George L. Brengelmann

Disparities Between Aortic and Peripheral Pulse Pressures Induced by Upright Exercise and Vasomotor Changes in Man

Blood pressures were recorded simultaneously from the aortic arch and radial artery using two manometric systems with identical static and dynamic sensitivities. Measurements were made in four normal young men at rest and upright exercise requiring 29, 49, 78, and 100% of maximal oxygen uptake. Average radial arterial pressure rose from 133/66 mm Hg at rest to 236/58 mm Hg at maximal exercise. At the same time, average aortic pressures were 112/68 and 154/70 mm Hg, respectively. From rest to maximal exercise, pulse pressures at central and peripheral sites increased by factors of 1.95 and 2.60, respectively. Inducing reactive hyperemia in the arm abolished peripheral amplification. This amplification also diminished with time during prolonged heavy exercise. Mean pressures were nearly identical at the two sites at any oxygen uptake; mean pressures rose from 87 to 104 mm Hg from mild to maximal exercise. We conclude that estimates of stress on aortic and cerebral vessel walls and central baroreceptors would be grossly overestimated by use of peripheral pulse pressures.

Human Cardiovascular Adjustments to Rapid Changes in Skin Temperature during Exercise

In 11 normal men, central circulatory responses were measured while skin temperature was changed in a square-wave pattern during uninterrupted exercise (26% to 64% maximal oxygen consumption). Skin temperature was changed at 30-minute intervals, beginning at 32°C. On raising it to 38.2°C at low oxygen consumption (V˙o2), cardiac output increased 2.5 liters/min, and central blood volume, aortic mean pressure, and stroke volume fell (7%, 7%, and 11%, respectively). Right atrial mean pressure fell 2.2 and 2.3 mm Hg during control and heating periods, respectively. All variables returned to control levels when skin temperature was reduced toward 26.9°C. Raising it to 40°C reproduced these changes with a more clear-cut drop in right atrial mean pressure. Results indicated reduced peripheral venous tone and cutaneous pooling of blood during heating and rapid reversal on cooling. On raising skin temperature to 38.7°C at high V˙o2, cardiac output increased 19% (3.1 liters/min), stroke volume decreased 14%, and central blood volume rose slightly. Aortic mean pressure fell during the control period and was maintained or rose during heating periods. On cooling, central blood volume and stroke volume rose, cardiac output remained elevated, and aortic mean pressure fell. Increases in cardiac output during heating were related to skin temperature and not to V˙o2 or body temperature. At high V˙o2, circulatory adjustments favor metabolic rather than thermoregulatory demands.

Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression

The onset of melatonin secretion under dim light conditions (DLMO) and the circadian temperature rhythm during a constant routine were assessed in 6 female controls and 6 female patients with winter depression (seasonal affective disorder, SAD) before and after bright light treatment. After sleep was standardized for 6 days, the subjects were sleep‐deprived and at bedrest for 27 h while core temperature and evening melatonin levels were determined. The DLMO of the SAD patients was phase‐delayed compared with controls (2310 vs 2138); with bright light treatment, the DLMO advanced (2310 to 2135). The minimum of the fitted rectal temperature rhythm was phase‐delayed in the SAD group compared with the controls (0542 vs 0316); with bright light treatment, the minimum advanced (0542 vs 0336).

Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression

Circadian temperature, cortisol, and thyroid-stimulating hormone (TSH) rhythms during a constant routine were assessed in 6 female controls and 6 female patients with hypersomnic winter depression (seasonal affective disorder, SAD) before and after morning bright light treatment. After sleep was standardized for 6 days, the subjects were sleep-deprived and at bed rest for 27 hours while rectal temperature, cortisol, and TSH levels were assessed. The minimum of the fitted rectal temperature rhythm was phase-delayed in the SAD group compared to the controls 5:42 AM vs. 3:16 AM (p < .005); with bright light treatment, the minimum advanced from 5:42 AM to 3:36 AM (p = .06). The minimum of the cortisol rhythm was phase-delayed in the SAD group compared to the control group, 12:11 AM vs. 10:03 PM (P < .05); with bright light treatment, the minimum advanced from 12:11 AM to 10:38 PM (P = .06) [corrected]. The acrophase of the TSH rhythm was not significantly phase-delayed in SAD subjects compared to control, though the trend appeared to be toward a phase-delay (p = .07). After bright light therapy, the TSH acrophase was not significantly different in the SAD subjects; the trend was a phase-advance (p = .09). Overall, the data suggest that circadian rhythms are phase-delayed relative to sleep in SAD patients and that morning bright light phase-advances those rhythms.

Temperature Regulation in the Neutral Zone

The impressive features of human thermoregulation are the powerful effectors that defend us against hyperthermia-active vasodilation of the blood vessels of the skin, and secretion of sweat. Together, these can keep body temperature within one or two degrees of normal in an exercising person who generates heat at anear-kilowatt rate for hours, for example, in a marathon race.’ Less impressive, in terms of power, is shivering, for cold-exposed humans do not maintain thermal steady states for long through high rates of shivering. Least impressive and least obvious is the subtle modulation of skin blood flow that regulates body temperature over long periods of sedentary or mild activity and “neutral” thermal conditions. Yet it is that unappreciated effector system that accomplishes the thermal balance that we associate with normal body temperature. Clearly, it accomplishes the alterations in steady-state body temperature associated with the diurnal and lunar rhythms and with disturbances in those rhythms. If it means something to state that the “set-point” of body temperature regulation changes with sleep onset, for example, it must be that the parameters of control of skin blood flow in relation to inputs derived from skin and core thermosensors change with sleep onset. Do they? The observed effect might have nothing to do with the thermoregulatory control system per se . For example, lying down alters skin blood flow2” and thus alters the equilibrium core temperature in fixed thermal conditions. Is the apparent set-point shift the consequence of this nonthermal influence? To be able to answer such questions we need better quantitative understanding of the control of skin blood flow and means of measuring the parameters of control.

Body temperature and diurnal type in women with seasonal affective disorder

Body temperature rhythms and diurnal type were explored in female controls and women with seasonal affective disorder (SAD) before and after phototherapy. Women with SAD reported being more like evening types than did controls. Morning phototherapy advanced the body temperature rhythms of women with SAD, and shifted their morningness/eveningness scores toward the morning end of the continuum. The implications of these results for our understanding of both SAD and depression in women are discussed.

Epidural anesthesia and the thermoregulatory responses to hyperthermia - Preliminary observations in volunteer subjects

Background: Clinical reports associate the use of epidural anesthesia with an increase in core temperature in women in labor. We tested the hypothesis that epidural anesthesia alters thermoregulatory responses to hyperthermia in human volunteers.

Temperature dependence of intraparenchymal bronchial blood flow.

Previous studies suggested that bronchial vascular resistance, like that of the skin, changes with the temperature of the surrounding tissue. To investigate this phenomenon, we recorded anastomotic (systemic to pulmonary) (Qbrs-p) and total (Qbr) bronchial blood flow over a temperature range centered on normal. In 7 open-chested dogs the in situ left lower lobe (LLL) was separately ventilated (30 degrees C, 5% CO2 in humidified air) and was suspended in a fabric net from a strain gauge for continuous recording of weight. The pulmonary circulation of the LLL was pump-perfused at 255 +/- 69 ml/min in a closed circuit with temperature set at 30, 33, 36, 39 and 42 degrees C. Qbrs-p was measured as overflow from the LLL vascular circuit corrected for LLL weight changes. Qbr, tracheal, mid-esophageal and coronary flow were measured with 15 mu radiolabelled microspheres injected in the left atrium. The animals core temperature and that of the humidified air around the LLL were held constant. Qbr and Qbrs-p were equal and reached a peak at 36 degrees C with lower levels of flow at higher and lower temperatures. Esophageal, tracheal and coronary flow and cardiac output did not change nor did pressures in the systemic and LLL pulmonary artery and in the LLL airways. An intralobar change in temperature above or below 36 degrees C decreases only the lobar bronchial blood flow and does not influence blood flow to other nearby tissues including those vascularized by the bronchial circulation.

Letter to the editor: Why persist in the fallacy that mean systemic pressure drives venous return?

to the editor: The work of Berger et al. ([3][1]), recently published in the American Journal of Physiology-Heart and Circulatory Physiology , has at its core the idea that steady-state venous return (F) is driven through the resistance to venous return (Rven) by the difference between mean systemic

Placement of esophageal stethoscope by acoustic criteria does not consistently yield an optimal location for the monitoring of core temperature

The esophageal stethoscope has evolved into a device for both acoustic and core temperature monitoring. To test whether routine placement according to acoustic criteria results in placement of the core temperature sensor in the region of contiguity between the esophagus and the heart, we determined the depth of placement electrocardiographically. All patients were undergoing nonthoracic elective operations requiring general anesthesia and tracheal intubation. First, we established that different observers selected the same esophageal depth within ±1 cm electrocardiographically, using the criterion of a symmetric biphasic P wave of maximal amplitude (7 patients). Then, in 30 more patients, we compared routine acoustic placements with the depths of the maximalamplitude biphasic P wave. Stethoscopes placed according to acoustic criteria were within ±3 cm of P-wave depths in 15 of 30 patients. In the remaining patients, measured discrepancies ranged up to 13.5 cm. We conclude that the prevailing stethoscope design, with a thermistor at the tip, below the acoustic window, does not ensure placement of the thermistor within the optimal region for monitoring of core temperature. A modification in design that would take advantage of the reliability of electrocardiographic positioning is suggested.