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Biomedical subjects

C S Thompson

Publications and source records attributed to C S Thompson.

At least 37 records · Page 2Linked to original sources
PubMed2001

Endovascular repair of AAA rupture 20 months after endoluminal stent-grafting.

PURPOSE: To demonstrate the feasibility of endovascular repair of a ruptured abdominal aortic aneurysm (AAA) previously treated with an endoluminal stent-graft. CASE REPORT: An 84-year-old man with a 9.5-cm AAA underwent endoluminal repair with an Endologix stent-graft, but a type I endoleak was detected postprocedurally. The patient was discharged and lost to follow-up. Twenty months later, he suffered an aneurysm rupture, which was repaired using endovascular techniques. Although he had a postoperative course complicated by aspiration pneumonia and renal failure, he recovered fully and was discharged from the hospital with no evidence of endoleak on the postprocedural imaging studies. CONCLUSIONS: Late ruptures after endoluminal AAA stent-grafting can be successfully treated with endovascular techniques.

Aged↗
PubMed2001

Alterations in cholinergic and purinergic signaling in a model of the obstructed bladder.

PURPOSE: There is increasing evidence that purinergic signaling may have a role in the generation of detrusor contractions in the pathologically unstable human bladder. However, study of the rabbit model of partial bladder outlet obstruction showed a loss in cholinergic and purinergic innervation after 3 months. We examined changes in the cholinergic and purinergic components contributing to nerve mediated detrusor contraction in a rabbit model of detrusor instability secondary to bladder outlet obstruction during the early hypertrophic stage. MATERIALS AND METHODS: Partial bladder outlet obstruction was surgically induced in adult male rabbits. At 3 weeks detrusor strips were obtained and contractions were produced by electrical field stimulation in the presence of 1 microM. atropine and/or 30 microM. of the P2-purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2'4'-disulfonic acid, and after adding 1 microM. tetrodotoxin. Purinergic and cholinergic components were calculated and compared with those from sham operated controls. RESULTS: The cholinergic or atropine sensitive component was frequency dependent, that is smaller at lower frequencies. The cholinergic component was decreased in the early obstructed bladder. The pyridoxalphosphate-6-azophenyl-2'4'-disulfonic acid sensitive purinergic component was frequency dependent, that is larger at lower frequencies. The purinergic component was increased in the early obstructed bladder. The overall electrical field stimulation response or the response to KCl was unaltered in the obstructed group. There was no difference in the response in strips from the bladder neck and dome. CONCLUSIONS: The purinergic component of nerve mediated detrusor contraction is increased and the cholinergic component is decreased in early stages of bladder obstruction in this rabbit model.

Animals↗
PubMed2001

Fibrinogen, lipoprotein (a) and lipids in patients with erectile dysfunction. A preliminary study.

BACKGROUND: Erectile dysfunction is associated with cardiovascular risk factors (e.g. hypertension, smoking, dyslipidemia and diabetes) and is more common in patients with cardiovascular disease. We therefore assessed the prevalence of two predictors of vascular events, fibrinogen and lipoprotein-a, in patients with and without erectile dysfunction. METHODS: Men with erectile dysfunction (48 non-smokers, 48 smokers), aged 45-70 years, were compared with controls (21 non-smokers, 21 smokers) with normal erectile function and no known pathology. RESULTS: Serum total cholesterol was significantly higher in non-smokers with erectile dysfunction compared to both control non-smokers and erectile dysfunction smokers. Men with erectile dysfunction who smoked had a significantly higher plasma fibrinogen level than control smokers. Similarly, men with erectile dysfunction, who did not smoke had higher levels of plasma fibrinogen compared to both smokers and non-smokers without erectile dysfunction. No significant difference in serum lipoprotein-a values was found. CONCLUSIONS: These findings support the concept that cardiovascular risk factors are predictors of erectile dysfunction and that this may be another manifestation of vascular disease.

Aged↗
PubMed2000

The hippocampal neurons of neuronal apoptosis inhibitory protein 1 (NAIP1)-deleted mice display increased vulnerability to kainic acid-induced injury.

The neuronal apoptosis inhibitory protein (NAIP) is a member of a novel family of inhibitor of apoptosis (IAP) proteins. The IAP genes are highly conserved from baculovirus to metazoans and suppress apoptosis induced by a variety of triggers both in vitro and in vivo. Here we describe the generation and characterization of mice with the targeted deletion of NAIP1. We demonstrate that the NAIP1-deleted mice develop normally. However, the survival of pyramidal neurons in the hippocampus after kainic acid-induced limbic seizures is greatly reduced in the NAIP1 knock-out animals. Thus, although NAIP1 is not necessary for normal development of murine central nervous system, the endogenous NAIP1 is required for neuronal survival in pathological conditions.

Animals↗
PubMed2000

Relaxation of rabbit lower urinary tract smooth muscle by nitric oxide and carbon monoxide: modulation by hydrogen peroxide.

Recent studies suggest that the body produces two gaseous messengers, nitric oxide (NO) and carbon monoxide (CO), both of which activate soluble guanylyl cyclase and thus modulate the activity of smooth muscle cells. In the present study, the effects of NO and CO on the smooth muscle of the lower urinary tract were compared. In addition, the modulation of tissue NO- and CO-induced relaxation by hydrogen peroxide was examined. NO, produced endogenously by electrical field stimulation (EFS) or applied exogenously as a solution, induced a concentration-dependent relaxation of rabbit cavernosal and urethral smooth muscle strips, but not of bladder tissues. The cavernosal tissue was found to be three times more sensitive to the actions of NO than the urethra. CO also induced relaxation of both tissue types, but with no apparent difference in sensitivity between the tissues. However, CO was much less potent than NO with respect to smooth muscle relaxation. The mechanism of action of the two mediators was cyclic guanosine monophosphate (cGMP)-dependent, as evidenced by enhanced formation of cGMP and inhibition of relaxation by the guanylyl cyclase inhibitor, oxadiazoloquinoxaline-1-one (ODQ.) The data suggests that NO is the dominant messenger in these tissues, but does not exclude a role for CO. In the presence of hydrogen peroxide, the relaxation responses induced by both NO and CO were significantly increased, regardless of tissue type. The mechanism for this effect is unclear, but evidence points to a requirement for the activation of guanylyl cyclase and enhanced formation of cGMP, since potentiation by the peroxide was blocked by a specific guanylyl cyclase inhibitor. We suggest that H(2)O(2) may play a positive role in the amplification or NO and CO-mediated responses.

Animals↗
PubMed2000

Inhibition of diabetic bladder smooth muscle cell proliferation by endothelin receptor antagonists.

Urinary bladder hypertrophy and hyperplasia are well recognised in diabetic cystopathy. The urinary bladder is known to synthesise endothelin-1 (ET-1), a potent vasoconstrictor peptide with mitogenic properties. Using diabetic New Zealand White (NZW) rabbits, we investigated the potential role of ET receptor subtypes (ETA and ET(B)) on the proliferation of bladder smooth muscle cells (SMC). Diabetes mellitus was induced in adult male NZW rabbits. After 6 months, control (n = 6) and diabetic (n = 6) bladders were removed and SMC from the dome and bladder neck were grown using standard explant methodology. At passage two, the cells were made quiescent and then further incubated in foetal calf serum (FCS), control age-matched rabbit serum (CRS) or diabetic rabbit serum (DRS) in the presence or absence of ET(A)-antagonist (BQ123) or ET(B)-antagonist (BQ788). SMC proliferation was then measured with 5-bromo-2'deoxy-uracil 24 h later and by cell counting (using a haemocytometer) at 48 h. Neither BQ123 nor BQ788 influenced detrusor or bladder neck SMC proliferation in FCS or CRS. However, in the presence of DRS, BQ123 and BQ788 significantly inhibited diabetic detrusor and bladder neck SMC proliferation at 30 and 100 nmol/l (P < 0.03 and P < 0.01, respectively). Cell counts were also significantly reduced from the diabetic detrusor and bladder neck (P < 0.01 and P < 0.03 with BQ123 and BQ788, respectively). These results suggest that ET may play a pathophysiological role in the bladder SMC hyperplasia associated with diabetes mellitus.

Animals↗
PubMed2000

Doxazosin modifies serotonin-mediated rabbit urinary bladder contraction. Potential clinical relevance.

5-Hydroxytryptamine (5-HT) induces rabbit detrusor contractions via 5-HT3 receptors. Similarly, 5-HT4 receptors are known to be present in the human bladder. Doxazosin, a non-selective alpha1 antagonist, is used for the symptomatic relief of bladder outflow obstruction. Previous work has shown that doxazosin inhibits 5-HT2-mediated platelet shape change. Hence, the aim of this study was to assess, using organ baths and autoradiography, whether doxazosin has any 5-HT-inhibiting activity in the rabbit detrusor. Detrusor strips from adult New Zealand White rabbits were placed in organ baths; phenoxybenzamine (10(-5) M) was added to block alpha-receptors. After KCl responses were assessed, the tissues were exposed to 10(-3) M 5-HT. Subsequently, the strips were incubated with doxazosin or ondansetron (10(-5) M; 5-HT3 antagonist) followed by a further exposure to 5-HT. In some experiments, after the initial 5-HT-induced contractions, the tissues were washed and then re-exposed to 5-HT. These latter experiments acted as controls. Low-resolution autoradiography was performed on detrusor sections to assess the effect of doxazosin on 5-HT binding. These sections were analyzed densitometrically. Doxazosin and ondansetron produced a significant reduction in 5-HT-mediated contractions. Inhibition by doxazosin was in a concentration-dependent manner. Autoradiography demonstrated a significant reduction in [3H]-5-HT binding by doxazosin. Doxazosin significantly inhibits 5-HT-mediated contractions in the rabbit detrusor. This effect appears to be mainly mediated via 5-HT3 receptor inhibition. Autoradiographic evidence suggests that doxazosin reduces 5-HT binding in the rabbit detrusor. The beneficial effects of doxazosin in bladder outflow obstruction may be due, at least in part, to 5-HT antagonism.

Animals↗
PubMed2000

Possible role of endothelin-1 in the rabbit urinary bladder hyperplasia secondary to partial bladder outlet obstruction.

OBJECTIVES: Urinary bladder hypertrophy and hyperplasia are common features of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endothelin-1 (ET-1), which is a potent vasoconstrictor peptide with mitogenic properties. Using an animal model of partial BOO, we investigated the potential role of ET-1 and its receptor subtypes (ET(A) and ET(B)) in bladder smooth muscle cell (SMC) proliferation. MATERIALS AND METHODS: Partial BOO was produced in adult male New Zealand White rabbits. After 3 weeks, the bladder was removed and SMCs from the dome and bladder neck were grown using standard explant methodology. At passage 2, the cells were made quiescent and then further incubated in foetal calf serum (FCS), control age-matched rabbit serum (CRS) or partial BOO serum (BRS) in the presence or absence of ET(A)-antagonist (BQ123) or ET(B)-antagonist (BQ788). SMC proliferation was then measured 24 h later with 5-bromo-2'deoxy-uracil and by cell counting using a haemocytometer at 48 h. Immunostaining for alpha-actin was performed on detrusor and bladder neck cells to confirm the presence of smooth muscle cells. RESULTS: BQ123 and BQ788 did not influence detrusor or bladder neck SMC proliferation in FCS or CRS. However, in the presence of BRS, BQ123 and BQ788 (100 nmol/L) significantly (p = 0.008) inhibited detrusor and bladder neck SMC proliferation. Cell counts were significantly reduced from the detrusor (p = 0.03, p = 0.01 with BQ123 and BQ788, respectively) and bladder neck (p = 0.01 for both BQ123 and BQ78). CONCLUSIONS: These results suggest that ET antagonists may have a role in preventing SMC hyperplasia associated with partial BOO.

Animals↗
PubMed2000

Altered cavernosal endothelin-B-receptor binding sites in the rabbit model of partial bladder outlet obstruction.

Erectile dysfunction (ED) is a common problem that significantly affects the quality of life. Benign prostatic hyperplasia (BPH) is the commonest known benign proliferative disorder. Recently there has been growing evidence to suggest that patients with high BPH symptom scores have an increased incidence of ED. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is thought to play an important role as a modulator of erectile physiology and dysfunction. We investigated whether there are any changes in the density and distribution of ET-1 and its receptor subtypes in the corpora cavernosa (CC) of a rabbit model of partial bladder outflow obstruction (BOO). ET-1, endothelin-A- and -B- (ET(A) and ET(B)) receptor binding sites were primarily localized to the smooth muscle cells (SMC) of the CC and the endothelium lining the cavernosal space. ET(B)-receptor binding sites were significantly decreased (p = 0.04) in the 6-week BOO cavernosal tissue. ET-1 may play a role in the pathophysiology of ED associated with BPH. This may be partly a result of enhanced vasoconstrictor actions and SMC proliferation secondary to a reduction in ET(B)-receptors. Further work is needed to evaluate this possibility.

Animals↗
PubMed2000

Endothelin-1 and urinary bladder hyperplasia following partial bladder outlet obstruction.

Urinary bladder hypertrophy and hyperplasia is a common feature of bladder outlet obstruction (BOO). The urinary bladder is known to synthesize endothelin-1 (ET-1). ET-1 is a potent vasoconstrictor peptide with mitogenic properties. Using an animal model of partial BOO we investigated the potential role of ET-1 and its receptor subtypes [endothelin-A and -B (ET(A) and ET(B))] in bladder vascular smooth muscle cells (SMC) proliferation. In the presence of 3-week-old BOO serum, ET(A) and ET(B) antagonists significantly (p = 0.008) inhibited detrusor and bladder neck SMC proliferation. Cell counts were significantly reduced from the detrusor (p = 0.03, p = 0.01 with ET(A) and ET(B) antagonists, respectively) and bladder neck (p = 0.01 for both ET(A) and ET(B) antagonists). These results suggest that ET-1 antagonists may prevent SMC hyperplasia associated with partial BOO.

Animals↗
PubMed2000

Urological aspects of female sexual dysfunction.

The aetiology of male sexual dysfunction has been extensively investigated over the past few decades. This has led to the development of effective treatment for this common problem. However, to date, female sexual dysfunction has received very little attention, particularly from a urological point of view. In this review, we discuss the anatomy and physiology of the female sexual organs as well as the aetiological factors that are associated with female sexual dysfunction. An improved awareness and understanding of this subject may, in the future, enable us to address female sexual dysfunction more appropriately and develop suitable treatment.

Female↗
PubMed2000

Normal and pathological erectile function: the potential clinical role of endothelin-1 antagonists.

Erectile dysfunction (ED) is a common problem, particularly in older men. The production of penile erection involves an interplay between autonomic nerves and locally released vasoactive mediators. Endothelin-1 (ET-1) is a peptide released from endothelium in the corpus cavernosum, which causes smooth muscle contraction. Recent studies have investigated the physiological significance of ET-1 in the control of erectile function and it may play a role in detumescence. There is also much evidence to link ET-1 to risk factors for ED. ET-1 antagonists may prove beneficial in the treatment of ED and also in prevention of long term deterioration of erectile function. These antagonists may also find a role when used in combination with agents, which are established for the treatment of ED.

Animals↗
PubMed1999

Nitric oxide and penile erection: is erectile dysfunction another manifestation of vascular disease?

There is convincing evidence that the prevalence of erectile dysfunction is increased among men with ischaemic heart disease. This association may be attributed to the fact that both erectile dysfunction and ischaemic heart disease share similar risk factors (e.g. hypertension, dyslipidaemia, diabetes and smoking). Nitric oxide (NO) activity is adversely affected, in penile and vascular tissue, by these risk factors. It is therefore not surprising that a defect in NO activity is thought to play a role in the pathogenesis of both erectile dysfunction and ischaemic heart disease. We consider this evidence and propose that defective NO activity provides a unifying explanation for the association between these two conditions. Further research in this area may improve our understanding of the pathogenesis of cardiovascular diseases as a whole.

Cardiovascular Diseases↗