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Biomedical subjects

B Vollmar

Publications and source records attributed to B Vollmar.

At least 163 records · Page 9Linked to original sources
PubMed1992

Coronary microcirculation during halothane, enflurane, isoflurane, and adenosine in dogs.

We investigated the effects of clinically administered volatile anesthetics and of adenosine on the microvasculature of the in situ beating canine heart. Thirteen dogs were studied during general anesthesia with an opioid (piritramide), which was infused throughout the experiments. Measurements were obtained in each animal at control (piritramide only) and during hypotension (mean arterial pressure 60 mmHg) induced by halothane, enflurane, isoflurane, and adenosine. Using epiillumination and fluorescence microscopy, 354 arterial microvessels with diameters from 20 to 450 microns were examined through all experimental periods. Hypotension by halothane, enflurane, isoflurane, and adenosine reduced coronary vascular resistance by 13%, 23%, 40%, and 85%, respectively. Coronary venous PO2 was unchanged from control with halothane (+/- 0%) and enflurane (+7%) and significantly increased with isoflurane (+16%) and adenosine (+65%). Left ventricular blood flow decreased significantly during halothane (-35%) and enflurane (-23%); was unchanged from control during isoflurane (-9%); but significantly increased during adenosine (+397%). Coronary arterial and arteriolar diameters increased with all hypotensive agents. Vasodilation was least with halothane, intermediate with enflurane and isoflurane, and most pronounced with adenosine. Diameters increased considerably more in vessels with initial diameters below 100 microns as opposed to larger vessels. Calculation of microvascular segmental resistances revealed that the maximum conductance changes during volatile anesthetics were located in the vessel segments visualized by microscopy, i.e., in vessels larger than 20 microns. However, this was not the case with adenosine. We conclude that volatile anesthetics induce coronary vasodilation by preferentially acting on vessels with diameters from 20 microns to approximately 200 microns, whereas adenosine, in addition, has a pronounced impact on the small precapillary arterioles.

Adenosine↗
PubMed1992

Effect of leukopenia on pulmonary hypertension after heparin-protamine in pigs.

Heparin neutralization by protamine after cardiac surgery and cardiopulmonary bypass may be associated with complement activation, transient leukopenia, thromboxane A2 release, and severe pulmonary hypertension. The role of leukocytes in the heparin-protamine reaction was studied in leukopenic pigs (n = 9) and a control group (n = 8). Leukopenia was induced by pretreatment with cyclophosphamide (30 mg.kg-1.day-1) for 6-7 days. During general anesthesia and after catheterization, baseline recordings of hemodynamics were performed and blood samples were withdrawn. Heparin (250 IU/kg) was injected and measurements were repeated after 10 min. Protamine sulfate (100 mg) was then infused over 2 min and measurements were performed after 2, 5, and 15 min. Prostanoid concentrations were measured by radioimmunoassays. In additional in vitro experiments, the release of thromboxane B2 from washed platelets and leukocytes after heparin-protamine stimulation was measured. Pretreatment with cyclophosphamide reduced leukocyte counts by 95.5% and the number of neutrophils by greater than 99.9%. Protamine infusion increased mean pulmonary arterial pressure by 74 and 46% and pulmonary vascular resistance by 185 and 384% in control and leukopenic animals, respectively. Thromboxane B2 concentrations increased in both groups. Stimulation by heparin, protamine, or heparin and protamine in sequence did not induce any thromboxane A2 release from washed blood cells. It is concluded that leukocytes do not contribute to pulmonary hypertension after heparin-protamine.

Animals↗
PubMed1992

Modified retrograde orotracheal intubation technique for airway access in rabbits.

Anatomical features of the oral fissure and pharynx of rabbits make orotracheal intubation a difficult task with a high failure rate. We have developed a versatile technique for retrograde intubation of rabbits which consists of the following steps: (1) assessment of the trachea through a cervicotomy (2) insertion of a guidewire into its lumen, (3) delivery of the guide through the mouth, and (4) introduction of the orotracheal tube over the guide. This procedure was performed in 58 rabbits under pentobarbital anesthesia and resulted in successful orotracheal intubation in 56 animals. Awakening from anesthesia and extubation were uneventful. No complications related to this technique were observed during a follow-up period of 5-14 days. The described technique is a simple and safe method to access the airways of rabbits and can be useful in chronic experiments.

Anesthesia↗
PubMed1992

Systemic and regional hemodynamics of isoflurane and sevoflurane in rats.

The authors studied the effects of sevoflurane and isoflurane on systemic hemodynamics and regional blood flow distribution (microsphere technique) in 15 rats during general anesthesia with intravenous chloralose and controlled ventilation. Inhaled anesthetics were applied to reduce mean arterial blood pressure (MAP) to 70 mm Hg (1.66 vol% sevoflurane and 0.96 vol% isoflurane) and 50 mm Hg (MAP 50; 3.95 vol% sevoflurane and 2.43 vol% isoflurane). Control recordings were obtained with intravenous chloralose only. At a MAP of 70 mm Hg, both anesthetics reduced heart rate, cardiac output, and systemic vascular resistance to a similar degree. Isoflurane decreased systemic vascular resistance markedly at a MAP of 50 mm Hg and thereby maintained cardiac output at higher levels than sevoflurane. The left ventricular rate-pressure product decreased comparably with both anesthetics. Cerebral blood flow increased dose-dependently with both inhaled anesthetics but to a greater degree with isoflurane. Total hepatic blood flow remained unchanged from control at a MAP of 70 mm Hg but decreased at a MAP of 50 mm Hg. This was due to reductions of hepatic arterial and portal venous tributaries. Renal blood flow was reduced with only the high concentrations of the anesthetics. Myocardial blood flow was reduced at all concentrations of volatile anesthetic; however, the decrease was less with isoflurane. This would indicate a more pronounced coronary vasodilation by isoflurane as the rate-pressure product, as a measure of the actual left ventricular oxygen demand, decreased by comparable degrees with both anesthetics. Our results indicate that sevoflurane and isoflurane (each approximately 0.7 MAC) have no dissimilar systemic and regional hemodynamic effects at a MAP of 70 mm Hg in this animal model. At higher concentrations (approximately 1.7 MAC), cerebral blood flow was more with isoflurane than with sevoflurane and was associated with a more pronounced vasodilation in the myocardium.

Anesthesia, General↗
PubMed1992

Blood flow and tissue oxygen pressures of liver and pancreas in rats: effects of volatile anesthetics and of hemorrhage.

The object of this investigation was to compare the effects of volatile anesthetics and of hemorrhage at comparable arterial blood pressures on splanchnic blood flow (radioactive microspheres) and tissue oxygenation of the liver and pancreas (surface PO2 [PSO2] electrodes). In contrast to earlier studies, we did not use identical minimum alveolar anesthetic concentration multiples as a reference to compare volatile anesthetics; rather, we used the splanchnic perfusion pressure. Under general anesthesia (intravenous chloralose) and controlled ventilation, 12 Sprague-Dawley rats underwent laparotomy to allow access to abdominal organs. Mean arterial pressure was decreased from 84 +/- 3 mm Hg (mean +/- SEM) at control to 50 mm Hg by 1.0 +/- 0.1 vol% halothane, 2.2 +/- 0.2 vol% enflurane, and 2.3 +/- 0.1 vol% isoflurane in a randomized sequence. For hemorrhagic hypotension, blood was withdrawn gradually until a mean arterial pressure of 50 mm Hg was attained. Volatile anesthetics and hemorrhage reduced cardiac output, and hepatic arterial, portal venous, and total hepatic blood flows by comparable degrees. Mean hepatic PSO2 decreased significantly from 30.7 +/- 2.6 mm Hg at control to 17.4 +/- 2 and 17.5 +/- 2 mm Hg during enflurane and isoflurane (each P less than 0.05) anesthesia, respectively. The decrease to 11.5 +/- 2.5 mm Hg was more pronounced during halothane anesthesia. Hemorrhagic hypotension was associated with the lowest hepatic PSO2 (3.4 +/- 1.3 mm Hg) and the highest number of hypoxic (0-5 mm Hg 86%) and anoxic PSO2 values (0 mm Hg 46%). Pancreatic blood flow and oxygenation remained unchanged from control during halothane and enflurane administration, whereas isoflurane increased both variables. Hemorrhagic hypotension slightly reduced pancreatic flow (-8%) but significantly decreased PSO2 from 58 +/- 5 mm Hg at control to 36 +/- 3 mm Hg, with 7% of all measured values in the hypoxic range. Thus, volatile anesthetics preserved pancreatic but not hepatic blood flow and tissue oxygenation in this rat model. Despite comparable effects on perfusion, the PSO2 of the liver and pancreas was the least during hemorrhagic hypotension compared to that with the anesthetics. Because the volative anesthetic-induced hypotension has such a different effect on splanchnic tissue oxygenation compared with hemorrhagic-induced hypotension, the authors conclude that the method of inducing hypotension may have different effects on oxygenation of various tissues.

Anesthetics↗
PubMed1992

[Delay phenomenon of the jejunum. Studies of nutritional blood supply and oxygen supply of the jejunum of the rabbit].

INTRODUCTION: Delay procedure has been shown to effectively improve microvascular perfusion in skin flaps. In analogy to skin, we have analyzed the effect of delay on regional blood flow and surface tissue PO2 of a proximal segment of the jejunum. METHODS: Under nembutal anesthesia (30 mg/kg BW) and mechanical ventilation a total of 15 rabbits were laparotomized. Regional blood flow of the jejunum was estimated using radioactive-labeled microspheres, and tissue PO2 was assessed by means of a platinum-multiwire surface electrode. In order to induce acute ischemia three consecutive jejunal arteries were ligated, and the proximal marginal vascular arch was temporarily occluded by a microvascular clip. Delay procedure was induced by 1) ligation of the jejunal arteries, 2) in situ-maintenance of the jejunal segment for two weeks followed by 3) relaparotomy and occlusion of the proximal marginal arch (n = 8). Regional blood flow of the jejunum and tissue PO2 were also assessed in sham-operated animals (n = 7). RESULTS: After acute ischemia regional blood flow (0.27 (0.05) ml x min-1 x g-1, mean (SEM)) and surface tissue PO2 (39 (3) mmHg) of the jejunal segment were found significantly (p < 0.05) reduced as compared to baseline (0.82 (0.12) ml x min-1 x g-1 and 66 (1) mmHg) and sham-operated animals (0.69 (0.12) ml x min-1 x g-1 and 62 (5) mmHg), respectively. In contrast, delay of the jejunal segment resulted in almost complete preservation of regional blood flow (0.56 (0.04) ml x min-1 x g-1) and surface tissue PO2 (65 (1) mmHg). CONCLUSION: We therefore like to propose that the jejunal delay phenomenon may be clinically used to reduce ischemic complications in jejunal transposition for esophagoplasty.

Animals↗
PubMed1992

[Anesthesiologic efficacy of propanidid as a liposome dispersion. An experimental study with rats].

BACKGROUND: Propanidid, an ultra-short-acting i.v. anaesthetic agent, was widely used in the 1960s. Reports of anaphylactoid reactions in patients associated with release of histamine following administration of the drug, however, led to withdrawal of this useful anaesthetic. Since the adverse side effects of the former solution could be attributed to the solvent cremophor, attempts have recently been made to produce a propanidid solution without addition of the solvent. We report on comparative investigations employing a new liposomal solution (B. Braun, Melsungen, FRG) and the conventional cremophor preparation with regard to anaesthetic properties, haemodynamic side effects, and electroencephalographic effects (EEG). METHODS: Sprague-Dawley rats (n = 46) were implanted with venous and arterial lines and epidural EEG electrodes during chloral-hydrate anaesthesia. The following day, arterial blood pressure (ABP), heart rate (HR), and EEG were monitored in awake animals and then after induction of anaesthesia by a bolus of the respective propanidid preparation, followed by an infusion period of 15 min in six different experimental groups. Animals of groups L-60, L-90, L-120, or C-60, C-90, or C-120 groups received 60, 90, or 120 mg.100 g-1.h-1 of the liposomal (L) or cremophor (C) preparation. During anaesthesia, the corneal reflex and nociception to tail-clamping were also tested. At termination of the infusion, blood samples were drawn for determination of plasma propanidid concentrations. RESULTS: Both preparations were similarly effective in induction and maintenance of anaesthesia in a dose-dependent manner; both similarly lowered ABP and HR. The corneal reflex and nociceptive responses to tail clamping were also comparably suppressed. However, whereas the liposomal preparation was well tolerated at higher dose levels, the cremophor preparation caused considerable dose-dependent mortality of 11%, 86%, and 86% in animals in groups C-60, C-90, and C-120, respectively. Both preparations were found to induce a burst-suppression pattern in the EEG associated with clonic seizures, with a lower incidence with the liposomal preparation (22% and 50% in groups L-90 and L-120) as compared to the cremophor preparation (100% and 89% in groups C-90 and C-120). A remarkable variability in propanidid plasma concentrations was found at the end of the infusion period, although no differences were observed between both preparations. Discontinuation of infusion of propanidid resulted in rapid awakening (less than 5 min), irrespective of whether the liposomal or conventional preparation was employed. CONCLUSION: The present findings demonstrate largely identical anaesthetic potencies of a new liposomal solution as compared to the conventional cremophor preparation of propanidid. The liposomal preparation, however, was superior as far as tolerance and incidence of clonic seizures was concerned. The present findings should prompt further studies on the suitability of liposomal propanidid as a short-acting anaesthetic agent in patients.

Anesthesia, Intravenous↗
PubMed1992

Dilation of coronary microvessels by adenosine induced hypotension in dogs.

An experimental model was established for fluorescence video microscopy of coronary microvessels. Nineteen dogs were anesthetized with a narcotic. Catheters were placed for hemodynamic monitoring and sampling of arterial and coronary venous blood. Myocardial perfusion was measured with radioactive microspheres. Following thoracotomy, movements of the myocardial surface area under investigation were restricted by a specially designed heart holder. Plasma was stained with FITC labelled dextran. Diameters were determined in arteriolar and venular microvessels greater than or equal to 20 microns. Measurements were performed during baseline conditions, i.e. only the basic anesthetic drug was applied, and during coronary vasodilation by continuous infusion of adenosine in a randomized sequence. Mean arterial pressure was reduced from 85 +/- 2 mmHg during baseline to 59 +/- 1 mmHg by infusion of 16.9 +/- 2.2 mg.kg-1.h-1 adenosine. Adenosine increased left ventricular blood flow by 253%, left ventricular oxygen demand remained unchanged. A total of 495 arteriolar and 170 venular diameters were measured during baseline condition and during adenosine infusion. Arteriolar diameters increased in all vessel segments between 20 and 600 microns, however, arterioles below a critical size of 100 microns had a greater dilating capacity than larger arterioles. Maximal decrease of segmental resistance occurred in 20-40 microns arterioles and amounted to 74%, which is less than the 82% decrease of total coronary resistance. Venular diameter changes, too, were more pronounced in smaller vessels.

Adenosine↗
PubMed1991

Oleic acid induced pancreatitis in pigs.

An experimental model of edematous pancreatitis in pigs was established and measurement of pancreatic macro- and microcirculatory parameters and determinations of pancreatic enzymes (lipase, phospholipase A) and vasoactive mediators (prostanoids, kallikrein, kininogen) were performed. During general anesthesia the pancreas was isolated in situ. Pancreatic microcirculatory parameters were measured using videofluorescence microscopy after iv administration of FITC-Dextran. In hourly collected samples lipase and phospholipase A activities were determined enzymatically, concentrations of kallikrein, kininogen, and selected prostanoids were measured by radioimmunoassay. Two experimental groups were studied: (1) control (n = 9); (2) edematous pancreatitis induced by injection of oleic acid into the pancreatic artery (free fatty acid, ffa; n = 10). The animals were followed up for 6 hr. Systemic hemodynamic parameters remained constant in both groups. In the pancreatitis group pancreatic blood flow and O2-consumption decreased significantly (-55 and -49%), while pancreatic vascular resistance increased significantly (+50%). During baseline conditions 41% of all capillaries were perfused. In the pancreatitis group there were both areas with persistent stasis as well as areas with continuous perfusion. However, in the latter areas the portion of perfused capillaries decreased significantly to 27%. In the control group the portion of perfused capillaries remained constant. Liberation of lipase and phospholipase A especially into lymph and ascites fluid was measured during pancreatitis. Furthermore, considerable releases of kallikrein into lymph (+50%) and ascites (+800%) and a marked consumption of kininogen in lymph (+90%) and in ascites fluid (+80%) were measured. Activation of the arachidonic acid cascade and a significant release of prostacyclin and thromboxane A2 into pancreatic venous blood and lymph was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1991

Left ventricular surface tissue oxygen pressures determined by oxygen sensitive multiwire electrodes in pigs.

STUDY OBJECTIVE: Polarographic oxygen sensitive electrodes can be used to measure tissue oxygen pressures on the surface of the beating heart. The purpose of the study was to clarify the significance of these PO2 determinations. DESIGN: Changes in left ventricular surface oxygen pressures, subendocardial or subepicardial wall functions (ultrasonic dimension technique), and blood flow (radioactive microsphere technique) were correlated during different degrees of acute coronary artery stenoses in pigs. EXPERIMENTAL MATERIAL: 19 anaesthetised open chest pigs, 28-40 kg body weight, were studied during different degrees of constriction of the left anterior descending artery which did not influence overall left ventricular function or irreversibly damage the myocardium. MEASUREMENTS AND MAIN RESULTS: Highly significant (p less than 0.001) correlations (each % delta) were obtained for surface tissue oxygen pressures (y) with subepicardial (y = 0.002 e 0.10x; r = 0.89) and subendocardial (y = 1.44 e 0.04x; r = 0.98) blood flow values, as well as with subendocardial function (y = 82.4 + 0.22x; r = 0.89); a significant correlation was also obtained for subendocardial function (y) with subendocardial blood flow (y = 66.0 + 0.28x; r = 0.69). However, no significant correlation was obtained for polarographic tissue PO2 with subepicardial segment function, indicating that regional function was maintained when tissue PO2 recordings were not much above 0 kPa and when blood flow was reduced by 25 to 30%. CONCLUSIONS: Oxygen pressures of the superficial layers of the left ventricle are relatively high at normal values of oxygen consumption but decrease rapidly if blood supply is reduced. Regional wall function is preserved at low oxygen pressures. Polarographic surface PO2 electrodes hence can be used to study influences of experimental interventions on oxygenation of the normally perfused and of the moderately ischaemic myocardium.

Animals↗
PubMed1990

Epicardial oxygen tensions during changes in arterial PO2 in pigs.

Arterial hypoxemia decreased epicardial tissue PO2, measured by means of a multiwire surface electrode, as well as coronary venous PO2 and myocardial lactate extraction. Left ventricular blood flow increased, O2 delivery, O2 demand and O2 consumption of the left ventricle remained unchanged. Thus, epicardial and coronary venous PO2 indicated decreased capillary and interstitial PO2 rather than cellular hypoxia. A linear relation between mean epicardial PO2 and coronary venous PO2 proves both parameters equally effective in reflecting changes in myocardial tissue oxygenation. However, PO2 distribution curves provide additional information and epicardial PO2 is superior in models with regional changes of myocardial oxygenation.

Animals↗
PubMed1990

[Pancreatic circulation in experimental biliary pancreatitis].

Measurements of pancreatic micro- and macrocirculation were performed to evaluate the pancreatitis-induced changes. Pigs were anesthetized and ventilated mechanically. Hypotension induced side-effects were avoided by adequate volume replacement. After laparatomy, splenectomy and gastroectomy the animals were enterotomized. Systemic hemodynamic parameters were monitored as well as pancreatic blood flow (Q), which was measured electromagnetically, and arterial and portal-venous blood gases. Pancreatic microcirculatory parameters were observed using fluorescence-videomicroscopy after i.v. administration of FITC dextran 150 and FITC labeled autologous erythrocytes. The pigs were randomly assigned to a control (n = 9) and a pancreatitis group (n = 10), the later being induced by the retrograde infusion of sodium-taurocholate. Systemic and pancreatic macrohemodynamic parameters remained constant in both groups, except for avdO2 and O2-consumption (O2-c) decreasing significantly in the pancreatitis group. At baseline 42% of all capillaries were perfused in both groups. In pancreatitis we detected focal areas with persistent stasis and areas which were continuously perfused. In these areas the portion of capillaries perfused by erythrocytes increased significantly to 67%. This was accompanied by an extravasation of FITC dextran. The finding of an unchanged Q beside reduced O2-c and avdO2 during pancreatitis is explained by the changes in pancreatic microcirculation. Focal stasis was observed beside areas showing typical signs of an acute inflammation: increased macromolecular permeability and capillary recruitment, e.g. oedema and hyperaemia.

Acute Disease↗
PubMed1990

Pulmonary hypertension after heparin-protamine: roles of left-sided infusion, histamine, and platelet-activating factor.

Severe pulmonary hypertension after protamine neutralization of heparin is an infrequent but life-threatening event following cardiopulmonary bypass. The effect of left ventricular infusion of protamine on pulmonary hypertension as well as a possible role of platelet-activating factor (PAF) or histamine in the heparin-protamine reaction was investigated in 30 pigs in four different groups during general anesthesia. Group 1 animals received 250 IU/kg heparin, followed by 100 mg protamine intravenously after 15 min. In group 2 protamine was infused into the left ventricle. Group 3 animals received the histamine H1- and H2-antagonists clemastine and ranitidine 5 min before protamine infusion. In group 4 the PAF receptor blocker WEB 2086 was given 5 min before protamine. Platelet-activating factor was measured by a bioassay in serum samples of group 1 and group 4 animals. In all four groups protamine caused severe pulmonary hypertension, thromboxane A2 release, and a transient decrease in leukocyte counts. No PAF release was detected after protamine infusion. Neither left ventricular infusion of protamine nor histamine or PAF antagonists prevented or attenuated the reactions after protamine infusion. The authors conclude that left ventricular infusion of protamine provides no protection from pulmonary hypertension, and that histamine and PAF are not involved in the acute pulmonary vasoconstriction after protamine neutralization of heparin.

Animals↗
PubMed1989

Release of arachidonic acid metabolites during acute pancreatitis in pigs.

The pancreatic release of arachidonic acid metabolites was studied in a porcine model of acute pancreatitis. In situ isolation of the pancreatic gland enabled selective collection of pancreatic venous blood, pancreatic lymph, and ascites fluid. Three experimental groups were studied: 1) control (n = 9); 2) hemorrhagic pancreatitis induced by injection of 5% bile salt (sodium taurocholate) into the pancreatic duct (n = 10); and 3) edematous pancreatitis induced by injection of free fatty acid (FFA) into the pancreatic artery (n = 10). Determinations of cyclooxygenase metabolites were performed by radioimmunoassay; lipoxygenase metabolites (LTC4, LTD4) were measured by radioimmunoassay after purification by high-performance liquid chromatography. Prostaglandin (PG)F1 alpha, thromboxane B2, and PGF2 alpha concentrations were almost doubled in the lymph of the FFA group during pancreatitis, as were PGF1 alpha levels in pancreatic venous blood. However, concentrations of cyclooxygenase metabolites remained unchanged in the control group and in the bile salt group. Concentrations of LTC4 and LTD4 in lymph and ascites fluid of both pancreatitis groups increased from about 50 pg/ml to a mean level of 600 pg/ml at 6 h. Leukotriene concentrations in the control group were consistently below 50 pg/ml. The results of this study indicate that above all LTC4 and LTD4 are released from the organ and that these arachidonic acid metabolites may be also involved in the events following acute pancreatitis contributing to the systemic effects of the disease.

Acute Disease↗
PubMed1987

Weight percentile at birth. I. Clinical data of pregnancy and relevance for early childhood development.

The influence of the weight percentile at birth on childhood development was examined in a prospective study of 847 singleton pregnancies. In the first two years of life significant relationships between the birth weight percentiles and the infant's development could be proven, while at the age of four social factors were predominant. Though various clinical data in pregnancy and delivery were related to fetal growth, such as weight of the mother, previous abortions and diseases, additional biochemical and biophysical information is desirable for early recognition of intrauterine growth disorders.

Birth Weight↗
PubMed1987

Weight percentile at birth. II. Prediction by endocrinological and sonographic measurements.

In a prospective study of 847 singleton pregnancies, the importance of various endocrine methods (serum estriol, HPL, SP1, beta-HCG, estradiol-17 beta, urinary estrogen excretion) and of two sonographic measurements (biparietal and thoracic diameter) for the diagnosis of growth retardation in the third trimester was studied. HPL and estriol determinations were best suited for the diagnosis of growth retardation. The thoracic diameter correlated most closely with the birthweight of the newborns. Sensitivity in relationship to growth retardation was between 17 and 35% for the HPL and estriol determinations as well as for both sonographic methods. Specificity was around 90% for these methods. The validity for all methods improved as the time of birth approached. Through the simultaneous measurement of one of the hormones and the thoracic diameter, an antepartal diagnosis of up to 50% of the hypo- and hypertrophic growth disorders was achieved. In the first two years of life a relationship between development and the HPL and estriol concentrations could be observed which was independent of the weight percentile at birth.

Birth Weight↗