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Biomedical subjects

D L Jardine

Publications and source records attributed to D L Jardine.

At least 19 recordsLinked to original sources
PubMed2005

Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model.

The time course of cardiac sympathetic nerve activity (CSNA) following acute myocardial infarction (MI) is unknown. We therefore undertook serial direct recordings of CSNA, arterial blood pressure (MAP) and heart rate (HR) in 11 conscious sheep before and after MI, and compared them with 10 controls. Conscious CSNA recordings were taken daily from electrodes glued into the thoracic cardiac nerves. Infarction was induced under pethidine and diazepam analgesia by applying tension to a coronary suture. MI size was assessed by left ventricular planimetry (%) at postmortem, peak troponin T and brain natriuretic peptide levels (BNP). Baroreflex slopes were assessed daily using phenylephrine-nitroprusside ramps. The mean infarcted area was 14.4 +/- 2.9%, troponin T 1.88 +/- 0.39 microg l(-1) and BNP 8.4 +/- 1.3 pmol l(-1). There were no differences in haemodynamic parameters or CSNA between groups at baseline. MAP and HR remained constant following MI. CSNA burst frequency increased from baseline levels of 55.8 +/- 7.1 bursts min(-1) to levels of 77.5 +/- 8.7 bursts min(-1) at 2 h post-MI, and remained elevated for 2 days (P < 0.001). CSNA burst area also increased and was sustained for 7 days following MI (P= 0.016). Baroreflex slopes for pulse interval and CSNA did not change. CSNA increases within 1 h of the onset of MI and is sustained for at least 7 days. The duration of this response may be longer because the recording fields decrease with time. This result is consistent with a sustained cardiac excitatory sympathetic reflex.

Action Potentials↗
PubMed2005

Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep.

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

Adrenomedullin↗
PubMed2004

Variegate porphyria presenting with acute autonomic dysfunction, intussusception and renal infarction.

A 48-year-old man presented with abdominal pain, constipation and irritability one month after starting phenytoin treatment for a generalized seizure. He was hypertensive, tachycardic (BP 174/98, heart rate (HR) 100 bpm supine) and hypovolaemic. Abdominal CT demonstrated transient jejunal intussusception and infarction of the left kidney. Urinary porphobilinogen levels were increased and genetic analysis confirmed the diagnosis of variegate porphyria. Because of ongoing postural hypotension, the patient underwent further autonomic investigations. Levels of blood pressure (MBP), HR and muscle sympathetic activity (MSNA) were increased during the acute attack compared to recovery (131 versus 105 mmHg, 100 versus 60 bpm, 88 versus 26 bursts min(-1)). HR and MSNA did not increase during phase II Valsalva, whereas stroke volume (SV) decays were exaggerated (deltaMBP-56 versus 0-31 mmHg and SV 25% versus 40% baseline). Baroreflex failure causing increased sympathetic activity, decreased sympathetic and parasympathetic rapid responses, loss of splanchnic capacitance and renal salt wasting were the likely mechanisms for postural hypotension. Increased sympathetic activity may also have caused intussusception and focal renal vasoconstriction, both of which may be underdiagnosed causes of abdominal pain in acute porphyria.

Acute Disease↗
PubMed2004

Vasovagal syncope interrupting sleep?

Clinical data are reported for 13 patients who were referred with recurrent loss of consciousness at night interrupting their sleep. Most of the patients were women (10 of 13) with a mean age of 45 years (range 21-72 years). The histories were more consistent with vasovagal syncope than with epilepsy. This was supported by electroencephalographic and tilt test results. More polysomnographic monitoring data are required to confirm the diagnosis of vasovagal syncope interrupting sleep. This will be difficult because, although the condition may not be rare, the episodes are usually sporadic.

Adult↗
PubMed2003

A neural mechanism for sudden death after myocardial infarction.

By monitoring efferent cardiac sympathetic nerve activity (CSNA) directly in a conscious animal we observed, for the first time, that ventricular fibrillation (VF) following myocardial infarction (MI) was preceded by a paroxysm of CSNA which was not baroreflexmodulated. This observation has potential therapeutic implications.

Animals↗
PubMed2003

Respiratory failure secondary to diabetic neuropathy affecting the phrenic nerve.

We report a patient with Type 2 diabetes mellitus complicated by neuropathy affecting the phrenic nerves, resulting in fatal respiratory failure. Diabetic mononeuropathy is common and usually recovers spontaneously, but bilateral phrenic nerve involvement appears to be uncommon and difficult to treat. The pathology of diabetic mononeuropathy is not well understood and we believe this to be the first histological report of a phrenic nerve biopsy in this condition.

Aged↗
PubMed2002

Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope.

The importance of cardiac output (CO) to blood pressure level during vasovagal syncope is unknown. We measured thermodilution CO, mean blood pressure (MBP), and leg muscle mean sympathetic nerve activity (MSNA) each minute during 60 degrees head-up tilt in 26 patients with recurrent syncope. Eight patients tolerated tilt (TT) for 45 min (mean age 60 +/- 5 yr) and 15 patients developed syncope during tilt (TS) (mean age 58 +/- 4 yr, mean tilt time 15.4 +/- 2 min). In TT patients, CO decreased during the first minute of tilt (from 3.2 +/- 0.2 to 2.5 +/- 0.3 l x min(-1) x m(-2), P = 0.001) and thereafter remained stable between 2.5 +/- 0.3 (P = 0.001) and 2.4 +/- 0.2 l x min(-1) x m(-2) (P = 0.004) at 5 and 45 min, respectively. In TS patients, CO decreased during the first minute (from 3.3 +/- 0.2 to 2.7 +/- 0.1 l x min(-1) x m(-2), P = 0.02) and was stable until 7 min before syncope, falling to 2.0 +/- 0.2 at syncope (P = 0.001). Regression slopes for CO versus time during tilt were -0.01 min(-1) in TT versus -0.1 l x min(-1) x m(-2) x min(-1) in TS (P = 0.001). However, MBP was more closely correlated to total peripheral resistance (R = 0.56, P = 0.001) and MSNA (R = 0.58, P = 0.001) than CO (R = 0.32, P = 0.001). In vasovagal reactions, a progressive decline in CO may contribute to hypotension some minutes before syncope occurs.

Adult↗
PubMed2001

A Comparative Study of Blood Pressure Control with Short In-Center versus Long Home Hemodialysis.

We conducted a randomized crossover trial to establish, within patients, whether long-slow hemodialysis (HD) was associated with better blood pressure (BP) control than standard HD. Nine home HD patients, not on antihypertensive drugs, were dialyzed to the same eKt/V(urea) and target weights for 6-8 h (LD) at home and for 3.5-4.5 h (SD) in the dialysis center 3 times weekly in randomized sequence, with each phase lasting 8 weeks. Ambulatory BP, bioimpedance, neurohormones and autonomic function were measured in each phase. Pre- and postdialysis systolic, ambulatory systolic and diastolic BP were all higher with SD than with LD and intradialysis hypotension was more common. Weight, ECF volume and neurohormones did not differ between treatments. Muscle sympathetic activity was increased in both phases and cardiac sympathetic activity tended higher during SD. These findings suggest that additional factors to ECF volume may contribute to the superior BP control produced by long-slow HD.

Adult↗
PubMed2000

Baroreceptor denervation presenting as part of a vagal mononeuropathy.

A 48-year-old woman presented with a history of progressive cough, dysphonia, dysphagia, and postural symptoms. Subsequent neurological investigations were consistent with a bilateral vagal mononeuropathy, and neurosarcoidosis was diagnosed after scalene node biopsy. Autonomic investigations including microneurography, neurohormones, and heart rate variability demonstrated arterial and cardiopulmonary baroreflex failure. In addition, parasympathetic control of heart rate was absent and consistent with a bilateral, nonselective lesion in the proximal vagus.

Arginine Vasopressin↗
PubMed2000

Brain stem stroke causing baroreflex failure and paroxysmal hypertension.

BACKGROUND: Paroxysmal neurogenic hypertension has been associated with a variety of diseases affecting the brain stem but has only rarely been reported after brain stem stroke. The mechanism is thought to involve increased sympathetic activity and baroreflex dysfunction. We undertook microneurographic recordings of muscle sympathetic nerve activity (MNSA) during beat-to-beat blood pressure (BP) monitoring to investigate this hypothesis. CASE DESCRIPTION: We investigated a 75-year-old woman who developed paroxysmal hypertension (BP 220/110 mm Hg) after a large left-sided medullary infarct. The paroxysms were triggered by changes in posture and were accompanied by tachycardia, diaphoresis, and headache. Serum catecholamines were substantially increased (norepinephrine level, 23.9 nmol/L 9 days after stroke; normal level, <3.8 nmol/L), and heart rate variability, measured by spectral analysis, was decreased in both low- and high-frequency domains (0.04 and 0.06 ms(2), respectively; normal level, 0.14+/-0.02 ms(2)). MNSA was increased in frequency (61 bursts per minute; normal level, 34+/-18 bursts per minute), and the burst amplitude was not inversely related to diastolic BP. BP and MNSA responses to cold pressor and isometric handgrip stimuli were intact. CONCLUSIONS: Extensive unilateral infarction of the brain stem in the region of the nucleus tractus solitarius may result in partial baroreflex dysfunction, increased sympathetic activity, and neurogenic paroxysmal hypertension.

Aged↗