["Mobile" ECMO]. / Extracorporeal membrane oxygenation "mobile".

ECMO (extracorporeal membrane oxygenation) is a cardiac or respiratory support which uses the principle of extracorporeal circulation (ECC). It consists of a pump generating an output as well as a membrane oxygenating blood and removing CO2. Thanks to an ECMO mobile team, expert caregivers can now perform the circulatory support in primary centers and then transfer patients under assistance to the referral center. After a brief summary of the two different anatomical approaches (veno-arterial and veno-venous) as well as their indications, the authors will share their experience of two transferred patients under ECMO to Geneva. Referral center and ECMO mobile team concepts will then be detailed focusing on the present situation in Switzerland.

Plateletpheresis before redo CABG diminishes excessive blood transfusion.

BACKGROUND: Blood conservation remains an important element for patients undergoing cardiac operations with cardiopulmonary bypass. Preoperative platelet-rich plasma (PRP) harvest is an autologous blood conservation method. The efficacy of preoperative PRP harvest and post-cardiopulmonary bypass reinfusion on postoperative bleeding and need for postoperative blood transfusion was evaluated in patients undergoing redo coronary artery bypass grafting in a prospective, randomized manner. METHODS: All adult patients admitted for redo coronary artery bypass grafting entered into the study. The PRP harvest aim was 20% or more of the total estimated circulating platelets. Immediately preoperatively three sequestration cycles were performed. The PRP was reinfused after weaning from cardiopulmonary bypass. One hundred seven parameters/patient were recorded. There were 20 patients in the RPR group and 20 controls (without PRP harvest). RESULTS: Patient characteristics, operative data, and preoperative hematologic parameters did not differ between the groups. In the PRP group, the mean platelet count in the PRP was 864 +/- 139 x 10(3)/microL, and the platelet yield was 27% +/- 5% (range, 20% to 37%). The average total chest tube blood loss was 423 mL (PRP) compared with 1,462 mL (controls; p < 0.001). Fourteen patients in the control group required blood transfusions postoperatively compared with only 1 patient in the PRP group (p < 0.001). Postoperative fluid requirements were also significantly greater in the control group (p < 0.001). Postextubation gas exchange was significantly better in the PRP group compared with controls (p < 0.01). Postoperative ventilation time and intensive care stay were significantly shorter in patients in the PRP group. CONCLUSIONS: A preoperative PRP harvest of 20% or more of the total platelets and reinfusion of the PRP after cardiopulmonary bypass resulted in significantly less postoperative blood loss and decreased fluid and blood transfusion requirements compared with controls. Postextubation gas exchange, ventilation time, and time required in the intensive care unit were also better, and the method was found cost-effective.

Autologous platelet sequestration in patients undergoing coronary artery bypass grafting.

OBJECTIVES: Blood conservation remains an important issue for patients undergoing cardiac surgery with cardiopulmonary bypass. Platelet sequestration (PSQ) is an aggressive autologous blood conservation method, whose effectiveness is still debated. The main objective of the present study was to evaluate whether PSQ reduces postoperative blood transfusion requirements in patients undergoing coronary artery bypass grafting (CABG) and to determine if PSQ is a cost-effective blood conservation method. MATERIAL AND METHODS: All adult patients admitted for CABG entered the study. Exclusion criteria were: recent blood transfusion (<7 days), a platelet count of 150x10(3)/microl or less, hematocrit less than 35% and body weight 50 kg or less. The sequestration was aim 20% or more of the total platelet plasma volume. The sequestration protocol was three sequestration cycles performed just prior to surgery. The concentrated platelet portion was reinfused after weaning from the cardiopulmonary bypass. Hundred seven parameters/patients were recorded. Sixty patients entered the study; 30 in the PSQ group and 30 controls (CTR). RESULTS: Patient characteristics, operation data, preoperative hematology and coagulation parameters did not differ between the groups. In the PSQ group a mean of 433+/-34 ml concentrated platelet portion was collected. The mean platelet count in the concentrated platelet portion was 749+/-157x10(3)/microl, resulting in a platelet yield of 28+/-6% (2040%). The average total chest tube blood loss was 423 ml (PSQ) compared to 858 ml (CTR), p<0.001. A greater number of CTR patients required blood transfusion postoperatively (23) compared to PSQ (3), P<0.001, and fluid requirements were also significantly increased in the control group, P<0.001. No statistical differences in hematology and coagulation parameters between the groups were observed. The hospital mortality was low and the incidence of postoperative complications was few and without group differences. Post-extubation gas exchange was better in PSQ patients compared to CTR. CONCLUSIONS: A preoperative PSQ of a minimum 20% of the total platelet plasma volume resulted in significantly lower postoperative blood loss and fluid and blood transfusion requirements compared to controls. Post-extubation gas exchange was also better after PSQ. Only one patient did not tolerate the sequestration. No other adverse effects of the procedure were observed.

Contractor responses of the isolated colon of the mouse to morphine and some opioid peptides.

Morphine (1 X 10(-8) - 1 X 10(-4)M), fentanyl (1 X 10(-9) - 1 X 10(-5)M) and alfentanyl (1 X 10(-10) - 1 X 10(-5)M) as well as methionine enkephalin [Met5]enkephalin (1 X 10(-11) - 1 X 10(-8)M), [D-Ala2, Met5]enkephalin (1 X 10(-12) - 1 X 10(-8)M) and dynorphin A(1 - 13) (1 X 10(-9) - 1 X 10(-6)M) caused a contractor response of the longitudinal musculature of the terminal colon of the mouse. These effects were competitively antagonized by naloxone. The pA2 values obtained for naloxone antagonism of morphine and opioid peptides and the high sensitivity of the preparation to enkephalins suggest the presence of delta-opiate receptors in this preparation but mu- and kappa-receptors may also be present. Opiate-induced contractions in the mouse colon were abolished by tetrodotoxin and after incubation with indomethacin. It is concluded that the excitatory actions of the opiates in the mouse colon are mediated via opiate receptors located on nerves which do not release acetylcholine, noradrenaline or 5-hydroxytryptamine. The opiates may produce their action by removing an inhibitory neural influence (the nature of which remains to be elucidated) allowing a prostaglandin-mediated effect to predominate, thereby increasing muscle tone.

Effect of dopamine on dog distal colon in-vitro.

The effects of dopamine, isoprenaline, adrenaline and noradrenaline in dog isolated colon strips were studied. All these drugs produced in the preparation relaxations which were inhibited by propranolol and sotalol or, in the case of noradrenaline, by a mixture of propranolol and phentolamine. A selective beta 1-adrenergic antagonist, practolol, had the same inhibitory effects on the relaxations induced by all the agonists, suggesting the existence of beta 1- and beta 2-adrenoceptor subtypes in the dog distal colon. There is no evidence for the presence of specific dopaminergic receptors in this preparation.

Potentiation by sulphydryl agents of the responses of guinea-pig isolated ileum to various agonists.

Sulphydryl agents (dithiothreitol, mercaptoethanol, monothioglycerol, cysteine, glutathione) increase non-specifically the potency of various agonists (acetylcholine, 5-hydroxytryptamine, nicotine, bradykinin, prostaglandin E2) on the guinea-pig ileum. These effects are of non-cholinergic origin and are not related to prostaglandin synthesis. Sulphydryl agents act directly on the smooth muscle cells of the guinea-pig ileum most probably by reducing disulphide bonds located on the membrane surface and by this mechanism modulate the muscular contractile activity.

Adrenoceptors and regulation of intestinal tone in the isolated colon of the mouse.

Adrenaline, noradrenaline, phenylephrine, dopamine, clonidine and apomorphine at low concentrations (from 10(-9) M to 10(-6) M) contracted the longitudinal muscle of the isolated distal colon of the mouse. Phentolamine, tetrodotoxin and indomethacin antagonized these contractile responses. Yohimbine antagonized them at lower concentrations than prazosin. Dopamine and clonidine had the same contractile activity on preparations from mice pretreated with 6-hydroxydopamine (6-OHDA). Isoprenaline (10(-9) to 3 X 10(-7) M) induced relaxations of the colon which were antagonized by propranolol. At higher concentrations, adrenaline and noradrenaline (from 3 X 10(-7) M), dopamine (from 3 X 10(-5) M), phenylephrine (from 3 X 10(-6) M) and apomorphine (from 10(-4) M) relaxed the colon. Clonidine (10(-6) to 3 X 10(-5) M) inhibited the spontaneous activity of the colon but never induced relaxations. At 10(-4) and 10(-3) M clonidine elicited contractions. Prazosin antagonized the inhibitory effect of phenylephrine and clonidine, a mixture of propranolol and prazosin antagonized the relaxations to adrenaline, noradrenaline and dopamine and unmasked contractions that were sensitive to yohimbine and tetrodotoxin. The relaxations induced by apomorphine and the contractions induced by clonidine (greater than 10(-6) M) were resistant to all these antagonists. Electrical field stimulation (1 ms, 2 Hz, 2-20 V) of the mouse colon induced contractile responses which increased with the frequency of the stimulus. After cessation of stimulation at 4 Hz a rebound contraction was generally observed, followed by a progressive decline in tone. In the presence of atropine, the contractile response to field stimulation was abolished and transformed into a rapid and sustained relaxation. A rebound contraction was always observed after cessation of stimulation. The responses to electrical stimulation (in the presence or absence of atropine) were abolished by tetrodotoxin. The rebound contractions were abolished by indomethacin. The relaxations induced in the presence of atropine were not modified by phentolamine, propranolol, guanethidine, methysergide, mepyramine, cimetidine or naloxone. Tetrodotoxin (from 3 X 10(-8) M) caused a sustained contraction of the colon with increased spontaneous activity. This contraction was not modified by atropine, phentolamine, propranolol, guanethidine, methysergide, mepyramine, cimetidine, naloxone, but was abolished by preincubation of the preparation with indomethacin. These results indicate that, at low concentrations, various sympathomimetics contracted the mouse distal colon by stimulating alpha 2 presynaptic adrenoceptors. The responses appeared provided intramural prostaglandin synthesis was unaffected. Higher concentrations of sympathomimetics induced relaxations by stimulation of postjunctional alpha 1- and beta-adrenoceptors. Electrical field stimulation of the mouse colon produced cholinergically mediated contractions or, in the presence of atropine, non-adrenergic non-cholinergic (NANC) relaxations followed by rebound contractions, provided prostaglandin synthesis was unaffected. 6 These data suggest that in the mouse isolated colon, muscle tone and contractility are regulated by 2 opposing mechanisms: (1) a neurogenic cholinergic activity and a local prostaglandin synthesis leading to an increase in muscle tone; (2) a neurogenic NANC inhibitory control the nature of which remains to be elucidated. alpha 2-Presynaptic receptors, when activated inhibit the neurogenic inhibitory control and liberate the mechanism by which muscle tone is increased, causing a contraction.

The effects of substituted benzamides on frog rectus abdominis.

The substituted benzamides metoclopramide, bromopride, tiapride and sulpiride (10(-5) and 10(-4) M) significantly increased the sensitivity of frog rectus abdominis muscle to exogenous acetylcholine but not to carbachol. This supersensitivity could be correlated with the anticholinesterase activity of these drugs measured in homogenates from frog skeletal muscle. Sultopride, like procainamide, has only inhibitory effects on the responses of the rectus abdominis to acetylcholine and has no anticholinesterase activity in this preparation.

A study of the effects of amodiaquine on the guinea-pig isolated ileum.

Amodiaquine (3.5 . 10(-7) mol/l), a 4-amino-quinoline antimalarial, increases the responses of the guinea-pig isolated ileum to direct (acetylcholine, histamine, barium, chloride), partially (5-hydroxytryptamine, PGE1 and F2 alpha) and totally (electrical stimulations, nicotine) indirect agonists. Moreover it reverses inhibitions of the electrical induced contractions by acetylcholine antagonists (atropine), acetylcholine release blocking agents (morphine, tetrodotoxin, procaine, noradrenaline) and prostaglandin synthesis inhibitors (indomethacin, ibuprofen, flufenamine acid, hydrocortisone). From 2.7 . 10(-6) mol/l, it induces dose-related tonic contractions which are totally and reversibly abolished by indomethacin as well as by the prostaglandin antagonist, polyphloretin phosphate, but not by atropine, morphine and tetrodotoxin. This indicates that amodiaquine exerts both a direct muscular non selective ileal sensitization to various agonists and, but at higher concentrations, a contractile effect apparently dependent on prostaglandin synthesis and release. At even higher concentrations (5.4 . 10(-6) mol/l) an effect of amodiaquine on acetylcholine release was demonstrated by the observation of phasic contractions inhibited by atropine, morphine and tetrodotoxin. These effects are different from those found by us with several other antimalarial compounds in the same preparation.

Potentiation by D-penicillamine and other sulfhydryl agents of the vascular response to histamine in the anaesthetized dog.

D-penicillamine (80 mg/kg) potentiates the fall in blood pressure produced by an i.v. injection of histamine in the anaesthetized dog but is inactive on the effects of acetylcholine and prostaglandin E1. Other sulfhydryl agents (alpha-thioglycerol, 2-mercaptoethanol, 2,3-dimercapto-l-propanol, DL-cysteine, glutathione, diethyldithiocarbamate) can similarly modify the effects of histamine on blood pressure but two metal complexing agents (CaNa2 EDTA and orthophenantroline) are inactive. After pretreatment with indomethacin (10 mg/kg) or cimetidine (0.5 mg/kg/min) D-penicillamine still increases the effect of histamine but not after pretreatment with pyrilamine maleate (1 mg/kg). Moreover D-penicillamine does not modify the blood pressure drop due to dimaprit but increases that to 2-(2-pyridyl) ethylamine. It is concluded that D-penicillamine and some other sulfhydryl agents can increase the blood pressure lowering effects of histamine at the level of vascular H1-receptors by a sensitizing mechanism which might involve the rupture of a disulfide bridge.

The effects of antiinflammatory steroids on the response of the guinea-pig isolated ileum to acetylcholine, histamine, nicotine, 5-hydroxytryptamine and electrical stimulation.

High concentrations of antiinflammatory steroids (2.5-40 microgram/ml) reversibly inhibited the electrically induced contractions of the guinea-pig isolated ileum. At 40 microgram/ml they also reversibly inhibited contractions elicited by acetylcholine, histamine nicotine and 5-hydroxytryptamine. PGE1 (2.5 ng/ml), PGE2 (2.5 ng/ml) and PGF 2 alpha (25 ng/ml) antagonized these effects. The inhibition of contractions elicited by direct agonists were less pronounced than those elicited by indirect or partly indirect agonists. The inhibitory effect of steroids may be related to non-specific actions on biological membranes. An overall sensitization of the smooth muscle by PG's may explain their antagonism to inhibition by steroids.

Pharmacological analysis of the effects of metoclopramide on the transmurally stimulated guinea-pig ileum.

The effects of metoclopramide (Mcp), a benzamide derivative, have been quantitatively analyzed on the responses of the isolated guinea-pig ileum to transmural stimulation. Mcp (0.03 microgram ml-1 upwards) increased these responses but this effect which was calcium-dependent was not concentration-dependent (up to 30 micrograms ml-1). Mcp antagonized the inhibitor effects of noradrenaline, dopamine, procaïne, adenosine triphosphate, bufexamac and hydrocortisone on the ileal responses, but not those of tetrodotoxin and verapamil.

Inhibition of caerulein and physalaemin-induced contractions of guinea-pig isolated ileum by non-steroidal antiinflammatory drugs and various steroids and their reversal by prostaglandin E1.

Two non-steroidal antiinflammatory drugs, two antiinflammatory steroids and two sex steroids were found to potently and reversibly inhibit caerulein-induced and physalaemin-induced contractions of guinea-pig isolated ileum. The effects of these drugs were reversed by small amounts of PGE1.

Pharmacological analysis of the effects of substituted benzamides on the isolated guinea-pig ileum. Study of metoclopramide, sulpiride, bromopride, tiapride and sultopride.

The effects of metoclopramide (Mcp), sulpiride (Sp) and some of their derivatives: bromopride (Br), tiapride (Ti) and sultopride (Stp) have been compared on the guinea-pig isolated ileum. 1. Br and Ti have, like Mcp, and indirect cholinergic stimulating effect on the intestinal smooth muscle. Sp and Stp are devoid of such an effect. 2. At high doses, all the benzamides have a direct inhibitory effect on the ileum. 3. Mcp, Br and Ti (10(-5)M) potentiate the responses of the ileum to acetylcholine (ACh). At high doses (10(-4)M) the effects of all benzamides on the responses to ACh as well as to histamine (H) are mostly inhibitory. 4. Mcp and Br (10(-5)M) inhibit the responses of the ileum to serotonin (5HT) while Ti, Sp and Stp potentiate them. 5. Neural pathways and calcium mechanisms are involved in the potentiations of ACh and 5HT responses since the enhancements observed are abolished in the presence of tetrodotoxin or in the absence of Ca++.