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Biomedical subjects

A H Goodman

Publications and source records attributed to A H Goodman.

69 records · Page 4Linked to original sources
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The effect of heart rate on indices of myocardial contractility in the dog.

1. Changes in heart rate were evoked by atrial pacing in anaesthetized dogs with no pretreatment and in dogs given reserpine or guanethidine for 72 h. The effect of alterations in heart rate were related to two indices of myocardial contractility: the maximal rate of change of left ventricular pressure (dp/dt), and an index which was independent of initial fibre length (dp/dt)/IIT, where IIT is integrated isometric tension. 2. An increase in heart rate in control dogs was accompanied by a rise in both dp/dt and (dp/dt)/IIT confirming that the Bowditch staircase does exist in the intact ventricle. The regression line relating heart rate to (dp/dt)/IIT was significantly steeper than that relating heart rate to dp/dt because the reduction in left ventricular preload at high heart rate tends to attenuate the rise in dp/dt. 3. Reserpine, but not guanethidine pretreatment was accompanied by either a slight decrease or no change in (dp/dt)/IIT during pacing. 4. Acute elevation of (dp/dt)/IIT by either calcium or isoprenaline infusion in reserpine pretreated dogs did not restore the Bowditch effect. 5. Acute depression of (dp/dt)/IIT by propranolol and pentobarbitone was accompanied by a greater rise in (dp/dt)/IIT with pacing in control dogs and a rise rather than a fall in reserpine-pretreated dogs.

Animals↗
PubMedDate not supplied

Transient pressure-flow responses in the resting canine hindlimb--analysis as responses to rapid stretching of the resistance microvessels.

The transient hyperaemia caused by sudden elevation of arterial pressure and reactive hyperaemia after interruption of arterial pressure for 3, 5, 10, 20 and 40 s were studied in the perfused resting hindlimb of anaesthetized areflexic dogs. Experiments were performed using steady-state pressures ranging from 50-150 mmHg. The component of the hyperaemia response (delta Q) that was attributable to resistance vessel distension by a sudden rise in pressure (delta P), was measured as the difference between peak hyperaemic flow change and the flow change predicted for that delta P in a system having constant resistance. Over the range of steady-state pressures used, vascular conductance was approximately constant, indicating that steady-state flow autoregulation was weak. delta Q was a linear function of delta P for both the hyperaemia of sudden pressure elevation and reactive hyperaemia, and the delta Q/delta P relationships were independent of steady-state perfusion pressure. The delta Q/delta P relationships for sudden pressure elevation and reactive hyperaemia after 40 s occlusion did not differ significantly. For a given delta P, however, delta Q decreased with decreasing occlusion time. The magnitude of reactive hyperaemia after brief occlusion depended not only on the degree of resistance vessel relaxation achieved during occlusion but also on the pressure step resulting from restoration of pressure. Using data from these experiments in a simple mathematical model of an idealized resistance vessel, a series of distensibility curves were constructed that showed that as active wall tension increased with increasing steady-state pressure, resistance vessel distensibility decreased.

Animals↗