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Biomedical subjects

I R Mahy

Publications and source records attributed to I R Mahy.

8 recordsLinked to original sources
PubMed1996

Disturbance of peripheral microvascular fluid permeability by the onset of atrioventricular asynchrony in patients with programmable pacemakers.

BACKGROUND: In vitro and in vivo evidence suggests that atrial natriuretic peptide can enhance fluid flux from intravascular to extravascular compartments. The relevance of this to human pathophysiology remains unclear. OBJECTIVES: To determine whether a central haemodynamic change associated with increased plasma concentrations of atrial natriuretic peptide produces detectable change in the capillary filtration coefficient in a peripheral microvascular bed. PATIENTS: 12 patients with programmable dual chamber permanent pacemakers. METHODS: Calf capillary filtration coefficient (using a modified plethysmographic technique) and plasma atrial natriuretic peptide concentrations were measured during atrioventricular synchronous and ventricular pacing. RESULTS: Atrioventricular asynchrony was associated with higher mean (SD) concentrations of atrial natriuretic peptide (231.9 (123.1) v 53.5 (38.8) pg/ml) and an increased mean (SD) calf capillary filtration coefficient (4.2 (1.1) v 3.6 (1.1) ml/min.mm Hg.100 ml x 10(-3)), but there was no correlation between the magnitude of the change in these variables in individual patients. CONCLUSIONS: The peripheral capillary filtration coefficient may change in response to altered central haemodynamics. Atrial natriuretic peptide remains one potential candidate mechanism, but other factors are also likely to be involved.

Adult↗
PubMed1995

Capillary pressure during and after incremental venous pressure elevation in man.

1. The relationship between capillary pressure and venous pressure was investigated during incremental venous pressure elevation in seven healthy volunteers. Pressure was measured simultaneously at the apex of finger nailfold capillaries and in the dorsal vein of the ipsilateral hand. Elevation of venous pressure was accomplished by inflation of a sphygmomanometer cuff around the upper arm. 2. As venous pressure rose, apical capillary pressure (Pc) approached venous pressure (Pv). For changes in Pv greater than 20 mmHg, the increment in Pc was invariably less than the increment in Pv. 3. Above a cuff pressure of 20 mmHg, capillary pulse pressure amplitude (CPPA) tended to decline. At 50 mmHg cuff pressure, CPPA was lower than at baseline for all subjects. At baseline, CPPA was 4.2 +/- 2.0 mmHg (mean +/- S.D.) and at 50 mmHg it was 2.3 +/- 1.1 mmHg (P = 0.02). 4. In the period between 1 and 6 min following cuff release, both Pc and CPPA were lower than at baseline. (At baseline, Pc was 16.1 +/- 2.3 mmHg and following cuff release it was 11.2 +/- 1.5 mmHg (P = 0.02). At baseline, CPPA was 4.2 +/- 2.0 mmHg and following cuff release it was 1.8 +/- 1.1 mmHg (P = 0.03).) 5. Estimated changes in the ratio of pre- to postcapillary resistance (Ra/Rv), using arterial blood pressure (Pa) measured in the contralateral arm, and taking (Pa-Pc)/(Pc-Pv) to approximate to Ra/Rv, closely mirrored changes in CPPA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Disturbance of peripheral microvascular function in congestive heart failure secondary to idiopathic dilated cardiomyopathy.

OBJECTIVES: Previous studies of peripheral microvascular function in human heart failure have concentrated on changes in flow, and there is little information concerning the impact of heart failure on the principal determinants of transcapillary fluid exchange. This study investigated whether alterations in capillary pressure and microvascular fluid permeability can be detected in subjects with idiopathic dilated cardiomyopathy. METHODS: Finger nailfold capillary pressure and calf capillary filtration coefficient (CFC) were measured in parallel studies of two overlapping groups of 12 non-oedematous subjects with idiopathic dilated cardiomyopathy and mild to moderate heart failure and in age- and sex-matched healthy controls. Capillary pressure was measured by direct cannulation using an electronic resistance feedback servonulling technique, and CFC by mercury-in-silastic strain gauge plethysmography using a modification of the technique which avoids assumptions concerning isovolumetric venous pressure. RESULTS: Following correction for differences in skin temperature, capillary pressure was lower in the subjects with heart failure (P = 0.02). Both CFC and isovolumetric venous pressure were greater in the subjects with heart failure than in controls (3.4 +/- 0.9 vs. 2.6 +/- 0.7 ml.min-1.mmHg-1.100 ml-1, P = 0.03; 27.1 +/- 8.4 vs. 17.2 +/- 7.2 mmHg, P = 0.01). CONCLUSIONS: These data suggest that factors other than changes in arterial inflow and venous outflow pressures are likely to play an important role in the disruption of microvascular homeostasis which occurs in heart failure. Changes in capillary hydraulic conductance may contribute to the pathogenesis of oedema.

Adult↗
PubMed1994

The peripheral microcirculation in atrial fibrillation: preservation of capillary pressure and filtration coefficient.

OBJECTIVE: The aim was to assess whether atrial fibrillation results in disturbances of capillary pressure and capillary filtration coefficient in man. METHODS: Finger nailfold capillary pressure and calf capillary filtration coefficient were measured in subjects in atrial fibrillation and in matched healthy controls in sinus rhythm. Capillary pressure was measured by direct cannulation using an electronic resistance feedback servonulling technique, and capillary filtration coefficient by mercury-in-Silastic strain gauge plethysmography using a technique believed not to invoke the venoarteriolar response. RESULTS: Mean capillary pressure did not differ significantly between subjects in atrial fibrillation and those in sinus rhythm [18.4(SD 5.1) mm Hg in atrial fibrillation v 18.0(2.9) mm Hg in sinus rhythm]. In a subgroup of patients restored to sinus rhythm (n = 7) by dc cardioversion there was no significant alteration in capillary pressure [15.3(4.2) mm Hg v 16.6(2.8) mm Hg]. Capillary filtration coefficient was also similar in subjects in atrial fibrillation to that in healthy controls in sinus rhythm [2.81(0.65) kfu in atrial fibrillation v 2.87(0.69) kfu in sinus rhythm]. CONCLUSIONS: These data would suggest that under resting conditions autoregulatory mechanisms are able to preserve microvascular homeostasis despite the central changes associated with atrial fibrillation.

Atrial Fibrillation↗
PubMedDate not supplied

Capillary pulse waveform in aortic stenosis.

The importance of the dynamic nature of perfusion pressure within the peripheral microcirculation is increasingly recognised. Capillary pressure is determined not only by arterial inflow pressure, but is also subject to a variety of local and systemic influences which have been shown to affect both mean pressure and the capillary pulse waveform. To what extent changes in central pulse waveform influence capillary pressure has yet to be determined. By using a dynamic technique of capillary pressure measurement in human subjects with aortic stenosis, we have been able to show that the characteristics of the pulse waveform typically associated with large vessels in this condition are also readily detectable at a capillary level despite local influences. However, changes in the rate of pulse wave transmission described in large arteries were not apparent at a microvascular level. Unlike mean capillary pressure and capillary pulse pressure, pulse waveform in the capillary mimics central haemodynamics.

Aged↗
PubMedDate not supplied

Postural vasoconstrictor response in human heart failure.

In order to study whether posturally induced vasoconstriction is impaired in subjects with heart failure, laser Doppler fluximetry was used to measure blood flow in the cutaneous microvascular bed of the foot at rest and during passive lowering of the extremity below heart level, in subjects with idiopathic dilated cardiomyopathy and in healthy controls. Two sites were studied: the toe pulp where arteriovenous anastomoses are numerous and the dorsum of the foot where such anastomoses are absent. Despite demonstrating a marked reduction in cutaneous blood flow at rest at each site [dorsum 3.0 AU (1.8-4.5) [median (range)] in heart failure patients vs 4.5 AU (1.8-31.6) in controls; toe 8.7 AU (3.1-33.5) in heart failure vs. 44.7 AU (5.2-280.0) in controls, p < 0.01], the results suggest that in non-oedematous subjects with severe left ventricular dysfunction there is no major disturbance of the postural vasoconstrictor response, either at a site rich in highly innervated anastomoses [43.6% (14.5-89.4) vs. 43.7% (15.6-91.1)] or in a site with few such anastomoses [79.7% (39.6-92.3) vs 69.6% (10.1-94.9)].

Adult↗