one or more brief periods of occlusion, the infarct size is reduced with respect to the area at risk. Also the ischaemia reperfusion injury is remarkably reduced. Such effects form the ischaemic preconditioning. Ischaemia-reperfusion injury is attributed to a Ca2+ overload of the myocardial fibres together with an inadequate resynthesis of ATP, a loss of membrane phospholipids and a release of free oxygen radicals. The inadequate resynthesis of ATP is responsible for an increased concentration of nucleosides and purinic bases with swelling of the myocardial fibres. The cell Ca2+ overload depends on a reduced activity of the ionic pumps caused by the oxygen lack during ischaemia. During reperfusion the vascular endothelial cells of the previously ischaemic area release free oxygen radicals in response to the activity of the xanthine-oxidase on hypoxanthine produced by the ischaemic myocardium. This initial release of oxygen radicals is responsible for the adhesion of neutrophils to the endothelium. After adhesion also the neutrophils release free radicals due to the activity of NADPH-oxidase on molecular oxygen. Myocardial, neural and endothelial mechanisms account for the protective effect of preconditioning. Myocardial mechanisms include the release of adenosine as well as of antioxidant enzymes. Adenosine, which activates protein-kinase C, favours the phosphorylation of a protective protein, whereas the antioxidant enzymes impair the activity of the free oxygen radicals. Preconditioning may also involve the synthesis of a heat shock protein. Neural mechanisms are represented by a reduced release of noradrenaline from the sympathetic nerve endings and a reduced sensitivity of myocardium to noradrenaline. Finally, vascular endothelial cells take part in preconditioning by means of an increased production of nitric oxide which seems to exert a protection against arrhythmias.

Animals↗
PubMed1996

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. There were two spontaneous abortions and three intrauterine deaths. One pregnancy was electively terminated after extensive thrombosis in the splanchnic district requiring surgical entero-resection. In five pregnancies the mother received no treatment; in ten pregnancies acetylsalicylic acid (ASA) was prescribed to the mother as soon as she was found pregnant, subcutaneous heparin was added from the middle trimester in seven cases. In patients treated with ASA and subcutaneous heparin pregnancies had a good outcome. Administration of ASA and heparin during pregnancy appears to improve the outcome in patients with PT and can prevent severe maternal complications, but requires close monitoring.

Adult↗
PubMed1996

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 2.5 min. In addition to the reduction of the size of a subsequent infarction, preconditioning is responsible for the attenuation of the ischemia-reperfusion injury. The protection has a short duration and does not exceed two hours. Myocardial, neural and endothelial factors are involved in preconditioning. The myocardial component includes an increased release of adenosine with activation of A1 adenosine receptors, the activation of a protein-kinase C and possibly of antioxidant enzymes. The neural component includes a reduction in the release of noradrenaline from the postganglionic sympathetic fibers and a reduced myocardial sensitivity to noradrenaline. The increased myocardial release of adenosine, together with the reduced adrenergic activity, is consistent with the reduction in myocardial metabolism which has been observed after preconditioning. The coronary vascular endothelium is concerned in an increased release of nitric oxide which seems to be responsible for a prevention of reperfusion arrhythmias. In addition to the protective effect exerted on the myocardium, ischemic preconditioning seems to be responsible for a change in the coronary responsiveness to short periods of occlusion followed by release. This change in responsiveness is mainly represented by a greater velocity of the increase in flow occurring in the coronary reactive hyperemia.

Animals↗
PubMed1996

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. The effect of changes of baroreceptor stimulation was prevented using an arterial pressure reservoir. 3. After NO-inhibitor (Nitro-L-arginine), heart rate decreased by 8% in spite of an unchanged pressure. 4. When upstream pressure was increased by constriction of the descending aorta, heart rate decreased by 4% before and after inhibition. Owing to the vagotomy this decrease was attributed to a sympathetic tone reduction following baroreceptor stimulation. 5. The results show that NO-inhibition reduces heart rate independently of an increased baroreceptor stimulation and does not reduce the basal sympathetic control on the sinus-atrial node.

Anesthesia, General↗
PubMed1995

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. In contrast to previous investigations, the inhibition of nitric oxide synthesis was prevented from causing an increase in blood pressure by the use of a blood-pressure-compensating device. The results observed during each of the three techniques, suggest that the initial cause of the vasodilatation is not the result of the increase of the production of nitric oxide. However, subsequent to the initiation of vasodilation, an increase in the shear stress can result in an increase in the release of nitric oxide from the vascular endothelium, thus prolonging the vasodilatation obtained using each technique.

Acetylcholine↗
PubMed1995

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. The flow in the left descending and circumflex coronary arteries is reduced in systole because of the compression exerted by the contracting myocardium on the intramyocardial vessels. Due to the thinner wall of the right ventricle, this reduction is not obvious in the right coronary artery. The intramyocardial pump model provides a satisfactory explanation of the mechanism by which contraction reduces the flow. It also explains the attenuation of the diastolic-systolic oscillations of flow which occurs in the presence of a stenosis of a large epicardial artery. The varying elastance model shows the dependence of the extent of the reduction of the flow in systole on myocardial contractile force rather than on the pressure developed in the ventricle by the contraction. However, although the ventricular systolic pressure does not affect the flow in hearts with a relatively thick wall, it contributes to the systolic reduction of flow in hearts with a relatively thin wall. Owing to a mechanism involving the coronary capacitance, contraction is also responsible for the level of coronary flow in diastole.

Animals↗
PubMed1994

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. A 10 s coronary occlusion was performed before and after intracoronary infusion of Nitro-L-arginine (LNNA), at the dose of 100 mg in 20 min. The effect of LNNA in preventing the release of NO by the endothelium was demonstrated by the reduced coronary hyperaemia which follows the intracoronary infusion of acetylcholine. After LNNA the baseline coronary flow was not altered. Following the release of the coronary occlusion the peak amplitude of the reactive hyperaemia was not significantly changed, while the duration was reduced to almost a half of the control. The results suggest that in the intact dog NO is not important in the regulation of the baseline coronary vasomotor tone. It may also be argued that the peak amplitude of the hyperaemia is not significantly affected by LNNA either because the inhibition of the release of nitric oxide is counteracted by a greater production of adenosine, or because a mechanism not affected by nitric oxide (e.g. a myogenic mechanism) is involved in the reactive hyperaemia. In contrast the reduction of the duration of the hyperaemia after the inhibitor may depend on a reduced effect of the shear stress of the blood on the endothelium during the reactive hyperaemia.

Animals↗
PubMed1994

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. Nitric oxide release occurs under basal conditions, in response to chemical stimuli (acetylcholine, bradykinin, thrombin, prostacyclin, serotonin, etc.) and in response to changes in shear stress (effects of blood velocity on vascular endothelium). 3. Analogues of L-arginine inhibit NO and are widely used to study the effects of NO on the cardiovascular system: in intact animals, these inhibitors cause vasoconstriction, leading to an increase in arterial blood pressure (ABP) and bradycardia. 4. Bradycardia induced by NO inhibitors is due, in part, to baroreceptor activity following the increase in ABP and in part to a direct effect on the sino-atrial node. 5. In the intact animals and isolated perfused heart, NO inhibitors cause coronary vasoconstriction and hence a reduction in basal coronary flow. This effect, however, is not seen in isolated coronary vessels. 6. From experiments in which ABP did not change, NO does not appear to have an important role in regulating coronary vasomotor tone under basal conditions. 7. Nitric oxide appears to be involved in the duration of reactive hyperaemia following coronary vascular occlusion but is not involved to any significant extent in the peak amplitude of hyperaemia. 8. Responses to vasodilator stimuli which do not involve NO in the initiation of the vasodilation may be prolonged by the effect of increased blood flow (shear stress) which releases NO and potentiates hyperaemia.

Animals↗
PubMed1994

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. Transient (10 s) increases in intravascular blood pressure in a range above 70 mm Hg were produced by mechanical constriction of the descending thoracic aorta. In the presence of a normal vasomotor tone the increase in blood pressure caused an autoregulatory increase in the mean diastolic coronary inflow resistance. After maximal vasodilatation by dipyridamole, no change in inflow resistance was induced by the increase in intravascular blood pressure. It may be argued that while a non-maximal vasodilatation is reported to increase coronary distensibility, at a blood pressure of 70 mm Hg the complete suppression of the vasomotor tone brings the vascular radius to a size which cannot be further distended by an increase in blood pressure.

Animals↗
PubMed1993

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 energy cost of track running per unit distance (Cr) was then obtained from the ratio of steady-state VO2, corrected for lactate production, to speed; it was found to be independent of speed, its overall mean being 3.72 +/- 0.24 J.kg-1 x m-1 (n = 58; 1 ml O2 = 20.9 J). Maximal VO2 (VO2max) was also measured on the same subjects. Theoretical record times were then calculated for each distance and subject and compared with actual seasonal best performances as follows. The maximal metabolic power (Er max) a subject can maintain in running is a known function of VO2max and maximal anaerobic capacity and of the effort duration to exhaustion (te). Er max was then calculated as a function of te from VO2max, assuming a standard value for maximal anaerobic capacity. The metabolic power requirement (Er) necessary to cover a given distance (d) was calculated as a function of performance time (t) from the product Crdt-1 = Er. The time values that solve the equality Er max(te) = Er(t), assumed to yield the theoretical best t, were obtained by an iterative procedure for any given subject and distance and compared with actual records.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

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. Complete occlusion of the major individual ventricular branches and partial occlusion of the main right coronary artery did not impair right ventricular performance. Only complete occlusion of the main artery affected right and left ventricular function as revealed by echocardiogram. Reduced output by the ischemic right ventricle caused a reduction in left ventricular diastolic and systolic dimensions and in left ventricular developed pressure without any effect on left ventricular end-diastolic pressure.

Animals↗
PubMed1993

"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. Effects of abrupt changes of resistance obtained by removing an aortic constriction are also analyzed according to the same basic Windkessel equation and the results show the same close relationship to resistance.

Animals↗