[Changes in cerebral vasomotor reactivity in relation to respiratory and metabolic stimuli: an analysis of its behavior in hypertensive and normotensive subjects]. / Modificazioni della reattività vasomotoria cerebrale in relazione a stimoli respiratori e metabolici: analisi del comportamento in soggetti ipertesi e normotesi.

We know that increases in the arterial blood pressure determines changes in the behaviour of the cerebrovascular resistance and also the possible lack of vasomotor reactivity. In order to clarify the pathway of circulatory vasomotor reactivity in arterial hypertension, we carried out a study on a group of hypertensive subjects (20 patients) who were compared to a group of normotensive controls (18 patients). A transcranial doppler (TCD) study was performed with rebreathing tests (apnea and hyperventilation) and it was carried out in both groups of subjects. The TCD was repeated after an administration of sublingual pill of nitroglycerin. In both groups the hyperventilation caused a significant reduction in the velocity peak in the middle cerebral artery (norm.: 84.88 +/- 4.86 cm/sec 60 +/- 5.2 cm/sec; hyperten. 84.50 +/- 7.1 cm/sec 58.80 +/- 5.47 cm/sec) in contrast apnea induced a major increase in the velocities (norm.: 84.88 +/- 4.86 cm/sec 102.50 +/- 4.89 cm/sec; hyperten.: 84.50 +/- 7.1 cm/sec 101.59 +/- 10.6 cm/sec). We noticed a statistical significant difference between the velocities recorded in the different tests (Anova test p < 0.0001). The behaviour of the velocities in the rebreathing tests after nitroglycerin was similar when compared to the same test were performed without the drug. This study suggests that there is no difference in the behaviour of the cerebral reactivity between normotensives and the hypertensive subjects without vascular or cardiac compliance. Finally we would emphasize the role of TCD in the recording changes of cerebrovascular resistances due to pressure or metabolic causes.

Transcutaneous PCO2 level as an index of tissue resistance to ischemia.

The authors performed a retrospective study on a data base of 525 patients with peripheral arterial disease, to analyze the pathophysiologic meaning of resting transcutaneous pressure of carbon dioxide (PCO2) and of CO2 production during three minutes of local ischemia. The resting and postischemic PCO2 and its maximum increase related to rest (PCO2 production) were measured with Kontron 7640 equipment. The results show a significant increase of PCO2 production in the Fontaine stage 2A (183 patients, 4.61 mmHg, P < 0.0001), in stage 2B (194 patients, 5.22 mmHg, P < 0.0001), in the third stage (83 patients, 6.10 mmHg, P < 0.0001), and in the fourth stage (53 patients, 8.66 mmHg, P < 0.0001). Only the patients at the first stage showed an insignificant increase, perhaps because of the small number (12) in this group. The authors feel that the measurement of tcPCO2 production during local ischemic stress can be a very important parameter for evaluating peripheral arterial disease as an expression of metabolic tissue performance and, overall, of the tissue resistance to ischemia.

Iloprost, stable analogue of the prostacyclin, is able to improve the tissue resistance to ischaemia.

On 10 patients, suffering from peripheral arterial disease, with critical limb ischaemia, the CO2 production during ischaemia has been evaluated at 1st and at 28th day of treatment with iloprost. The study demonstrated that the drug is able to improve the tissue resistance to ischaemia, with a significant (p < 0.05) reduction of the CO2 production. The authors underline that this study is one of the first confirmations, in vivo and on the man, of the previous experimental findings, made in isolated arterial tissue.

Three-month therapy with calcium-heparin in comparison with ticlopidine in patients with peripheral arterial occlusive disease at Leriche-Fontaine IIb class.

Forty patients with a mean age of 62.6 +/- 6 years, 36 men and 4 women, with peripheral arterial occlusive disease (PAOD) at Leriche-Fontaine IIb class, were randomly allocated to one of two treatment groups, receiving either 12,500 IU/day of subcutaneous (sc) calcium-heparin (CAE) or 250 mg/day of oral ticlopidine, each given for ninety days. The following parameters were evaluated before the start of the active treatment period and after thirty and ninety days of treatment: pain-free walking distance (PWD), maximum walking distance (WDmax), systolic and diastolic blood pressure (BP), posterior tibial arterial pressure and Winsor index at rest and after exercise (treadmill), transcutaneous oxygen and carbon dioxide pressures at rest (TcPO2 and TcPCO2 respectively), and time to 50% TcPO2 recovery after three-minute ischemia. Both treatments induced an improvement in PWD/WDmax, which, at the end of the study, were increased by 50.7/58.7% and 31.7/36.2%, respectively, for CAE and ticlopidine treatments, respectively.