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P R Freund

Publications and source records attributed to P R Freund.

34 records · Page 2Linked to original sources
PubMed1987

Unaltered norepinephrine-heart rate relationship in exercise with exogenous heat.

We measured plasma norepinephrine (NE) concentration, an index of sympathetic nervous activity, and epinephrine (E), an index of adrenal medulla activity, in six normal young men during mild to severe exercise, with and without superimposed heat stress. The primary objective was to observe whether the normally close relationship between heart rate and log NE concentration in upset when heart rate at a given work load is increased by heat stress. Exercise, beginning at 50 W, was graded in 50-W increments lasting 10 min each up to 200 W, which lasted 5-10 min. Each subject went through the protocol twice, once with skin temperature kept low by a water-perfused suit and then with skin temperature raised to 38 degrees C. Exogenous heart stress raised log circulating NE concentration in proportion to the rise in heart rate at a given work load so that the usual relationship between these variables, previously observed during other stresses, was preserved. In contrast to some other stresses, heat stress had no added effect on E concentration, indicating that this stress during exercise raises sympathetic neural activity (as reflected in the rise in NE) without stimulating additional adrenal release of E.

Adult↗
PubMed1987

Effect of spontaneous sighs on arterial oxygenation during isoflurane anesthesia in humans.

The presence, frequency, and volume of spontaneous sighs was evaluated in 21 (ASA 1-2) supine patients aged 44 +/- 15.2 (SD) yr, during isoflurane-nitrous oxide anesthesia. Before induction the inspiratory capacity of each patient was determined. After induction of anesthesia and tracheal intubation patients breathed spontaneously except for three manual inflations to each patient's predetermined inspiratory capacity at the beginning and end of surgery. Arterial blood gas tensions were measured before and 5 min after each set of mechanical deep breaths and each hour during surgery, the mean duration of which was 2 +/- 0.09 hr. Spontaneous sighs occurred in 13 of 21 patients. The average frequency was 6 +/- 4 sighs/hr. At FIO2 = 0.5, nonsighing patients had an initial PaO2 of 229 +/- 59 mm Hg and sighers had an initial PaO2 of 162 +/- 57 mm Hg (P less than 0.05). Arterial oxygen did not change in sighing patients during the course of surgery, while in nonsighing patients the PaO2 decreased from the initial value of 229 +/- 60 mm Hg to 170 +/- 63 mm Hg (P less than 0.05). Mechanical deep breaths administered at the end of surgery produced no improvement in oxygenation in either sighers or nonsighers. The presence or absence of sighs did not correlate with PaO2 or PACO2. Though the results suggest that spontaneous sighs in some patients may function to help maintain arterial oxygenation, all patients maintained their PaO2 while breathing spontaneously under general anesthesia in the supine position.

Adult↗
PubMed1987

Respiratory effects of nalbuphine and butorphanol in anesthetized patients.

A double-blind, randomized study was conducted in 16 patients who were anesthetized with 50% nitrous oxide in oxygen and given either 0.17 mg/kg butorphanol or 0.86 mg/kg nalbuphine, and whose respiratory depression was assessed by the response of minute ventilation to increasing carbon dioxide concentrations. The slopes of the carbon dioxide ventilatory response curves [delta VE/delta PCO2(L.min-1 X %CO2(-1)] were 7.45 +/- 1.17 with nalbuphine and 2.42 +/- 0.56 with butorphanol. Butorphanol caused significantly (P less than 0.025) greater respiratory depression than nalbuphine. The results of this study caution against the indiscriminate use of butorphanol in the perianesthetic setting.

Anesthesia, General↗
PubMed1985

Sweat rate vs. forearm blood flow during lower body negative pressure.

Skin blood flow is inhibited when hyperthermia and added hypovolemic stresses are superimposed. We tested the hypothesis that part of this inhibition is a reduced drive for cutaneous active vasodilatation (AVD) with sweat rate (SR) taken as an indirect measure of the efferent drive for cutaneous AVD. We also inquired whether SR itself changes with redistribution of blood volume. Six healthy supine men were subjected to lower body negative pressure (LBNP) after heating in water-perfused suits increased esophageal temperatures (Tes) to a mean of 37.2 degrees C and at least doubled SR and forearm vascular conductance (FVC). Heating continued throughout LBNP and recovery. Sweat rate did not decrease with LBNP onset, although SR-Tes slopes during LBNP were reduced 28% from control. In four subjects the SR-Tes slope did not recover when LBNP was discontinued. These observations suggest that SR is not an effector of the low-pressure baroreflex. In contrast to SR, FVC abruptly fell 22% at the onset of LBNP. Thereafter, FVC-Tes slopes near zero or less occurred. The major effector for FVC inhibition with LBNP appears to be the neural vasoconstrictor system. A minor component due to reduced drive for cutaneous AVD probably occurs as well.

Adult↗
PubMed1985

Plasma renin activity and forearm blood flow in paraplegic humans.

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28-47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

Adult↗
PubMed1984

Attenuated skin blood flow response to hyperthermia in paraplegic men.

To clarify how skin and internal temperatures interact in control of skin blood flow, five male paraplegic subjects (lesions at the level of thoracic vertebrae 1-11) (29-47 yr old) were heated in water-perfused suits to elevate oral temperature (To) 1-1.5 degrees C. In part I only the insensate skin was heated; sensate skin was kept at 32-34 degrees C. No appreciable elevation of forearm blood flow (FBF) or sweating occurred, even with To at 38 degrees C. In part II the suit was applied to the whole body so that skin temperature was 40 degrees C, except for one arm that remained at 32-34 degrees C for FBF measurement. Sweating was noted above the lesion in all but one subject. FBF increased in all subjects but was far below levels previously reported for hyperthermic normal men; also, thresholds appeared elevated. To the extent that effector connections are intact, attenuated FBF response implies that either 1) some vasoconstrictor bias associated with cardiovascular regulation is active or 2) thermoregulatory effector outflow is diminished. If the latter is true, it follows that the effector outflow reduction relates to diminished afferent input. But the component of the effector outflow contributed by peripheral thermoreception is small; thus these findings may indicate that what is lacking in the afferent input is central thermoreception from below the lesion, possibly from the spinal cord itself.

Adult↗
PubMed1984

Caudal anesthesia with lidocaine or bupivacaine: plasma local anesthetic concentration and extent of sensory spread in old and young patients.

Continuous caudal peridural anesthesia with 2% lidocaine (6 mg/kg) or 0.75% bupivacaine (2.2 mg/kg), both with epinephrine 1:200,000, was studied in two groups of male patients, younger than 40 or older than 55 yr old, respectively. Patients receiving lidocaine in the younger group (n = 6) were 32 +/- 5.2 (mean +/- SD) yr old and weighed 75 +/- 12 kg, while those in the older group (n = 16) were 66 +/- 5.3 yr old and weighed 72 +/- 8.2 kg. Patients receiving bupivacaine in the respective groups were 27 +/- 7.0 yr old (n = 5), and 76 +/- 10 kg compared to 69 +/- 10 yr (n = 14) and 75 +/- 10 kg. Anesthesia was satisfactory in all patients. Extent of sensory anesthesia, peak plasma lidocaine or bupivacaine concentrations, and area under the plasma concentration-time curves were independent of age. No local anesthetic toxicity was observed and peak drug concentrations were below those commonly associated with toxicity.

Adult↗
PubMed1982

Splanchnic vasoconstriction in heat-stressed men: role of renin-angiotensin system.

We conducted a two-part study to determine whether the renin-angiotensin system contributes to the rise in splanchnic vascular resistance (SVR) during heat stress (rectal temperature was raised 1 degree C). In experiment 1 (control) seven men on a normal salt diet were directly heated (water-perfused suits) for 40-50 min. Arterial pressure (85 Torr) was unchanged; plasma renin activity (PRA) rose from 102 to 239 ng angiotensin I.100 ml-1.3 h-1; and SVR increased 73% (from 63 to 109 units). Experiment 2 was a repetition of experiment 1 on the same subjects, except that propranolol (10 mg iv) was given at the onset of heating to block renin release. Propranolol attenuated the rise in heart rate and reduced mean arterial pressure from 82 to 72 Torr; it blocked the rise in PRA with heating in two subjects, reduced it in three, but increased it in two. Although changes in SVR paralleled those in PRA in three subjects, SVR still rose 60% (from 58 to 99 units) after PRA rise was blocked. In both experiments, plasma norepinephrine concentration rose indicating increased sympathetic nervous activity. During mild heat stress, increased PRA is not a major factor in the increase of SVR.

Adult↗
PubMed1982

Cutaneous vascular response to exercise and acute hypoxia.

Six normal young men were studied during 50 min of moderate exercise (100-137 W) that included one 15-min (protocol 1) or two 10-min periods of breathing 11-12% O2 (in N2) (protocol 2). Absolute work intensity was kept constant for each subject, but relative severity increased during hypoxia owing to reduction in maximum O2 uptake. Our question was whether hypoxia causes cutaneous vasoconstriction; this in turn should cause a rise in esophageal temperature (Tes) and a shift in the forearm skin blood flow (SkBF)-Tes relationship. In all subjects forearm blood flow (FBF) (venous occlusion plethysmography) rose throughout exercise and Tes tended to stabilize. Neither 10- nor 15-min periods of hypoxia caused systematic changes in FBF or Tes or their relationship to each other. We conclude that hypoxia equivalent to that incurred at 4,500-5,000 m does not significantly alter the short-term regulation of SkBF and body temperature during moderate exercise. Net cutaneous vasoconstriction is not elicited by arterial chemoreflexes under these conditions.

Adult↗
PubMed1981

Absence of active cutaneous vasodilation associated with congenital absence of sweat glands in humans.

In the rare syndrome, hereditary anhidrotic ectodermal dysplasia (AED), sweat glands are congenitally absent. Assuming normal vasculature and normal central mechanisms, presence or absence of active cutaneous vasodilation (AVD) in hyperthermic subjects with AED critically tests the hypothesis that AVD is a consequence of sudomotor activity. Three men with full expression of the syndrome and a woman who is mosaic were heated in water-perfused suits until oral temperature was 1.4-1.7 degrees C above control. The men showed no sweat gland imprints on iodine-treated paper nor significant elevation in forearm blood flow (FBF, determined plethysmographically). In the woman, we observed sweat gland activity, approximately 9 and 22 glands/cm2, on the right and left side, respectively, and vasodilation, slight on the right and more on the left. Cutaneous vasoconstriction in response to negative pressure applied to the lower body was observed (3 subjects) and local FBF increased in response to local heating (2 subjects). Therefore, in AED, with apparently normal cutaneous vasculature and sympathetic innervation, AVD is absent as well as sweat glands.

Adolescent↗
PubMed1981

Vasomotor control in healed grafted skin in humans.

Do the vasomotor functions unique to skin recover in a skin graft? To determine whether locally mediated vasodilation and active reflex vasodilation recovery, we applied direct heating and whole-body heating, respectively. Also, presence of sympathetic cutaneous vasoconstriction was tested with application of lower body negative pressure (LBNP) during local heating. Subjects were six men who had been severely burned. Forearm blood flow (FBF) was recorded (venous occlusion plethysmography) in regions with healed split-thickness circumferential grafts. All subjects responded normally to local heating of the forearm (irrigation with 42 degrees C water). All but one showed cutaneous vasoconstriction in response to LBNP. Three subjects responded normally to whole-body heating with water-perfused suits (oral temperature elevation approximately 1.5 degrees C); two subjects had attenuated responses. No active vasodilation was normal cutaneous vasomotor functions return in (or under) split-thickness skin grafts, recovery and associated thermoregulatory function may be attenuated or absent, perhaps in relation to the survival of dermis.

Adolescent↗
PubMed1979

Blockade of the pressor response to muscle ischemia by sensory nerve block in man.

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.

Adult↗
PubMed1978

Cardiovascular responses to muscle ischemia in man--dependency on muscle mass.

We sought to determine whether the pressor response to exercise-induced muscle ischemia is related to the mass of tissue rendered ischemic. Six men repeatedly exercised for 5 min at a fixed load between 75 and 150 W (bicycle ergometer). Thirty seconds before the end of exercise, circulation to one calf, two calves, one leg, and two legs was arrested with pneumatic cuffs in successive tests with 15-min recovery periods interspersed. Each occlusion was maintained until the 3rd min of exercise recovery. During postexercise occlusion we observed 1) mean arterial pressure (MAP) was elevated in proportion to the mass of ischemic muscle, 2) forearm blood flow (FBF) was elevated during the overlap of occlusion with exercise but did not show a uniform response during the following 3 min of occlusion--either vasoconstriction or vasodilation occurred, 3) heart rate (HR) was elevated only when two legs were occluded, and 4) occlusion did not affect ventilation or endtidal CO2. We conclude that the ischemic pressor response is muscle mass-dependent. Our findings suggest that the baroreflex alters peripheral vascular resistance so as to aid in the maintenance of elevated MAP.

Adult↗
PubMedDate not supplied

Calcium channel blockers do not enhance increases in plasma potassium after succinylcholine in humans.

STUDY OBJECTIVE: To determine whether chronic calcium channel blocker therapy exaggerates the rise in plasma potassium concentration ([K+]) after succinylcholine administration. DESIGN: Prospective clinical study. SETTING: University and Veterans Affairs hospitals. PATIENTS: 36 ASA physical status III and IV male patients: 21 patients taking chronic calcium channel blockers and 15 patients not receiving calcium channel blockers, all of whom were scheduled for inpatient surgical procedures with general anesthesia. INTERVENTIONS: In all patients, anesthesia was induced with high-dose opioids plus a sedative-hypnotic, and intubation was facilitated with 1 to 1.5 mg/kg succinylcholine without nondepolarizing neuromuscular blocker pretreatment. MEASUREMENTS AND MAIN RESULTS: Plasma [K+] was measured prior to induction and 1, 3, 5, 8, 11, and 15 minutes after succinylcholine was administered. A modest average peak rise of 0.5 mEq/L in plasma [K+] was observed, but there were no differences between patients who were or were not receiving calcium channel blockers. CONCLUSIONS: Patients receiving chronic calcium channel blocker therapy are at no greater risk of hyperkalemia after succinylcholine than those not taking such medications.

Anesthesia, Intravenous↗