Late changes in aorto-renal vein transplants

The results of 152 renal artery reconstructions in 128 hypertensive patients were reviewed 1 to 15 years postoperatively in 89 of 98 survivors. Forty-seven (52.8%) patients were normotensive, 29 (32.6%) are improved, and 13 (14.6%) were not improved. Angiography was performed 1 to 11 years after the operation. Only 2 of the 31 vein implants showed an adequate lumen. Four vein grafts were occluded. In 2 out of 4 stenosed transplants stenosis was functionally significant, and the patients with recurrent hypertension underwent re-reconstruction. The causes of the stenoses were severe constriction by scar tissue and extensive subintimal cellular proliferation of the vein graft. Twelve of 31 vein bypass grafts were dilated by an average of 22%. The average increase in caliber of the remaining 9 vein grafts was 106%. The possible contributory factors were forceful distension, excessive adventitial dissection, inadequate storage of the vein, ischemic damage of the vein wall (especially in younger patients), and the increase flow rate through the transplant.     

Measurement of the Fowler dead space in patients with pulmonary emphysema using C18O2

In patients with lung emphysema, changes in lung volumes as well as changes in airway resistance are well known. The change in airway resistance is caused by obstruction of central airways, which is supposed to reduce the respiratory dead space. Until now, it was not possible to measure the respiratory dead space in patients with lung emphysema using the method of Fowler [2], because in this method distinction of the three phases of an inert gas expirogram is essential. While this distinction is easy in healthy subjects (fig. 1; expirogram 3), the separation of the three phases in patients with lung emphysema is not possible due to gradual transition of phase II into phase III in these patients (fig. 1; expirogram 2). The use of C18O2 as tracer gas allows to separate phase II and phase III even if the patients have severe emphysema (fig. 1; expirogram 1). CO2 labeled with the stable oxygen isotope 18O (C18O2) is completely taken up in the gas exchanging region of the lung, but not from the conducting airways. Therefore C18O2 is only expired from the dead space of the lung, but not from the alveolar region. Hence, C18O2 allows exact measurement of the respiratory dead space in patients with lung emphysema. 21 healthy nonsmoking subjects and 29 patients with clinical signs of lung emphysema participated in this study. There was a good correlation between respiratory dead space, measured by the use of Ar-gas and C18O2-gas in healthy subjects (fig. 2). This indicates, that the use of C18O2 is a valid method to measure the functional dead space. As expected, there was also a correlation between the airway resistance and respiratory dead space in patients with lung emphysema (fig. 3), but not in healty subjects. There was no significant difference of the mean values of the respiratory dead space between these two groups (223 +/- 43 ml in healthy subjects vs. 227 +/- 52 ml in patients), even though there were large differences in airway resistance (0.20 +/- 0.10 kPa/l/s vs. 0.49 +/- 0.27 kPa/l/s). This may be due to a loss of alveolar function in the area of the terminal bronchioli, which is typical for emphysematous patients. This entails a shift of functional dead space towards lung periphery and therefore causes an increase of the volume of functional dead space. But this enlargement may be compensated by the volume reduction, caused by the airway obstruction. Hence, these two oppositional mechanisms may result in only minimal change of dead space volume.     

Heart rate variability and circulating catecholamine concentrations during steady state exercise in healthy volunteers.

OBJECTIVES--To assess whether exercise induced suppression of heart rate variability in the low frequency domain (0.06-0.15 Hz) is related to the increase in circulating catecholamine concentrations. DESIGN--Randomised crossover trial of three exercise tests characterised by different workloads. Pharmacological simulation of exercise-induced changes in vagal and sympathetic activity. PARTICIPANTS--Six healthy men with a mean age of 31.2 (SD 3.0) years. INTERVENTIONS--Three different workloads of steady state cycling ergometry: control state without cycling, cycling at a target heart rate of 100 beats/min, and cycling at a target heart rate of 150 beats/min. Intravenous infusion of atropine (target heart rate 100 beats/min) followed by the additional infusion of adrenaline and noradrenaline. MAIN OUTCOME MEASURES--Fast Fourier analysis of heart rate variability; blood pressure; and venous plasma concentrations of lactate, adrenaline, and noradrenaline. RESULTS--During the control exercise period there were no changes in the assessed variables compared with the preceding resting period. During exercise at a heart rate of 100 beats/min systolic blood pressure increased and heart rate variability decreased. During exercise at a heart rate of 150 beats/min systolic blood pressure and lactate, adrenaline, and noradrenaline concentrations increased. In addition, low frequency (LF) was lower than during exercise at 100 beats/min, high frequency (HF 0.15-0.80 Hz) resembled that during exercise at 100 beats/min, and diastolic blood pressure was reduced. Infusion of atropine caused no changes in blood pressure or plasma concentrations of lactate, adrenaline, and noradrenaline and decreased heart rate variability. The additional infusion of adrenaline and noradrenaline completely suppressed heart rate variability and increased blood pressure. CONCLUSIONS--The reduction in LF and HF during exercise at a heart rate of 100 beats/min, which is not characterised by increased plasma catecholamine concentrations, and during atropine infusion suggests that heart rate variability in the supine state is largely influenced by vagal activity. The additional reduction in LF during exercise at 150 beats/min and during catecholamine infusion may reflect a negative feedback of circulating catecholamines on the sympathetic control of heart rate.     

Maturational gonadotropin from the African catfish, Clarias gariepinus: purification, characterization, localization, and biological activity.

A gonadotropic hormone of the African catfish, Clarias gariepinus, was was purified and chemically characterized. Its biological activity was tested and its localization in the gonadotropic cells of the pituitary demonstrated. An ethanolic extract of 500 pituitaries of adult male and female African catfish was subjected to ion-exchange chromatography on DE-52. The 31- to 38-kDa fraction was further purified on Sephadex G-75. On rpHPLC over an ODS 120T column two major components appeared as single bands after SDS-PAGE. From the amino acid composition and sequence analysis of these fractions, compared with those of salmon and carp GTH II-alpha and salmon GTH II-beta it was concluded that they represent catfish GTH alpha- and II-beta-subunits. The biological activity of the complete hormone (the 31- to 38-kDa fraction from the G-75 column) was tested on the production of 11 beta-hydroxyandrostenedione and 17 alpha-hydroxy-20 beta-dihydroprogesterone by catfish testis in vitro. Polyclonal antibodies were raised against the purified beta-subunit. Immunocytochemical study using these showed them to bind specifically to hypophysial gonadotropic cells. To date only one form of GTH has been demonstrated in the African catfish.     

Increased fine particle deposition in women with asymptomatic nonspecific airway hyperresponsiveness

Previous studies suggest that lung function tests using monodisperse aerosols can help to identify early stages of lung diseases. We investigated intrapulmonary particle loss and aerosol bolus dispersion-a marker of convective gas transport-in 32 women with asymptomatic nonspecific bronchial hyperresponsiveness (BHR) compared with 60 women without BHR. Deposition of inhaled particles (0.9 micrometer mass median aerodynamic diameter [MMAD]) was calculated from particle losses of inhaled aerosol boluses consisting of di-2-ethylhexyl sebacate droplets. Convective gas mixing was assessed by the aerosol bolus dispersion method. Women with BHR, nonsmokers as well as smokers, showed significantly increased deposition of aerosol particles (nonsmokers: 45.6 +/- 8.8%; smokers: 49.2 +/- 5.4%; mean +/- SD) compared with the control group of female nonsmokers without BHR (38.2 +/- 9.1%; mean +/- SD) (p < 0.01). Aerosol bolus dispersion values showed a trend for higher values in subjects with BHR (nonsmokers: 572 +/- 122 cm3; smokers: 587 +/- 85 cm3) compared with the control group (542 +/- 88 cm3) (p = 0.2). Also, the maximal expiratory flow at 25% vital capacity (MEF25) showed a trend for decreased values in nonsmokers with BHR compared with nonsmokers without BHR (64 +/- 16% of predicted versus 78 +/- 24% of predicted; p = 0.03). These results suggest that deposition of inhaled particles (0.9 micrometer MMAD) administered by the aerosol bolus technique is a sensitive index of peripheral lung injury that is usually not assessable by conventional methods.     

A recalcitrant, erythematous, desquamating disorder associated with toxin-producing staphylococci in patients with AIDS.

Although staphylococcal infections are common in patients with AIDS, staphylococcal toxin-related disorders have rarely been described. Five cases of a staphylococcal toxin-associated syndrome characterized by prolonged erythema, extensive cutaneous desquamation, hypotension, tachycardia, and multiple organ involvement are described in patients with AIDS. These illnesses were recurrent and recalcitrant with a mean duration of 50 days. Toxic shock syndrome toxin-1-producing staphylococci were isolated from three and staphylococcal enterotoxins B and A from one patient each. Sources of organisms were blood, one patient, and soft tissues and nasal accessory sinuses, two patients each. Three of the five patients died of renal failure and central nervous system abnormalities. One survivor required intubation for respiratory failure. All individuals manifested a marked diminution of CD4+ cells. Other laboratory abnormalities included azotemia and prolongation of partial thromboplastin time. Oliguria occurred in three patients. Thus, this recalcitrant erythematous desquamative disorder appears to be a variant of staphylococcal toxic shock syndrome in certain subsets of immunocompromised individuals.     

Regulation and cellular localization of the membrane-bound thyrotropin-releasing hormone-degrading enzyme in primary cultures of neuronal, glial and adenohypophyseal cells

Using monolayer cultures from murine brain and reaggregate cell cultures of rat anterior pituitary we observed that TRH (pyroGlu-His-Pro-NH2) added to the culture medium was not taken up by these cells but hydrolyzed at the pyroGlu-His bond by an enzyme obviously located at the cell surface. This enzyme exhibited a high degree of substrate specificity and other characteristics of the membrane-bound TRH-degrading enzyme. Relatively high enzymatic activity was associated with cultured neuronal cells from embryonic rat brain while glial cells were almost devoid of this peptidase activity. Rather low, but significant activity was found on anterior pituitary cell aggregates. In agreement with previous in vivo studies we observed that the TRH-degrading ectoenzyme on adenohypophyseal cells was regulated by estradiol and stringently controlled by T3, but that the activity of the brain enzyme was not. When pituitary cells were separated according to their size and density and established in reaggregate cell culture, a close correlation was always observed between enzyme activity and the distribution of lactotrophic cells regardless of the animal models (eu- and hypothyroid adult male rats) used and the cell fractionation techniques (velocity sedimentation and sequential velocity/buoyant density sedimentation) employed. Such a close correlation was not observed with other cell types, such as the somatotrophic cells, the folliculo-stellate cells, the ACTH-producing AtT20 pituitary cells, or thyrotrophic cells. In conclusion, the high degree of substrate specificity, the tissue-specific regulation, and the very heterogeneous distribution of the TRH-degrading ectoenzyme on brain and pituitary cells strongly support the hypothesis that this enzyme serves very specialized functions in the transmission of TRH signals at specific target sites.