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Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 109 records · Page 6Linked to original sources
PubMed1996

Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure.

OBJECTIVE: The effect of high-volume plasmapheresis on hepatic encephalopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) was investigated in patients with fulminant hepatic failure (FHF). METHODS: Twelve consecutive patients (8 women, 4 men, median age 34 years (range 19-51), were studied before and after high-volume plasmapheresis with 10-16 litres fresh frozen plasma, while PaCO2 and body temperature were maintained at 30 (23-34) mmHg and 37.6 degrees C (36.6-38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriovenous oxygen difference (AVDO2) and oxygen extraction (AVDO2 divided by arterial oxygen content). CBF was determined by a xenon-133 clearance method in eight patients and CMRO2 calculated as AVDO2 times CBF. Cerebral perfusion pressure (CPP) was determined as the difference between mean arterial and subdural pressures in eight patients. RESULTS: High-volume plasmapheresis was initiated 22 (6-168) h after the development of hepatic encephalopathy and 11 patients had grade 4 encephalopathy. Following high-volume plasmapheresis the grade of encephalopathy improved in four patients. The CBF increased from a median of 31 (16-86) to 45 (18-97) ml/100 g/min and as oxygen extraction remained unchanged (32 (9-41) vs. 29 (7-39)%), CMRO2 increased from 1.24 (0.96-1.82) to 1.86 (1.00-2.07) ml/100 g/min (P < 0.05). The CPP increased from 62 (19-76) to 92 (50-105) mmHg (P < 0.01), whereas the intracranial pressure remained unchanged (19 (3-45) vs. 11 (5-33) mmHg). No statistical difference was found between the relative changes in the above parameters in survivors compared to non-survivors. CONCLUSION: Although the clinical status did not improve in all patients, both CBF and CMRO2 increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect partial removal of neuroinhibitory plasma factors.

Adult↗
PubMed1996

Subcutaneous blood flow in man during sleep with continuous epidural anaesthesia.

BACKGROUND: Subcutaneous blood flow increases during sleep and we evaluated if this increase is affected by epidural anaesthesia. METHODS: Lower leg subcutaneous blood flow was determined by 133Xenon clearance in ten subjects during continuous epidural anaesthesia at L2-L3 including eight hours of sleep, while the upper abdominal subcutaneous blood flow served as control. RESULTS: Epidural anaesthesia to the level of the umbilicus was followed by an increase in the lower leg subcutaneous blood flow from 3.4 (1.8-6.3) to 7.8 (3.6-16.9) ml min-1 100 g-1 (median and range; P < 0.001) and returned to 3.5 (2.4-7.6) ml min-1 100 g-1 after 88 (45-123) min. In contrast, until the period of sleep the upper abdominal region blood flow remained at 5.2 (3.2-6.4) ml min-1 100 g-1. During sleep, lower leg subcutaneous blood flow did not change significantly, but the upper abdominal flow increased to 6.2 (5.2-7.2) ml min-1 100 g-1 after 34 (29-70) min (P < 0.01), and it remained elevated for 125 (100-164) min. CONCLUSIONS: The results indicate that although epidural anaesthesia induced only a temporary increase in lower leg subcutaneous blood flow, it hindered the rise in subcutaneous blood flow normally manifest during early sleep.

Abdominal Muscles↗
PubMed1996

Lymphocytes and NK cell activity during repeated bouts of maximal exercise.

Effects on the immune system of 6-min "all-out" ergometer rowing were investigated over 2 days (2 x 3 bouts) in eight male oarsmen with a maximal oxygen uptake of 5.5 +/- 0.1 l/min (mean +/- SE). Blood samples were obtained before, during, and 2 h after each bout and on the day after the last bout. Compared with levels at rest, the first bout of exercise increased the concentration of leukocytes (2-fold); neutrophilic granulocytes (2-fold); lymphocytes (2-fold); monocytes (2-fold); the blood mononuclear cell (BMNC) subsets CD3+ (2-fold), CD4+ (2-fold), CD8+ (3-fold), CD16+ (8-fold), CD19+ (2-fold), and CD14+ (2-fold); the NK cell activity (2-fold); and plasma interleukin-6 (3-fold) (P < 0.05). During the last bout even higher levels were noted for leukocytes (3-fold); neutrophilic granulocytes (3-fold); lymphocytes (4-fold); the BMNC subsets CD4+ (3-fold), CD8+ (5-fold), CD16+ (13-fold), CD19+ (5-fold), and CD14+ (3-fold); and for the NK cell activity (4-fold) (P < 0.05). During the recovery periods all values were at or above the level at rest, and elevated concentrations of leukocytes (38%), neutrophilic granulocytes (48%), and lymphocytes (46%) reflected in the BMNC subsets and increased NK cell activity (119%) were also noted on the day after the last bout (P < 0.05). The results show that maximal exercise with large muscle groups provokes higher immune responses during repetitive bouts.

Adult↗
PubMed1996

Hormonal and metabolic responses to electrically induced cycling during epidural anesthesia in humans.

Hormonal and metabolic responses to electrically induced dynamic exercise were investigated in eight healthy young men with afferent neural influence from the legs blocked by epidural anesthesia (25 ml of 2% lidocaine) at L3-L4. This caused cutaneous sensory anesthesia below T8-T9 and complete paralysis of the legs. Cycling increased oxygen uptake to 1.90 +/- 0.13 (SE) l/min, and fatigue developed after 22.7 +/- 2.7 min. Compared with voluntary exercise at the same oxygen uptake and heart rate, concentrations of blood and muscle lactate (musculus vastus lateralis) as well as plasma potassium increased more while muscle glycogen decreased more during electrically induced exercise. Hepatic glucose production always rose during exercise. However, during involuntary exercise with sensory blockade, it did not match the rise in peripheral glucose uptake and plasma glucose decreased (P < 0.05). Plasma glycerol increased less in electrically induced vs. voluntary exercise, and free fatty acids and beta-hydroxybutyrate decreased only during electrically induced exercise. Epinephrine, growth hormone, adrenocorticotropic hormone, and cortisol levels were higher during involuntary vs. voluntary exercise (P < 0.05). In conclusion, neural and humoral mechanisms exert redundant control with regard to responses of catecholamines and pituitary hormones (growth hormone and adrenocorticotropic hormone). In contrast, neural input from motor centers and feedback from working muscle are important for glucose production and lipolysis during exercise in humans. Humoral feedback is apparently not sufficient to trigger normal mobilization of extramuscular fuel stores.

Adult↗
PubMed1996

Mechanisms regulating regional cerebral activation during dynamic handgrip in humans.

Dynamic hand movement increases regional cerebral blood flow (rCBF) of the contralateral motor sensory cortex (MS1). This increase is eliminated by regional anesthesia of the working arm, indicating the importance of afferent neural input. The purpose of this study was to determine the specific type of afferent input required for this cerebral activation. The rCBF was measured at +5.0 and +9.0 cm above the orbitomeatal (OM) plane in 13 subjects during 1) rest; 2) dynamic left-hand contractions; 3) postcontraction ischemia (metaboreceptor afferents); and 4) biceps brachii tendon vibration (muscle spindles). The rCBF increased only during dynamic hand contraction; contralateral MS1 (OM +9) by 15% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05); supplementary motor area (OM +9) by 11% to 69 +/- 9.8 ml.100 g-1.min-1 (P < 0.05); and there were also bilateral increases at MS2 (OM +5) [by 16% to 64 +/- 8.6 ml.100 g-1.min-1 (P < 0.05)]. These findings suggest that the rCBF increase during dynamic hand contraction does not require neural input from muscle spindles or metabolically sensitive nerve fibers, although the involvement of mechanoreceptors (group III or Ib) cannot be excluded.

Adult↗
PubMed1996

Subcutaneous oxygen and carbon dioxide tensions during head-up tilt-induced central hypovolaemia in humans.

The effect of hypovolaemic shock on subcutaneous oxygen and carbon dioxide tensions was studied in man. Subcutaneous oxygen (Psc,O2) and carbon dioxide (Psc,CO2) tensions were monitored, during 50 degrees head-up tilt (anti-Trendelenburg's position)-induced central hypovolaemia, in two females and eight males, using a silicone tonometer on the lateral upper aspect of the right arm. All cardiovascular variables remained stable at rest. Incremental tilting to 50 degrees increased heart rate (HR) and mean arterial pressure (MAP) (p < 0.01), while stroke volume (SV), cardiac output (CO) and central venous saturation (SvO2) decreased (p < 0.05). Presyncopal symptoms appeared after 28 (8-48) min (mean and range) as HR decreased from 82 (63-108) to 52 (36-70) beats min-1 (p < 0.05), MAP from 88 (61-106) to 46 (37-54) mmHg and SvO2 from 0.68 (0.56-0.76) to 0.58 (0.39-0.70) (p < 0.01). On return of the tilt table to the horizontal position HR, MAP, SV, CO and SvO2 immediately re-established resting values. The Psc,O2 was 83 (72-102) mmHg at rest and during tilting it increased to 89 (82-111) mmHg followed by a decrease to 72 (58-97) mmHg (p < 0.01) at the appearance of presyncopal symptoms. Psc,O2 returned to the pretilt level over 45 (30-60) min of recovery. Arterial oxygen, carbon dioxide and Psc,CO2 did not change significantly. Subcutaneous oxygen tension decreases during marked central hypovolaemia and it returns slowly to the resting level during recovery. Psc,O2 is a more sensitive marker of impaired tissue oxygenation than arterial oxygen pressure.

Adult↗
PubMed1996

Plasma magnesium during human liver transplantation.

Patients with severe liver disease and accompanying malnutrition may exhibit electrolyte disturbances including the magnesium balance. In 18 patients plasma magnesium (p-Mg) was determined at the start of the liver transplantation and during the anhepatic and reperfusion phases of the operation. The blood loss was 6.9 (2.5-8.8) 1 (median and range) and the cumulative transfusion volume was 10.2 (5.0-17.2) 1 of which 5.9 (2.5-14.2) 1 was with fresh frozen plasma. p-Mg was 0.72 (0.58-0.88) mmol.l-1 and it did not change significantly during the operation. Thus, in 4 patients it was at or below the lower reference value of 0.67 mmol.l-1. In 11 patients it changed less than 0.05 mmol.l-1, while in 4 patients the concentration was rose, and in 3 patients we noted a fall in each of 0.08 mmol.l-1. There was no correlation between p-Mg and the blood loss or the administered volume of fresh frozen plasma. In 10 randomly chosen fresh frozen plasma units, the p-Mg was 0.64 (0.61-0.71) mmol.l-1. These observations do not support a need for close monitoring or substitution of magnesium during human liver transplantation. On the other hand, the finding of a low value in 4 of 18 patients suggests that plasma magnesium should be monitored and eventually corrected while the patient is on the waiting list.

Adolescent↗
PubMed1995

[Free oxygen radicals during transplantation surgery].

Free oxygen radicals are a highly reactive species of molecules characterized by an unpaired electron in the outer electron ring. They are formed continuously in the organism as part of enzymatic reactions, or as byproducts of oxidation processes. Antioxidants are able to eliminate free oxygen radicals, but during ischaemic reperfusion, the capacity of these systems is exceeded resulting in tissue injury, cell necrosis, destruction of enzymes and DNA-damage. Free oxygen radicals thereby play a major role in the tissue injury seen in organs after transplantation surgery and aorta operations. When the endogenous antioxidative capacity is exceeded, protection of lipid membranes against attack by free oxygen radicals by antioxidant supplementation is an alternative strategy for reduction of tissue injury. Since antioxidants are atoxic, they could also be of importance even in small operations, where the tissue blood supply is often periodically cut off.

Antioxidants↗
PubMed1995

Naloxone-provoked vaso-vagal response to head-up tilt in men.

A double-blind paired protocol was used to evaluate, in eight male volunteers, the effects of the endogenous opiate antagonist naloxone (NAL; 0.05 mg.kg-1) on cardiovascular responses to 50 degrees head-up tilt-induced central hypovolaemia. Progressive central hypovolaemia was characterized by a phase of normotensive-tachycardia followed by an episode of hypotensive-bradycardia. The NAL shortened the former from 20 (8-40) to 5 (3-10) min (median and range; P < 0.02). Control head-up tilt increased the means of thoracic electrical impedance [from 35.8 (SEM 2.1) to 40.0 (SEM 1.8) omega; P < 0.01] of heart rate [HR; from 67 (SEM 5) to 96 (SEM 8) beats.min-1, P < 0.02], of total peripheral resistance [TPR; from 25.5 (SEM 3.2) to 50.4 (SEM 10.5)mmHg.min.1-1, P < 0.05] and of mean arterial pressure [MAP; from 96 (SEM 2) to 101 (SEM 2)mmHg, P < 0.02]. Decreases were observed in stroke volume [from 65 (SEM 12) to 38 (SEM 9) ml, P < 0.01], in cardiac output [from 3.7 (SEM 0.7) to 2.5 (SEM 0.5) 1.min-1, P < 0.01], in pulse pressure [from 55 (SEM 4) to 37 (SEM 3)mmHg, P < 0.01] and in central venous oxygen saturation [from 73 (SEM 2) to 59 (SEM 4)%, P < 0.01]. During NAL, mean HR increased from 70 (SEM 3); n.s. compared to control) to only 86 (SEM 9) beats.min-1 (P < 0.02 compared to control) and MAP remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Arterial diameter during central volume depletion in humans.

The luminal diameter of the radial artery was followed by high frequency ultrasound during 50 degrees head-up tilt-induced central volume depletion in ten healthy subjects of whom six were tilted twice and pretreated with the serotonin receptor antagonist methysergide or placebo following a double-blind randomized design. Eight subjects without active treatment experienced presyncopal symptoms after 16-45 (mean 32 min). Central volume depletion was indicated by an increase in mean thoracic electrical impedance [from 31.5 (SEM 1.6) to 33.4 (SEM 1.7) omega; P < 0.05]. Cardiac output decreased [from 4.1 (SEM 0.3) to 2.2 (SEM 0.3) 1.min-1] and heart rate [HR, from 64 (SEM 3) to 100 (SEM 7) beats.min-1], mean arterial pressure (MAP, from 77 (SEM 4) to 89 (SEM 2) mmHg [10.3 (SEM 0.53 to 11.9 (SEM 0.27) kPa]) and total peripheral resistance (TPR, from 19 (SEM 2) to 34 (SEM 4) mmHg.min.1-1 [2.5 (SEM 0.27) to 4.5 (SEM 0.53) kPa.min.1-1]) increased; but with the appearance of presyncopal symptoms, HR, MAP and TPR were reduced to 65 (SEM 8) beats.min-1, 46 (SEM 4) mmHg [6.1 (SEM 0.53) kPa] and 18 (SEM 3) mmHg.min.1-1 [2.4 (SEM 0.4) kPa.min-1.1-1], respectively (P < 0.05). Vascular resistance was reflected in the arterial diameter which decreased from 2.42 (SEM 0.17) to 2.27 (SEM 0.14) mm during head-up tilt and increased to 2.71 (SEM 0.14) mm with the appearance of presyncopal symptoms (P < 0.05). Methysergide reduced the resting radial (15 +/- 2%) and temporal artery diameters (10 +/- 3%) (P < 0.05); however, it affected neither tilt-tolerance nor the central cardiovascular response to tilt. The results suggested a serotonergic influence on arterial tone at rest, and demonstrated that vessels as large as the radial artery participated in vascular control during central volume depletion independent of such a serotonergic influence.

Adult↗
PubMed1995

The venous pump does not affect the indifference point for electrical impedance in humans.

We have used regional electrical impedance at 2.5 and 100 kHz over nine body sections (two thoracic, one abdominal, two thigh, two around the knee, and two lower leg) in eight subjects to determine the volume indifference point defined as the level at which fluid volume remained constant independent of body position changes in space. Passive head-up tilt and tilt with activation of the venous muscle pump of the legs were performed in 10 degrees increments from 0 to 60 degrees over 6 min. The impedance changes in relation to 0 degree were similar for the two frequencies. Over the thorax it increased in proportion to the head-up tilt angle by a mean of 3.8 (range 1.9 to 9.3) omega (100 kHz) at 60 degrees (P < 0.05), while the abdominal impedance did not change significantly. Over the thigh it decreased with increasing head-up tilt angle by a mean maximum of -2.3 (range -9.4 to -0.4) omega and over the lower leg by a mean of -2.7 (range -6.0 to -0.8) omega. There were only marginal changes around the knee, mean -1.5 (range -2.3 to -0.2) omega (P < 0.05), and no change around the ankle indicating that little or no fluid was accumulated in these regions. Changes in impedance during passive and active head-up tilt did not differ significantly in any but one position: between the greater trochanter and the mid thigh, where during passive tilt it decreased by a mean of -4.8 (range -9.4 to -1.9) omega, and with activation of the venous pump by a mean of only -1.2 (range -1.9 to -0.4) omega (P < 0.05). These results indicated that the vascular volume indifference point was positioned between the navel and iliac crest both during the passive and active head-up tilts although during the passive tilt, apparently more fluid was accumulated in the vessels of the thigh.

Adult↗
PubMed1995

Functional loss of cerebral blood flow autoregulation in patients with fulminant hepatic failure.

In management of patients with fulminant hepatic failure, it is recommended that mean arterial pressure should be raised if cerebral perfusion pressure is lower than 50 mmHg, but the influence of such therapy on cerebral blood flow is unknown. We examined cerebral blood flow autoregulation in seven consecutive patients with fulminant hepatic failure during treatment of imminent insufficient cerebral perfusion pressure. Cerebral perfusion was evaluated by transcranial Doppler assessed mean flow velocity in the middle cerebral artery and by the arterio-venous difference for oxygen. Intracranial pressure was recorded by a subdural transducer and cerebral perfusion pressure calculated as the difference between mean arterial pressure and intracranial pressure. After 20 (range 10 to 43) min, mean arterial pressure was raised from 74 (43-80) to 94 (76-114) mmHg by i.v. noradrenaline, cerebral perfusion pressure increased from 49 (26-75) to 82 (50-108) mmHg (p < 0.01) as the intracranial pressure remained unchanged at 26 (3-35) mmHg. The mean flow veolocity increased from 68 (30-134) to 108 (48-168) cm s-1 and the arterio-venous difference for oxygen by 46 (10-82)% (p < 0.05). Both mean flow velocity (r = 0.63) and arterio-venous difference for oxygen (r = 0.71) were correlated to mean arterial pressure (p < 0.001), and a lower blood pressure limit of autoregulation could not be identified in any of the patients. These data suggest that the cerebral blood flow is not autoregulated in patients with fulminant hepatic failure and therefore cerebral blood flow should be "clamped" within the normal physiologic range by manipulation of arterial blood pressure in order to avoid cerebral hypoxia and/or hypertensive induced cerebral oedema.

Acute Disease↗
PubMed1995

Restricted pulmonary diffusion capacity after exercise is not an ARDS-like injury.

Pulmonary diffusion capacity (DLCO) is reduced 2 h after various types of exercise, such as rowing, treadmill running, arm cranking and marathon running. The decrease in DLCO may involve alterations in the alveolar-capillary membrane as well as depletion of the central blood volume. We hypothesized that the reduction in DLCO might also be influenced by oxygen free radicals, acute phase proteins and endotoxin, which are also involved in the adult respiratory distress syndrome (ARDS). Ten competitive male oarsmen performed a 6 min 'all-out' ergometer row. Single breath DLCO was determined before and 2 h after rowing and venous blood samples were also obtained during the row. Absolute DLCO decreased by 11% (range 0-20%) 2 h after rowing, whereas the concentration of endotoxin did not change significantly and interleukin (IL)-1-alpha, IL-8 and tumour necrosis factor (TNF)-alpha were below the levels of detection before, during and 2 h after rowing. Oxygen free radicals were evaluated by oxidative modification of amino acids and DNA. Corrected for creatinine in urine voided 3 h post-exercise, the DNA repair product 8-oxo-7,8-dehydro-2-deoxyguanosine (8-oxodG) did not change significantly. The ratio of fluorescence due to dityrosine to that due to tryptophan in plasma proteins increased after exercise. This might reflect an effect of oxygen free radicals, but it might also indicate an altered relative composition of plasma proteins. These results suggest that the reduced pulmonary diffusion capacity following exercise is unrelated to factors typically associated with ARDS.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1995

Thoracic electrical impedance and fluid balance during aortic surgery.

Indices of fluid balance were evaluated during and after aortic surgery in 16 consecutive patients. Thoracic electrical impedance (TI), heart rate (HR), central venous (CVP), pulmonary artery mean (PAMP), pulmonary wedge (PWP) and mean arterial (MAP) pressure as well as fourteen arterial and venous blood gas variables were followed. Consistent with a reduction of T1 by 4.2 (-5.2 to 9.2) Ohm (median and range) during the operation, fluid balance was in excess of 1.8 (-0.1 to 3.3) 1 when evaporation was not taken into account, and it remained elevated by 1.3 (0.0 to 5.4) 1 on the first postoperative morning. The HR, MAP and PWP remained stable, while CVP and PAMP decreased by 6 (-2 to 13) and 6 (-1 to 22) mmHg, respectively. Of the determined variables only TI revealed a meaningful correlation to fluid balance (rho = -0.41; P < 0.01). Haemoglobin concentrations increased in proportion to the administered packed erythrocytes, while arterial oxygen saturation, pH and base excess decreased in proportion to the excess fluid. The results indicate that while central venous and pulmonary artery mean pressures gave the impression of a volume deficit, the positive fluid balance was mirrored by thoracic electrical impedance, and that even a minor increase of fluid balance may affect pulmonary function in patients subjected to aortic surgery.

Aged↗
PubMed1995

A maximal central venous oxygen saturation (SvO2max) for the surgical patient.

Before induction of anaesthesia, 23 patients scheduled for major abdominal surgery had blood samples drawn from a central venous catheter for oxygen saturation (SvO2) after graded infusion of isotonic saline. The infusion of saline was continued until further administration resulted in a stable SvO2 (SvO2max). The SvO2 increased from 69 (53-83) to 72 (66-83) % (median and range; P < 0.0001), when the patients received 10 (0-26) mL.kg-1, average 500 mL, of saline. At the same time central venous haematocrit decreased from 38 (32-47) to 36 (23-47) % which suggests that the intravascular volume was expanded by 420 (180-3070) mL or by 72 (18-174) % of the administered volume. The results demonstrate that volume expansion by saline can establish a maximal venous oxygen saturation in the surgical patient.

Abdomen↗
PubMed1995

Cardiovascular and hormonal responses to anaphylactic shock in the pig.

Cardiovascular and hormonal responses to anaphylactic shock were evaluated in anaesthetized pigs sensitized by natural exposure to Ascaris suum as verified by antibodies. In six animals with such antibodies, Ascaris antigen injection produced a plasma histamine increase of 52 (42-196) fold (median and range; P < 0.05), while four pigs without such antibodies served as controls with only insignificant increases in histamine. In the anaphylactic group, two of the animals died during the investigation due to cardiovascular collapse. In the sensitized pigs resting heart rate (HR), 104 (86-118) beats min-1, increased to 204 (164-240) beats min-1 as mean arterial pressure (MAP) decreased from 94 (83-102) to 45 (31-90) mmHg (P < 0.05). In contrast, the non-sensitized pigs maintained the resting HR of 101 (79-113) beats min-1, as MAP decreased to 50 (41-97) mmHg (P < 0.05). In the sensitized group systemic vascular resistance (SVR) fell from 1114 (843-1811) to 990 (588-1173) dyne s-1 cm-5 and then increased to 3617 (2593-4166) dyne s-1 cm-5, while in the control group there was only a reduction to a minimum value of 730 (458-1307) dyne s-1 cm-5 (P < 0.05). Thoracic electrical impedance increased only in the sensitized group [from 28.3 (24.7-31.4) to 29.9 (24.0-31.4)], indicating central volume depletion. Plasma catecholamines increased markedly only in the sensitized pigs, and plasma pancreatic polypeptide, vasopressin, aldosterone and renin responses confirmed to those established during central hypovolaemia. During anaphylaxis, this study demonstrated cardiovascular responses similar to those established during a major blood loss. However, as indicated by plasma catecholamines, sympathetic activity was many times that previously demonstrated during haemorrhage, and sympathoactivation may explain the marked vasoconstriction noted in the sensitized pigs.

Anaphylaxis↗
PubMed1995

Cerebral perfusion during human liver transplantation.

During transplantation of the liver cerebral perfusion was monitored by transcranial Doppler determined middle cerebral artery mean flow velocity (Vmean) and pulsatility index (PI) in six fulminant hepatic failure patients and 11 patients with chronic liver disease. In both groups of patients Vmean, PI and central haemodynamic variables were recorded during (1) the last preanhepatic hour; (2) the anhepatic phase; (3) the first 15 min of reperfusion; and (4) for the following 45 min of reperfusion. No significant differences were detected between the two groups of patients with respect to changes of variables with time. The Vmean (40 +/- 13 cm s-1 [mean +/- SD]), thoracic electrical impedance (TI) (30 +/- 7 Ohm), heart rate (97 +/- 19 beats min-1), mean arterial pressure (84 +/- 9 mmHg) and arterial carbon dioxide tension (PaCO2, 4.5 +/- 0.4 kPa) remained stable in the anhepatic phase, while cardiac output (CO, 7.6 +/- 2.7 to 5.4 +/- 1.41 min-1), stroke volume (SV, 79 +/- 26 to 56 +/- 15 ml) and PI (1.2 +/- 0.3 to 0.9 +/- 0.2) decreased (P < 0.05). During reperfusion, CO (9.9 +/- 4.01 min-1), SV (105 +/- 40 ml), PaCO2 (5.5 +/- 0.6 kPa), Vmean (57 +/- 17 cm s-1) and PI (1.2 +/- 0.2) became elevated. Taken together, during the anhepatic phase of the liver transplantation a maintained central blood volume as indicated by the constant TI served for a stable blood pressure and in turn cerebral perfusion, whereas revascularization of the graft increased cerebral perfusion concomitant with an elevated carbon dioxide tension.

Adult↗