Biomedical subjects
Publications and source records attributed to D B Friedman.
In the 1946 film 'A Matter of Life and Death', complex partial seizures were portrayed in detail and with surprising accuracy. This study was conducted to determine the nature of the medical collaboration in the preparation of the film as well as the reasons why the creative team of Michael Powell and Emeric Pressburger included these details, but elected to make them invisible to all but those with medical educations.
1. Heart rate response to reversible central hypovolaemia can be divided into three stages. In the first stage (corresponding to a reduction of the blood volume by approximately 15%) a modest increase in heart rate (< 100 beats/min) and total peripheral resistance compensate for the blood loss, and a near normal arterial blood pressure prevails (preshock). During the second stage, a reduction of the central blood volume by approximately 30% results in a decrease in heart rate, total peripheral resistance and blood pressure due to activation of unmyelinated vagal afferents (C-fibres) from the left ventricle. In the third stage, blood pressure falls further as haemorrhage continues and tachycardia (> 120 beats/min) is manifest. This stage may proceed into irreversible shock with death from cardiac arrest probably related to the formation of free oxygen radicals. 2. Recognition of the vasodepressor-cardioinhibitory reaction to a reduced circulating blood volume is important and suggests the need for immediate treatment with volume expansion in critically ill patients.
We have measured the cardiovascular responses during voluntary and nonvoluntary (electrically induced) one-leg static exercise in humans. Eight normal subjects were studied at rest and during 5 min of static leg extension at 20% of maximal voluntary contraction performed voluntarily and nonvoluntarily in random order. Heart rate (HR), mean arterial pressure (MAP), and cardiac output (CO) were determined, and peripheral vascular resistance (PVR) and stroke volume (SV) were calculated. HR increased from approximately 65 +/- 3 beats/min at rest to 80 +/- 4 and 78 +/- 6 beats/min (P < 0.05), and MAP increased from 83 +/- 6 to 103 +/- 6 and 105 +/- 6 mmHg (P < 0.05) during voluntary and nonvoluntary contractions, respectively. CO increased from 5.1 +/- 0.7 to 6.0 +/- 0.8 and 6.2 +/- 0.8 l/min (P < 0.05) during voluntary and nonvoluntary contractions, respectively. PVR and SV did not change significantly during voluntary or nonvoluntary contractions. Thus the cardiovascular responses were not different between voluntary and electrically induced contractions. These results suggest that the increases in CO, HR, SV, MAP, and PVR during 5 min of static contractions can be elicited without any contribution from a central neural mechanism (central command). However, central command could still have an important role during voluntary static exercise.
Regional cerebral blood flow (rCBF) was measured at orbitomeatal (OM) plane +5.0 and +9.0 cm in 10 subjects at rest and during dynamic hand contractions before and after axillary blockade. Handgrip strength was significantly reduced, and rating of perceived exertion increased after blockade. During hand contractions before blockade, contralateral hemispheric cerebral blood flow (CBF) at OM +9.0 increased from a resting value of 58 (49-75) to 63 (52-82) ml.100 g-1.min-1; contralateral motor sensory rCBF at OM +9 from 58 (50-77) to 71 (64-84); motor sensory rCBF at OM +5 from 67 (54-76) to 77 (64-87) and 70 (62-84) contralaterally and ipsilaterally, respectively; and supplementary motor area (SM) rCBF from 64 (53-69) to 75 (67-88) ml.100 g-1.min-1. During dynamic hand contractions after axillary blockade, CBF did not increase at OM +5 or in the SM. Furthermore, contralateral motor sensory rCBF at OM +9 increased much less. Axillary blockade had no effect on resting CBF, rCBF, or increases in the two during hand contractions of the opposite hand. Thus neural feedback from the contracting muscle is necessary for the increases in SM bilateral OM +5 motor sensory rCBF and the maximal increase in contralateral OM +9 motor sensory rCBF during dynamic hand contractions.
Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)
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We describe a case of generalized, asymptomatic, chronic annular lichen planus. The centers of the large annular lesions were atrophic and had lost their elasticity. Histologic examination revealed an absence of elastic fiber in the center. Electron microscopy revealed fragmented elastic fibers. Examination of early lesions showed that elastolysis had already begun in the heavy cellular infiltration. We conclude that the annular configuration resulted from the elastolytic activity of the inflammatory cells with the formation of foci of localized acquired cutis laxa.
We evaluated regional electrical impedance (Z degree) at 2.5 and 100 kHz to separate intra- and extracellular fluid changes and correlated Z degree over the thorax (TI) to relative changes in the central blood volume (CBV) induced by head-up tilt. In nine experiments head-up tilt resulted in normotensive central hypovolaemia associated with a 3.7 +/- 0.4 Ohm (mean +/- SE) increase in TI100 kHz after 60 min. In 24 experiments pre-syncopal symptoms were induced after 43 +/- 2 min, when TI100 kHz had increased 4.2 +/- 0.2 Ohm. Head-up tilt instantly decreased the activity of technetium labelled erythrocytes (99Tcm) over the thorax by 24 +/- 2%, and increased 99Tcm over the thigh by 68 +/- 10% (P less than 0.01, n = 8) with no further changes during the sustained tilt. Haematocrite increased during head-up tilt from 43.1 +/- 0.3 to 47.9 +/- 0.6% (P less than 0.01, n = 8). Accordingly, the increase in TI (6.3 +/- 0.6 vs. 4.5 +/- 0.4 Ohm, n = 6) and the decrease in Z degree through one leg (7.2 +/- 1.2 vs. 2.8 +/- 0.5 Ohm, n = 6) at 2.5 kHz was more pronounced than at 100 kHz. Also the changes in TI were correlated to CBV as calculated from 99Tcm and haematocrite (r = 0.90, P less than 0.01). The results suggest that: (1) Hypovolaemic shock is associated with a faster increase of TI than normotensive head-up tilt. (2) Head-up tilt is characterized by an initial decrease in CBV followed by a further decrease in plasma volume, which eventually leads to hypovolaemic shock. (3) Blood volume changes during head-up tilt are reflected in regional Z degree.
Regional cerebral blood flow (rCBF) was determined at rest and during static handgrip before and after regional blockade with lidocaine. A fast rotating single photon emission computer tomograph system with 133Xe inhalation was used at orbitomeatal plane (OM) +2.5 and +6.5 cm in eight subjects. Median handgrip force during the control study was 41 (range 24-68) N, which represented 10% of the initial maximal voluntary contraction (MVC) and was 24 (18-36) N after axillary blockade (P less than 0.05), which represented 21% of the new MVC. During static handgrip, the rating of perceived exertion was 14 (10-16) exertion units before and 18 (15-20) after blockade (P less than 0.05). Hemispheric mean CBF did not change during handgrip. However, premotor rCBF increased from 55 (44-63) to 60 (50-69) ml.100 g-1.min-1 (P less than 0.05) and motor sensory rCBF from 57 (46-65) to 63 (55-71) ml.100 g-1.min-1 (P less than 0.05) to both the ipsilateral and contralateral sides during handgrip before, but not after, axillary blockade. There was no change in rCBF to other regions of the brain. Regional anesthesia with lidocaine did not alter resting rCBF. However, despite a greater sense of effort during static handgrip, there was no increase in rCBF after partial sensory and motor blockade. Thus bilateral activation occurs in the premotor and motor sensory cortex during static handgrip, and this activation requires neural feedback from the contracting muscles.
This study was designed to evaluate the relative importance of intended effort ("central command") and of the absolute intensity of dynamic exercise to the cutaneous vasoconstrictor response to the onset of exercise in humans. Skin blood flow (laser-Doppler flowmetry) was measured from the forearm in six healthy individuals during 3-min periods of high- and low-intensity exercise with and without partial neuromuscular blockade. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure and expressed as a percent change from rest. A rating of perceived exertion (RPE) was expressed as a subjective measure of intended effort. Under control conditions, CVC decreased by 22% (median; range 7-42%, P less than 0.05) during high-intensity exercise [218 (186-268) W; RPE 16 (14-19) exertion units]. In contrast, during control low-intensity exercise [106 (88-128) W; RPE 10 (9-14) exertion units], during low-level exercise with curare [77 (54-98) W; RPE 13 (11-16) exertion units], and during maximal exercise with curare [106 (88-124) W; RPE 19 (18-20) exertion units], CVC did not change significantly. These results suggest that factors related to the activity of the exercising muscle and its metabolism rather than intended effort determine the cutaneous vasoconstrictor response to the initiation of intense dynamic exercise in humans.
BACKGROUND: Endurance athletes have a high incidence of orthostatic intolerance. We hypothesized that this is related to an abnormally large decrease in left ventricular end-diastolic volume (LVEDV) and stroke volume (SV) for any given decrease in filling pressure. METHODS AND RESULTS: We measured pulmonary capillary wedge (PCW) pressure (Swan-Ganz catheter), LVEDV (two-dimensional echocardiography), and cardiac output (C2H2 rebreathing) during lower body negative pressure (LBNP, -15 and -30 mm Hg) and rapid saline infusion (15 and 30 ml/kg) in seven athletes and six controls (VO2max, 68 +/- 7 and 41 +/- 4 ml/kg/min). Orthostatic tolerance was determined by progressive LBNP to presyncope. Athletes had steeper slopes of their SV/PCW pressure curves than nonathletes (5.5 +/- 2.7 versus 2.7 +/- 1.5 ml/mm Hg, p less than 0.05). The slope of the steep, linear portion of this curve correlated significantly with the duration of LBNP tolerance (r = 0.58, p = 0.04). The athletes also had reduced chamber stiffness (increased chamber compliance) expressed as the slope (k) of the dP/dV versus P relation (chamber stiffness, k = 0.008 +/- 0.004 versus 0.031 +/- 0.004, p less than 0.005; chamber compliance, 1/k = 449.8 +/- 283.8 versus 35.3 +/- 4.3). This resulted in larger absolute and relative changes in end-diastolic volume over an equivalent range of filling pressures. CONCLUSIONS: Endurance athletes have greater ventricular diastolic chamber compliance and distensibility than nonathletes and thus operate on the steep portion of their Starling curve. This may be a mechanical, nonautonomic cause of orthostatic intolerance.
Continuous blood pressure measurement by a non-invasive means is of clinical utility in many situations where changes in cardiovascular hemodynamics and blood volume distribution are likely to occur. We have compared blood pressure measurements using the Penaz principle (Finapres, Ohmeda) to an intra-arterial catheter system during head-up tilt (reverse Trendelenburg's position) which models central hypovolemia. Twelve healthy volunteers were raised to a 60 degree head-up tilt position for 60 min or until presyncope occurred. Seven subjects developed presyncopal symptoms at a mean time of 38 +/- 6 min with blood pressure measured by the Penaz principle falling from 140 +/- 8/72 +/- 4 to 82 +/- 10/54 +/- 6 mmHg (18.7 +/- 1.1/9.6 +/- 0.5 to 10.9 +/- 1.3/7.2 +/- 0.8 kPa) (P less than 0.01), at which point they were returned to a horizontal position with an immediate rise in blood pressure. During the maximal drop in blood pressure, heart rate decreased from 82 +/- 7 to 45 +/- 5 (P less than 0.01). Overall, the non-invasive system had a correlation coefficient of 0.98 as compared to the intra-arterial method and ECG for blood pressure and heart rate in all 12 subjects during rest, tilt, and recovery. We conclude that the Penaz principle apparatus is a useful monitor of symptomatic hypotension during central hypovolemia.
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Ratings of student clinical performance were analyzed to determine consistency of supervisor and coordinator judgements of the same students as they progressed through medical school and on into the internship. The results suggested that students were consistently and progressively rated higher.
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