Calcium Entry Blockers and Tissue Protection

Assessment of intermittent claudication by quantitation of exercise-induced microalbuminuria.

The hypothesis that intermittent claudication initiates a systemic inflammatory response was investigated by studying the effect of exercise on markers of neutrophil activation and vascular permeability in 25 claudicants and 10 controls. Urinary albumin excretion, previously demonstrated to reflect vascular permeability, increased significantly after exercise in claudicants and was associated with decreased neutrophil filterability and increased serum lysozyme activity. No similar exercise-induced changes were seen in controls or in claudicants after successful arterial bypass surgery. These results suggest that intermittent claudication is associated with potentially deleterious systemic manifestations that are surgically reversible.

Effect of surgery on the systemic inflammatory response to intermittent claudication.

Thromboxane and neutrophil changes following intermittent claudication suggest ischaemia-reperfusion injury.

Regular physical exercise improves walking performance in patients affected with peripheral obliterative arterial disease (POAD). The mechanisms underlying the phenomenon are still controversial. In order to verify the hypothesis that physical conditioning of lower limbs on a treadmill and ischemic preconditioning of the heart could share some biological aspects, 14 POAD subjects underwent a training program on the treadmill consisting of five repeated submaximal exercises at five-minute and two-hour intervals preceding the maximal tolerance test. Moreover, a protocol with two daily submaximal walking exercises over one week was also performed. Pain-free and total walking distance were measured before and after they performed the program. Moreover, plasma levels of adenosine and adenosine triphosphate (ATP) were measured and polymorphonuclear (PMN) leukocyte activity was studied together with rheologic parameters. Pain-free distance was prolonged by 15.4% and 14.3%, and total distance was prolonged by 23.1% and 26.9%, in the exercises with five-minute and two-hour intervals, respectively. After one week of daily exercises, the onset of pain and the end of the test were delayed by 24% and 43.7%, respectively. An improvement in blood rheology and a reduced PMN reactivity were also observed with the three protocols, associated with an increase in plasma levels of adenosine and ATP. Similarly to ischemic preconditioning in the heart, the possibility is suggested that an adenosine-mediated mechanism may contribute to the development of physical conditioning in treadmill-trained POAD patients.

Experimental Model of Short-Time Exercise-Induced Preconditioning in POAD Patients

Effect of controlled physical activity on haemorheological and metabolic changes in poad patients

Drugs such as dipyridamole (200 μg/kg/min), an adenosine uptake in hibitor, and theophylline (300 μg/kg/min), an adenosine receptor antagonist, respectively increased and decreased postischemic hypere mia in normal subjects, as well as in POAD patients. Moreover, dipyrida mole pretreatment was able to antag onize the reduction of peak flow in duced by nifedipine, and the potenti ating effect of flunarizine on postis chemic hyperemia was affected sig nificantly by theophylline, thus sug gesting a possible interference of calcium entry blocker drugs with the endogenous adenosine system. In a cellular model (polymorphonuclear leukocytes — PMN) the inhibitory ef fect of calcium entry blockers on stimulated functions (degranulation and free radical production) was highly antagonized by theophylline. Finally, a1H-NMR spectroscopy study showed a binding interaction between adenosine and flunarizine on the cell membrane. An adenosine-re ceptor coupling to the calcium entry blocker channels is suggested.

In vivo and in vitro evidence of an adenosine-mediated mechanism of calcium entry blocker activities.

Haemodynamics, rheology and mechanism of action of iloprost in man

In the last few years we have accumulated some evidence that calcium entry blockers could interfere with an endogenous purinergic mechanism, namely, with membrane adenosine receptors’” This property seemed to be shared by different groups of such drugs, independently from their chemical structure, thus opening new questions on the molecular mechanism of action24 Among these substances, first flunarizine and then dihydropyridines claimed our attention, and now we want to summarize the findings of our studies, not following the logical development of the adenosine hypothesis in our mind, but assembling our data according to the type of experimental design In this paper the thread of the argument implies a continuous hypothetical comparison with the adenosine system Our studies dealt with clinical pharmacological investigations on the circulatory activity of flunarizine either in control subjects or in peripheral obliterative arterial disease (POAD) patients The design of the study included the plethysmographic investigation of the leg hemodynamics after flunarizine infusion and after treatment with drugs that either block adenosine receptors, such as theophylline, or inhibit adenosine uptake, such as dipyridamole Finally a cellular model was approached to clarify a possible interference of calcium entry blocker with adenosine a t the membrane receptor level

Pharmacological Basis and Therapeutic Efficacy of Flunarizine in Peripheral Artery Disease

/pdf/arterial-venous-differences-in-metabolic-and-rheological-456kxue8r5.pdf

Arterial-venous differences in metabolic and rheological parameters in peripheral obliterative arterial disease patients

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