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Biomedical subjects

F Nicolas

Publications and source records attributed to F Nicolas.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

[Hemodynamic effects of a new antidepolarizing agent: fazadinium bromide].

Studies concerning the hemodynamic effects of this new antidepolarizing agent are scarce and difficult to interpret because of drug interactions, and of an accentuation of vagal tonus related to the use of morphinomimetic analgesics. For a better approach of the effects proper to fazadinium, we have tried to perform a study freed, to a maximum, from any drug interference. We studied the hemodynamic effects to a single dose of 1 mg.kg-1 of fazadinium bromide during 35 minutes in coronary patients normal hemodynamically or rhythmically, non-premedicated, ventilated with 50 p. 100 nitrous oxide in oxygen, and bebore any surgical procedure. All hemodynamic modifications are moderate and maximal 10 minutes after injection. The stroke index decreases 16 p. 100, heart rate increases 6 p. 100 and cardiac index falls 10 p. 100. Total peripheral resistance remains unchanged and mean arterial pressure drops 10 p. 100. Finally pulmonary wedge pressure decreases slightly. None of these modifications are statistically significant. One may, therefore, conclude that fazadinium tolerance, when the drug is freed from any drug interference, in coronary patients normal hemodynamically and free from rhythm disorders is excellent from a hemodynamic and rhythmic point of view. However, other isolated observations of hypovolemic subjects, or patients with atrial fibrillation receiving fazadinium and studied hemodynamically suggest a poorer tolerance in these cases.

Aged↗
PubMedDate not supplied

[Deep hypotension induced by sodium nitroprusside in neurosurgery. I.--Systemic hemodynamic effects (author's transl)].

The systemic hemodynamic effects of deep hypotension (MAP: 38 +/- 6 mm Hg) induced by sodium nitroprusside (S.N.) were studied in 20 patients who underwent surgery for cerebral aneurysm. The hemodynamic measurements were performed four times.: (1) during the preoperative period, (2) during stable anesthesia just before hypotension, (3) during stable hypotension, (4) 20 minutes after stopping nitroprusside. All patients were mechanically ventilated with a constant tidal volume and rate. Parameters for acid-base balance and Pa O2 were also recorded. Nitroprusside produces arterial and venous dilatation which results in a decrease of afterload and preload. The mean dosage of S. N. was 18 mcg/kg/mn. Systemic vascular resistances decreased by 62 p. cent. Mean arterial pressure decreased by 53 p. cent; it reached 40 mm Hg. Fall in preload resulted in a decrease in pulmonary wedge pressure by 28 p. cent. This fall in preload produced a decrease in stroke index according to Frank-Starling's mechanisms. However tachycardia allowed a rise in cardiac index by 20 p. cent. Increase of pulmonary wedge pressure at 8-10 mm Hg by blood volume expansion maintains stroke index at control level. Under these conditions the elevation of cardiac index is due to tachycardia. Cardiac rhythm disorders (wandering pace-maker, nodal rhythm) are observed in 5 patients after having stopped nitroprusside.

Adult↗
PubMedDate not supplied

[Deep hypotension induced by sodium nitroprusside in neurosurgery. II.--Cerebral hemodynamic effects and metabolic rate of oxygen (author's transl)].

The cerebral hemodynamic effects of sodium nitroprusside (S. N.) have been the object of animal studies mainly. During the only human study performed, the drop in mean arterial pressure (MAP) is limited to 67 mm Hg. The study of the evolution of cerebral blood flow (CBF) in cases of more severe hypotension (MAP less than 45 mm Hg) seems of some interest. The study was composed of the measurement of the CBF using Xenon 133 and the calculation of cerebral vascular resistances (CVR) as well as cerebral metabolic rate of oxygen (CMRO2). Eleven patients with an average age of 37 years underwent surgery for cerebral aneurism 10 to 15 days after the inaugural hemorrhagic accident, under narconeuroleptanalgesia and stable ventilatory conditions. They are divided into 2 groups: Group I, 9 patients with normal levels of consciousness; Group II, 2 patients either agitated or obnubilated. The study is composed of 3 successive measures: (1) (T0) during stable anesthesia just prior to hypotension; (2) (T1) after 5 minutes of hypotension (MAP = 40 +/- 7 MM Hg); (3) (T2) 20 minutes after having stopped S. N. infusion. For the 9 patients in Group I, CBF remains unchanged at T1, the CVR decreases (p less than 0.001) and CMRO2 decreases (p less than 0.05). At T2 all of these parameters return to T0 values. The postoperative clinical evolution is favorable and uncomplicated. For the 2 patients in Group II the CBF, initially higher, falls from 20 to 30 p. cent at T1 with a drastic reduction in CMRO2. Despite the improvement of these parameters at T2, a prolonged postoperative coma is observed. This study suggests that CBF and CMRO2 are important parameters to monitor during controlled severe hypotension. Decrease in MAP must be less than 50 p. cent of control value and time-limited.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Aggravation following anaesthesia in a case of unknown lateral amyotrophic sclerosis (author's transl)].

A 66 year old man whose activity was almost normal underwent a lombar sympathectomy under general anesthesia (thiopental, gallamine, N2O). Immediately after recovery an acute respiratory distress became evident. It was due to a respiratory paralysis on which neostigmine had no effect. Neurologic examination showed the symptoms of an amyotrophic lateral sclerosis which had remained unknown so far. The respiratory paralysis persisted and one year later artificial ventilation is still necessary almost continuously. Two aspects of this very rare observation are discussed: first the cause and mecanisms of the aggravation of the neurologic disease following anesthesia, secondly the rather unusually important part played by the respiratory paralysis in this case of lateral amyotrophic sclerosis.

Acute Disease↗