Biomedical subjects

David Robertson

Publications and source records attributed to David Robertson.

78 records · Page 5Linked to original sources

PubMed2002

Bronchial artery embolization for hemoptysis in young patients with cystic fibrosis.

PURPOSE: To review the authors' 15-year experience with bronchial artery embolization (BAE) for treatment of hemoptysis in young patients with cystic fibrosis. MATERIALS AND METHODS: By searching the 1985-1999 radiology database, the authors identified 23 young patients who had been referred to the radiology department for angiography. Twenty of these patients underwent BAE. The 23 medical records were retrospectively reviewed with regard to embolization agents used, embolization success rates, number of repeat embolizations, survival times, and causes of death. RESULTS: BAE was performed on 38 occasions in 20 patients. The mean age of patients at first BAE was 15 years (age range, 7-19 years). The majority (n = 34 [89%]) of BAEs were performed by using polyvinyl alcohol. The immediate success rate after BAE (ie, no recurrent bleeding within 24 hours) was 95% (36 of 38 BAEs). Eleven (55%) patients required more than one BAE, and the median time between first and second embolizations was 4 months (range, 5 days to 61 months). Three patients died as a consequence of severe hemoptysis during induction of anesthesia with intermittent positive pressure ventilation in preparation for BAE. The median survival duration after the first BAE (Kaplan-Meier estimate) was 84 months (average follow-up, 61 months; range, 5 days to 169 months). CONCLUSION: BAE had a high success rate for short-term control of bleeding; however, more than half the patients required repeat embolization during the long-term follow-up.

Adolescent↗

PubMed2002

Increased sympathetic activation in idiopathic orthostatic intolerance: role of systemic adrenoreceptor sensitivity.

Idiopathic orthostatic intolerance (OI) is characterized by adrenergic symptoms with standing. Changes in central sympathetic tone or in adrenoreceptor sensitivity could contribute to this syndrome. In OI patients and control subjects, we determined heart rate (HR) and systolic blood pressure (SBP) changes after incremental bolus doses of isoproterenol and phenylephrine before and during ganglionic blockade with trimethaphan. SBP decreased by 17+/-1.6 mm Hg in patients and 3.9+/-3.8 mm Hg in control subjects (P<0.01) with trimethaphan. Patients with a larger decrease (28+/-3.8 mm Hg, n=7) in SBP with trimethaphan had greater supine SBP and supine and upright plasma norepinephrine levels than did patients with a lesser decrease (3.0+/-3.0 mm Hg, n=7) in SBP. Supine and orthostatic HRs were similar for the groups. The majority of patients had a normal HR response to isoproterenol before and during ganglionic blockade. Phenylephrine increased SBP similarly in patients and control subjects before and during blockade. Sympathetic support is increased in a subgroup of OI patients. Hyperadrenergic and nonhyperadrenergic subgroups have similar degrees of orthostatic tachycardia. Our findings suggest that the hyperadrenergic features of OI cannot be completely explained by systemic hypersensitivity of postsynaptic alpha(1)- and beta-adrenoreceptors but rather originates in enhanced sympathetic activation.

Adrenergic alpha-Agonists↗

PubMed2002

Expression of P-glycoprotein in human cerebral cortex microvessels.

P-Glycoprotein (P-gp) is an ATP-dependent efflux transporter that extrudes non-polar molecules, including cytotoxic substances and drugs, from the cells. It was initially found in cancer cells and then was shown to be a normal component of complex transport systems working at the blood-brain barrier (BBB). Previous studies have demonstrated that, in the brain, P-gp is localized on the luminal plasmalemma of BBB endothelial cells and that it may interact with the caveolar compartment of these cells. The aim of this study was to identify the site of cellular expression of P-gp in human brain in situ and to morphologically determine whether an association may exist between P-gp and caveolin-1, a structural and functional protein of the caveolar frame. The study was carried out on human cerebral cortex by immunoconfocal microscopy with antibodies to both P-gp and caveolin-1. The results show that P-gp marks the microvessels of the cortex and that the transporter is localized in the luminal endothelial compartment, where it co-localizes with caveolin-1. The demonstration of this co-localization of P-gp with caveolin-1 contributes a morphological backing to biochemical studies on P-gp/caveolin-1 relationships and leads us to suggest that interactions between these molecules may occur at the BBB endothelia.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed2002

The ageing female reproductive axis I.

The female reproductive axis includes the hypothalamo-pituitary unit, the ovaries and the uterus. While changes in the brain may contribute to reproductive ageing, the major focus of current research is on the ovary, where the progressive loss of follicles ultimately leads to absent follicular function and consequent permanent cessation of menstruation, the menopause. The pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone, stimulate ovarian secretion of oestradiol and the inhibins from follicular granulosa cells, and androgens from interstitial cells, including the theca. A primary event in the ageing of the reproductive axis appears to be a decline in the secretion of inhibin B as follicle numbers fall. This leads to a slow rise in FSH in women who continue to cycle regularly, particularly in the last decade of reproductive life. As the menopause approaches, decreasing concentrations of both oestradiol and inhibin B lead to more marked increases in the gonadotropins, which reach their postmenopausal peak 2-3 years after final menses. In contrast, total testosterone concentrations are maintained across the menopausal transition, with a fall in sex hormone binding globulin (SHBG) and hence a rise in free testosterone.

Aging↗

PubMed2002

Ageing and water homeostasis.

This review outlines current knowledge concerning fluid intake and volume homeostasis in ageing. The physiology of vasopressin is summarized. Studies have been carried out to determine orthostatic changes in plasma volume and to assess the effect of water ingestion in normal subjects, elderly subjects, and patients with dysautonomias. About 14% of plasma volume shifts out of the vasculature within 30 minutes of upright posture. Oral ingestion of water raises blood pressure in individuals with impaired autonomic reflexes and is an important source of noise in blood pressure trials in the elderly. On the average, oral ingestion of 16 ounces (473ml) of water raises blood pressure 11 mmHg in elderly normal subjects. In patients with autonomic impairment, such as multiple system atrophy, strikingly exaggerated pressor effects of water have been seen with blood pressure elevations greater than 75 mmHg not at all uncommon. Ingestion of water is a major determinant of blood pressure in the elderly population. Volume homeostasis is importantly affected by posture and large changes in plasma volume may occur within 30 minutes when upright posture is assumed.

Aging↗

PubMedDate not supplied

Human phenotypes and animal knockout models of genetic autonomic disorders.

Norepinephrine (NE) is a crucial neurotransmitter involved in autonomic regulation of blood pressure. Dopamine beta-hydroxylase (DBH), the norepinephrine transporter (NET), and the vesicular monoamine transporter subtype 2 catalyze intracellular NE biosynthesis, NE reuptake from the synapse, and vesicular transport, respectively. Genetic disorders in humans have been identified that render DBH, and the NET dysfunctional and result in cardiovascular and neurological abnormalities. Vesicular monoamine transporter subtype 2 (VMAT2) activity protects against neurotoxins, and reduced VMAT2 expression is implicated in drug addiction. Further investigation of the consequences of these genetic abnormalities has been achieved by the construction of mice strains deficient in the genes encoding DBH, NET, and VMAT2.

Animals↗