Studies on the Circulation in Normotensive Febrile Patients

Weinberg, Johannes; Innes, J A; Thomas, Kerkau; Tooke, JE; Guz, A.

doi:10.1113/expphysiol.1989.sp003273

Cited by 14 publications

(6 citation statements)

References 20 publications

(30 reference statements)

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“…Another weakness might be the fact that we had only one set of measurements from each subject while some of the studies we compare with make serial measurements in study subjects during hyperthermia. 5,6,7 Last, we did not have access to previous medications used by the patients.…”

Section: Discussionmentioning

confidence: 99%

Fever increases heart rate and respiratory rate; a prospective observational study of acutely admitted medical patients

et al. 2019

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Background: The relationship between increase in body temperature, heart rate, and respiratory rate has only been studied in young, healthy subjects. Aim: To show the changes in heart and respiratory rate associated with fever in acutely admitted medical patients. Design: A prospective observational cohort study Methods: Vital parameters from 4,493 patients were retrospectively extracted. Linear and multiple variable regression analysis was used to calculate the change in heart and temperature rate for every degree rise in temperature (i.e. ΔHR/°C and ΔRR/°C) in the entire study group and in those with low (<36.1°C), normal (36.1-38°C) and high (>38°C) body temperatures. Results: The ΔHR/°C and ΔRR/°C was 7.2±0.4 beats per minute (bpm) and 1.4 ±0.1 (1.2 to 1.62) breaths per minute (bpm). Adjusting for age, oxygen saturation and mean blood pressure, the results were 6.4±0.4 (5.7 to 7.1) bpm and 1.2±0.1 (1.0 to 1.4) bpm. In low, normal and high body temperature the ΔHR/°C were 2.7±1.9, 6.9±1.9 and 7.4±0.9 bpm, respectively; for ΔRR/°C the values were -0.5±0.5, 1.5±0.5 and 2.3±0.3 bpm, respectively. Conclusions: We only found a modest association between fever and changes in heart rate and respiratory rate.

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Section: Discussionmentioning

confidence: 99%

Fever increases heart rate and respiratory rate; a prospective observational study of acutely admitted medical patients

et al. 2019

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“…Our results demonstrate that although activation of neurons in the DMH is a potential source of the excitatory drive to increase the activity of rat tail CVC neurons and reduce cutaneous heat loss, the activity of neurons in the DMH is not necessary for the increase in tail CVC neuron discharge evoked by application of PGE 2 to the POA, a model of the febrile response, a component of the acute phase immune response in which heat retention mediated by cutaneous vasoconstriction contributes to an increase in T C (19,43,53,67). Our finding that disinhibition of DMH neurons increased CVC neuronal activity parallels the recent demonstration that excitatory amino acid injections into DMH can activate CVC fibers in the plantar nerve (62).…”

Section: Discussionmentioning

confidence: 99%

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

Rathner

Madden²,

Morrison³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

118

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Rathner JA, Madden CJ, Morrison SF. Central pathway for spontaneous and prostaglandin E2-evoked cutaneous vasoconstriction. Am J Physiol Regul Integr Comp Physiol 295: R343-R354, 2008. First published May 7, 2008 doi:10.1152/ajpregu.00115.2008.-A reduction of heat loss to the environment through increased cutaneous vasoconstrictor (CVC) sympathetic outflow contributes to elevated body temperature during fever. We determined the role of neurons in the dorsomedial hypothalamus (DMH) in increases in CVC sympathetic tone evoked by PGE2 into the preoptic area (POA) in chloralose/urethane-anesthetized rats. The frequency of axonal action potentials of CVC sympathetic ganglion cells recorded from the surface of the tail artery was increased by 1.8 Hz following nanoinjections of bicuculline (50 pmol) into the DMH. PGE2 nanoinjection into the POA elicited a similar excitation of tail CVC neurons (ϩ2.1 Hz). Subsequent to PGE2 into the POA, muscimol (400 pmol/side) into the DMH did not alter the activity of tail CVC neurons. Inhibition of neurons in the rostral raphé pallidus (rRPa) eliminated the spontaneous discharge of tail CVC neurons but only reduced the PGE2-evoked activity. Residual activity was abolished by subsequent muscimol into the rostral ventrolateral medulla. Transections through the neuraxis caudal to the POA increased the activity of tail CVC neurons, which were sustained through transections caudal to DMH. We conclude that while activation of neurons in the DMH is sufficient to activate tail CVC neurons, it is not necessary for their PGE2-evoked activity. These results support a CVC component of increased core temperature elicited by PGE2 in POA that arises from relief of a tonic inhibition from neurons in POA of CVC sympathetic premotor neurons in rRPa and is dependent on the excitation of CVC premotor neurons from a site caudal to DMH. rostral raphé pallidus; thermoregulation; fever; dorsomedial hypothalamus; preoptic hypothalamus IN BOTH HUMANS (19,20,43) and rats (53) cutaneous vasoconstrictor (CVC) tone regulates heat loss to the environment and contributes importantly to the maintenance of normal body temperature and to the development of fever. The essential role for the generation of PGE 2 in the preoptic area (POA) in the production of fever has led to the use of nanoinjections of PGE 2 into the POA to understand the neural pathways controlling thermoregulatory effectors during the febrile response. Similarly, observations of thermal effector responses elicited by changes in skin (T SK ) or core temperature (T C ) have provided important information on the central neural networks responsible for body temperature homeostasis. Such studies have been pursued most extensively with regard to the sympathetic neural regulation of non-shivering thermogenesis in rodent brown adipose tissue (BAT), a highly metabolic tissue in which heat production contributes significantly to the defense of body temperature in cold environments and to the elevation of body temperature during the febrile response. The neur...

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“…Säuglinge hingegen sind in der Lage, im vorhandenen braunen Fettgewebe ¹zitterfrei" Wärme zu bilden. [15,16] angegeben wird, einer Steigerung des Herzzeitvolumens [17] und des Sauerstoffverbrauches sowie der Serumkatechol− aminkonzentrationen [18]. Neben einer erhöhten Stoffwechsel− aktivität kommt es in Folge des starken Schwitzens zu extremen Flüssigkeits− (300 ± 500 ml m ±2 24 h ±1 8C ±1 ) [19] und Elektro− lytverlusten.…”

Section: Physiologie Der Thermoregulationunclassified

Fieber in der Intensivmedizin

Brüderlein

Strupp²,

Vagts³

2006

Anästhesiol Intensivmed Notfallmed Schmerzther

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Fever is an unspecific symptom of most intensive care patients during their stay on an intensive care unit. The reasons for the increase of body temperature often remain unclear, even extended diagnostic measures are performed. The pathogenetic relevance of fever is commonly underestimated and leads to unreflected treatment of every increase of body temperature above 38 C. But the development of fever in patients is quite often useful and should not be treated with antipyretics. Physical measures like ice packs and surface cooling are only allowed to be used, if the central set point is lower than the actual core body temperature. This gradient can be recognized, when the patient starts to sweat. Principally, the treatment of fever in cardiovascular risk patients, patients with high risk for adverse neurological outcome, pregnant women during the first trimenon and in children with seizures must start with pharmacological interventions,which can be followed by physical measures.

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Studies on the Circulation in Normotensive Febrile Patients

Cited by 14 publications

References 20 publications

Fever increases heart rate and respiratory rate; a prospective observational study of acutely admitted medical patients

Fever increases heart rate and respiratory rate; a prospective observational study of acutely admitted medical patients

Central pathway for spontaneous and prostaglandin E₂-evoked cutaneous vasoconstriction

Fieber in der Intensivmedizin

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