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Biomedical subjects

P A Watt

Publications and source records attributed to P A Watt.

At least 19 recordsLinked to original sources
PubMed2006

A serious and repeatable electrical hazard--compressed electrical cord and an operating table.

We describe a previously unreported hazard resulting from compression of an electrical cable by an operating theatre table. This resulted in a live wire contact to the operating table. Intermittent connection of the table to earth during a procedure resulted in triggering of a residual current device mitigating the effects of the hazard. The actual cause was not readily identified as the devices connecting the table to earth were considered most likely to be the source of the current. There was potential for significant injury to the patient and theatre staff which would have been diminished if staff had had a better understanding of the electrical safety equipment in use. We examine the underlying causes of the accident, discuss electrical safety and correct use of safety devices in the operating theatre, and propose guidelines for appropriate management.

Aged↗
PubMed1999

Altered small artery morphology and reactivity in critical limb ischaemia.

Although the pathophysiology of critical limb ischaemia is poorly understood, there is evidence that the condition of the small arteries may determine the outcome of revascularization procedures. This study was designed to investigate the effects of critical limb ischaemia on the structure and function of the small arteries in the leg. Small arteries (<500 microm) from proximal (non-ischaemic) and distal (ischaemic) sites were obtained from patients undergoing bypass surgery for critical limb ischaemia and mounted in a myograph. Reactivity and morphological measurements were carried out and compared with controls. Control vessels from the thigh and calf showed no difference in media to lumen ratio. However, a comparison of ischaemic and non-ischaemic vessels from the patients with critical limb ischaemia showed significant thinning of the ischaemic vessel wall. Contraction studies using noradrenaline and angiotensin II revealed a significant decrease in the response of ischaemic vessels compared with the non-ischaemic vessels from the same patient. Moreover, these differences in reactivity were still apparent after the responses were corrected for wall thickness. Endothelial function assessed using the endothelium-dependent agonists acetylcholine and bradykinin showed a significantly impaired relaxation response to acetylcholine but not to bradykinin in the ischaemic vessels, and acetylcholine-induced relaxation was not improved after incubation with indomethacin. There was no change in the response to the endothelium-independent cAMP-mediated vasodilator iloprost but a significant impairment to sodium nitroprusside which acts via cGMP. These results suggest that small arteries in critical limb ischaemia are altered in both structure and function, with vessel wall thinning and impaired responses to acetylcholine and sodium nitroprusside.

Acetylcholine↗
PubMed1997

Endothelial function in subcutaneous resistance arteries from elderly hypertensive and normotensive subjects.

1. Previous studies have indicated that younger hypertensive subjects may have abnormal endothelium-dependent relaxation, which could contribute to the elevated peripheral resistance seen in established hypertension. This study was designed to examine the functional behaviour of the endothelium of small arteries from elderly hypertensive and normotensive subjects. 2. Resistance arteries were obtained from gluteal biopsies taken under local anaesthesia in 28 subjects of mean age 70 (range 60-76) years, and studied in an isometric myograph. Eighteen subjects had untreated essential hypertension, and 10 were normotensive. 3. After measurement of the contractile response to noradrenaline, relaxation responses to a variety of endothelium-dependent (acetylcholine and bradykinin) and endothelium-independent (iloprost and sodium nitroprusside) mechanisms were assessed in vessels precontracted with noradrenaline. Endothelium-dependent responses were also studied after incubation with NG-nitro-L-arginine to inhibit nitric oxide synthase. 4. There were no significant differences in the contraction or relaxation responses between elderly subjects with or without high blood pressure. Inhibition of nitric oxide synthase prevented any relaxation with acetylcholine and significantly attenuated the relaxation with bradykinin. Near-complete relaxation was however achieved with the endothelium-independent vasodilator sodium nitroprusside. 5. Hypertension in elderly subjects is not associated with a reduction in endothelial vasodilating function in the subcutaneous vessels of the gluteal region compared with age-matched normotensive controls. The results of this study do not support the hypothesis of a defect of resistance artery endothelium-dependent relaxation in the pathophysiology of hypertension in the elderly.

Acetylcholine↗
PubMed1996

Randomized comparison of ultrasonic aspiration versus conventional electrocautery for dissection of the human internal thoracic artery.

The most common technique currently employed to harvest the internal thoracic artery for coronary artery bypass grafting is conventional electrocautery. This study compared an alternative method, electrocautery with an ultrasonic aspirator, for harvesting the internal thoracic artery. Patients were randomly assigned to one of six experimental groups (conventional electrocautery, ultrasonic aspirator at settings of 60%, 80%, and 100% power output, and ultrasonic aspirator in 100% CAVI-Pulse modes 1 and 3). Ring segments of internal thoracic artery were studied in an organ bath. Contraction responses were elicited with 123 mmol/L potassium physiologic salt solution, KPSS, KPSS solution containing noradrenaline, and a cumulative noradrenaline dose-contraction curve. Relaxation studies were performed with the vasodilators acetylcholine, bradykinin, and sodium nitroprusside. Forty percent of the electrocauterized vessels were traumatized or damaged and failed to respond to contractile stimuli, whereas only 10% of the vessels in ultrasonic aspirator groups 60%, 80%, and 100% failed to respond. All vessels in the group harvested by ultrasonic aspirator in 100% CAVI-Pulse mode 1 responded, whereas 20% of the vessels in the group harvested by ultrasonic aspirator in 100% CAVI-Pulse mode 3 failed to respond. All settings of electrocautery with an ultrasonic aspirator produced a greater contractile response to KPSS and noradrenaline. Acetylcholine and sodium nitroprusside produced similar relaxations in all groups, but the bradykinin responses were significantly improved in all groups undergoing 100% electrocautery with an ultrasonic aspirator. These results suggest that 100% electrocautery with an ultrasonic aspirator, particularly in 100% CAVI-Pulse mode 1, resulted in less damage and trauma than conventional electrocautery during harvesting of the internal thoracic artery.

Adult↗
PubMed1996

Reproducibility of the circadian blood pressure fall at night in healthy young volunteers.

The aim of this study was to evaluate the reproducibility of the circadian blood pressure (BP) change in normal healthy volunteers. The subjects were 32 healthy, young, normotensive volunteers who underwent 24 h ambulatory BP monitoring on two occasions, at least 4 weeks apart. Data were analysed using standard definitions of day and night (i.e. 07.00-22.00 for daytime and 22.00-07.00 for night time), event diaries to identify individual's day and night time and a time independent method (cusum analysis). Intraindividual variations of BP were assessed using the coefficient of variation (CV). The mean 24 h BP was very reproducible with a CV of 4.7%. Using the fixed definition of day and night, mean night time systolic blood pressure (SBP) was significantly reduced on the second visit compared to the first (P < 0.001). Using fixed times for day and night, day-night difference was poorly reproducible, with a CV of 52% for SBP and 59% for diastolic blood pressure (DBP), however this improved using diary based day-night to 40/41% and cusum analysis to 24.6/28.1%. We recommend that circadian BP changes are studied using individual definitions of day and night or time independent methods such as cusum analysis.

Adult↗
PubMed1995

The effect of insulin on the vascular reactivity of isolated resistance arteries taken from healthy volunteers.

Impaired reactivity of the resistance vasculature may contribute to the development of diabetic microangiopathy by altering microvascular haemodynamics. This study investigates the acute effects of insulin on the contractility and relaxation properties of isolated human resistance arteries (< 300 microns internal diameter) taken from gluteal subcutaneous fat of 33 (18 male: 15 female) normotensive healthy volunteers (supine blood pressure 115.6 +/- 1.6/70.0 +/- 1.5 mm Hg [mean +/- SEM], with no family history of hypertension or diabetes mellitus. Resistance arteries were mounted in a small vessel myograph to measure isometric tension. Contractile responses to noradrenaline were reduced after incubation in 1 mU/ml of insulin for 20 min (p < 0.01; Group 1). Increasing concentrations of insulin were found to reduce the contractile response to noradrenaline in a dose-dependent manner (Group 2; 0.1 mU/ml by 8% [p < 0.01], 1 mU/ml by 17% [p < 0.02] and 10 mU/ml by 22% [p < 0.01]). Sensitivity to insulin (ED50) only decreased at the highest concentration of insulin. However, acetylcholine-induced relaxation was not altered by insulin (Group 2). Time control studies (Group 3) showed that contractile and relaxation responses over the 4-h study period were unchanged. Furthermore, the length of time the vessels were exposed to insulin did not progressively impair responses (Group 4). These findings suggest that insulin may induce abnormalities in vascular smooth muscle contractility, a factor that may contribute to or exacerbate the abnormal haemodynamics observed in the capillary microcirculation of numerous vascular beds in diabetes.

Acetylcholine↗
PubMed1995

Pulse pressure and resistance artery structure in the elderly.

There has been recent interest in the possibility that resistance vessel structural adaptation in hypertension may be more closely related to pulse pressure than to other blood pressure parameters. We investigated the relation between blood pressure and resistance vessel structure in a group of subjects from an age group (older than 60 years) in which a widening of pulse pressure is a typical finding and characterized blood pressure parameters using 24-hour ambulatory blood pressure monitoring. We studied resistance vessels retrieved from biopsies of skin and subcutaneous fat taken from the gluteal region of 32 subjects under local anesthesia (age, 70 +/- 1 years [mean +/- SEM], 21 of whom were hypertensive and 11 normotensive. Media-lumen ratio was higher in the hypertensive than the normotensive subjects (18.6 +/- 1.6% versus 12.8 +/- 1.2%, P < .01) and correlated with age (r = .44, P < .05), clinic systolic pressure (r = .35, P < .05), 24-hour systolic pressure (r = .40, P < .05), and 24-hour pulse pressure (r = .56, P < .001). Stepwise multivariate regression analysis identified clinic and 24-hour pulse pressure as the only significant predictors of media-lumen ratio independent of age, other parameters of clinic blood pressure, and blood pressure variability (R2 = 41%, P < .05). These findings confirm those from animal models of hypertension in demonstrating the importance of pulse pressure in relation to cardiovascular structural adaptation and have important implications for the goals of treatment of hypertension in the elderly.

Aged↗
PubMed1994

Impaired contraction and endothelium-dependent relaxation in isolated resistance vessels from patients with insulin-dependent diabetes mellitus.

1. An increase in capillary blood flow and pressure has been implicated in the pathogenesis of diabetic microangiopathy. Abnormal vascular reactivity of the resistance vasculature may play a contributory role by permitting alterations in regional haemodynamics. 2. We have studied the contractile behavior of isolated resistance arteries from normotensive patients with insulin-dependent diabetes mellitus and non-diabetic matched control subjects. Contractile responses to potassium (123 mmol/l), noradrenaline (10(-8) to 3 x 10(-5) mol/l) and angiotensin II (10(-11) to 3 x 10(-8) mol/l) were recorded. Relaxation studies were performed in maximally contracted vessels using acetylcholine (10(-8) to 10(-5) mol/l) and bradykinin (10(-9) to 10(-6) mol/l) (endothelium-dependent) and sodium nitroprusside (10(-9) to 10(-5) mol/l) (endothelium-independent). 3. The maximal contractile responses to potassium (P < 0.05), noradrenaline (P < 0.01) and angiotensin II (P < 0.01) were depressed in diabetic patients. Relaxation to acetylcholine was impaired (P < 0.05), but was normal with bradykinin and sodium nitroprusside. 4. These results suggest that there may be a defect in the endothelial cell acetylcholine receptor excitation-coupling in diabetes mellitus rather than a decreased ability to synthesize and release endothelium-derived relaxing factor. Impaired contraction and endothelium-dependent relaxation of resistance arteries in diabetic patients may contribute to the development of diabetic microangiopathy by causing an increase in tissue blood flow, a rise in capillary pressure and, as a result, an increase in vascular permeability.

Acetylcholine↗
PubMed1993

The effects of intraoperative vasodilators and angiographic contrast medium on the endothelium and smooth muscle cells of vein grafts.

Cellular injury is a major cause of intimal hyperplasia in vein grafts. The effects of exposure of vein samples to iopamidol, papaverine and iloprost were studied in vitro in an organ chamber to determine whether these agents cause endothelial and/or smooth muscle cell injury. Smooth muscle cell function was assessed by eliciting a dose response curve to noradrenaline. Endothelial cell function was assessed by measuring the degree of endothelial-dependent relaxation of sub-maximally contracted vein samples. Iopamidol and iloprost did not have any deleterious effect on endothelial or smooth muscle cell function. Papaverine did not affect endothelial-dependent relaxation but did produce a significant decrease in smooth muscle contraction. The use of these intraoperative agents during femorodistal bypass does not appear to cause functional injury to the endothelial or smooth muscle cells.

Aged↗
PubMed1992

Contraction and relaxation of human internal mammary artery after intraluminal administration of papaverine.

The internal mammary artery has become the conduit of choice for coronary artery bypass grafting. Intraluminal papaverine treatment during operation reduces vasospasm and facilitates anastomosis. However, it has been suggested that papaverine may cause intimal damage, and accordingly we have investigated endothelial damage by comparing the responsiveness of internal mammary arteries before and after intraluminal exposure to papaverine (15 mg/mL). Control and papaverine-treated segments of internal mammary artery were obtained from 13 patients undergoing coronary artery bypass grafting and mounted as ring preparations in an organ bath. Cumulative dose contractions to noradrenaline were performed, and the dose producing a half maximal response was determined. Relaxation studies of submaximally contracted arteries were performed using the endothelium-dependent vasodilators acetylcholine and bradykinin and the endothelium-independent vasodilator sodium nitroprusside. In the human internal mammary artery the use of intraluminal papaverine increased the lumen size by 20% (p less than 0.05), and the contractions elicited by noradrenaline were significantly less in the papaverine group than in the control group (p less than 0.05). Endothelium-dependent relaxation to acetylcholine or bradykinin was not affected by papaverine treatment. Endothelium-independent relaxation was the same in both groups, with almost 100% relaxation achieved by sodium nitroprusside. These results indicate that intraluminal papaverine treatment during coronary artery bypass grafting causes a reduction of smooth muscle contraction and does not impair endothelium-dependent relaxation.

Acetylcholine↗
PubMed1992

Endothelial cell injury secondary to surgical preparation of reversed and in situ saphenous vein bypass grafts.

Failure of infra-inguinal vein grafts appears to be due to the development of intrinsic lesions (intimal hyperplasia, fibrous stenoses) within the graft which lead to narrowing of the lumen, poor blood flow and thrombosis. The cause of these lesions remains unknown but recently it has been suggested that endothelial injury might be an aetiological factor. The damage that can occur after preparation of reversed vein grafts includes loss of endothelial cells and functional impairment of those cells that remain, in that the ability to produce prostacyclin and endothelium-derived relaxing factor (EDRF) is reduced. The preparation of in situ grafts is different to that for reversed grafts in that a valvulotome is passed along the lumen of the vein to destroy the valves. However, little is known about the degree of endothelial injury that this technique causes. Vein samples were obtained from patients undergoing infra-inguinal and coronary artery bypass grafting. The veins were mounted in an organ bath system to measure isometric tension and exposed to the endothelium-dependent agents acetylcholine, bradykinin, adenosine, histamine and the endothelium-independent agent sodium nitroprusside. The results indicate that preparation of reversed vein grafts leads to some loss of endothelial cells with functional impairment of the cells that remain. However, preparation of in situ grafts leads to severe or total loss of endothelial cells which resulted in an absence of detectable EDRF release. These findings were confirmed by histological examination of the vein samples.

Aged↗
PubMed1992

Endothelium-dependent modulation of resistance vessel contraction: studies with NG-nitro-L-arginine methyl ester and NG-nitro-L-arginine.

1. The effect of NG-nitro-L-arginine methyl ester (L-NAME) and NG-nitro-L-arginine (L-NOARG) on noradrenaline (NA)-induced contractility and acetylcholine (ACh)-induced endothelium-dependent relaxation was studied in rat mesenteric resistance arteries. 2. Third order branches of mesenteric arteries were dissected and mounted on two forty micron wires in a Mulvany myograph. 3. Incubation with L-NAME and L-NOARG (10 microM) caused a time-dependent shift in the 50% response to NA (ED50) (0.01 microM-10 microM) but was not associated with an increase in the maximum contractile response. 4. L-NAME and L-NOARG (10 microM) caused a time-dependent inhibition of ACh (1 microM)-induced relaxation with a maximum effect after 120 min. 5. Following endothelium removal, incubation with either L-NAME or L-NOARG caused no significant shift in the ED50, although the residual relaxation response to ACh (1 microM) was further attenuated. 6. Incubation with the cyclo-oxygenase inhibitor, indomethacin, enhanced the relaxation to ACh and reduced the inhibitory effects of L-NAME and L-NOARG. 7. In conclusion, L-NAME and L-NOARG are potent inhibitors of acetylcholine-induced endothelium-dependent relaxation in mesenteric resistance arteries. The shift in ED50 associated with these inhibitors suggests a probable role for the endothelium in modulating the contractility of the resistance vasculature.

Acetylcholine↗
PubMed1991

Structural and functional smooth muscle injury after surgical preparation of reversed and non-reversed (in situ) saphenous vein bypass grafts.

Intimal hyperplasia and isolated stenoses are major factors in determining the long-term patency of reversed and in situ vein grafts. Surgical handling causes functional endothelial damage in reversed vein grafts but the effects of valvulotome use are unknown. Saphenous vein samples were taken after minimal dissection (control), distension with saline, or after the passage of a valvulotome. Rectangular strips of vein were mounted in an organ bath and cumulative noradrenaline (10(-8)-10(-5) M) dose contraction curves were performed. Compared with controls there was a significant reduction in the contractile response of both the distended and valvulotome-prepared veins (P less than 0.05). Histological studies revealed partial endothelial cell loss in the distended group and total endothelial cell loss with patchy necrosis of the smooth muscle in the valvulotome group. These results suggest that the current use of a valvulotome not only renders the valves incompetent but also seriously damages the function of the smooth muscle layer.

Aged↗
PubMed1991

Calcium dependent and independent endothelin-1-induced contraction of human omentum vessels.

Endothelin-1, an endothelium derived vasoconstrictor peptide, induced concentration-dependent contraction of isolated human omental resistance arteries. Pre-treatment with the calcium antagonist nicardipine or calcium depletion caused a significant reduction but did not abolish the contractile response. However, when calcium depletion was combined with pretreatment with the protein kinase C inhibitor (H7), endothelin-1 failed to produce a contraction. This study shows that a large component of endothelin-1 contraction is calcium-dependent, involving activation of dihydropyridine-sensitive voltage-dependent calcium channels but in addition there is a calcium-independent component produced by protein kinase C activation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗