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Biomedical subjects

K E Cooper

Publications and source records attributed to K E Cooper.

At least 19 recordsLinked to original sources
PubMed1997

Salivary glands, their hormones, and thermoregulation.

The effects of the removal of the submandibular glands (sialadenectomy) on the fever induced by bacterial lipopolysaccharide (LPS) were examined. Thermally sensitive radiotransmitters were implanted into the abdomens of adult male Sprague-Dawley rats that experienced at this time either a sham operation or a sialadenectomy, and one week later body temperatures were recorded by telemetry in these rats when conscious. The initial fever (up to 180 min following LPS) response, following the intraperitoneal injection of 150 micrograms/kg E. coli LPS, was similar in the two groups of rats, but the second phase of the fever (240 to 420 min post-LPS) was modestly, but significantly higher (mean = 0.26 degree C) in sialadenectomized rats. A submandibular gland peptide (compound T; 100 micrograms/kg), given one-half hour before the LPS, did not affect the early fever, but suppressed the late-phase fever by 0.37 degree C (mean). The submandibular glands, which form an integral part of the neuroendocrine mechanisms responsible for attenuating the responses of the immune system to inflammatory stimuli, also appear to modulate thermogenic responses to these stimuli.

Animals↗
PubMed1997

Submandibular glands: novel structures participating in thermoregulatory responses.

Since submandibular glands participate in the regulation of cardiovascular and immunological responses to bacterial endotoxin, we examined their role as modulators of endotoxin-induced fever. Core body temperatures were measured by telemetry in rats that had either a sham operation or a sialadenectomy 1 week previously and that were maintained at 23-24 degrees C. The sialadenectomized rats showed a circadian variation in body temperature similar to sham-operated rats, although their daytime body temperature was 0.24 +/- 0.01 degree C lower. The fever elicited by intraperitoneal injection of Escherichia coli endotoxin was biphasic, with an initial phase occurring between 2 and 3 h, and a broader second phase peaking between 4 and 8 h after endotoxin injection. The initial fever was similar in the two groups of rats, but the second phase of fever was significantly higher by 0.28 +/- 0.09 and 0.26 +/- 0.07 degree C in sialadenectomized rats receiving 50 or 150 micrograms/kg of endotoxin, respectively. Intravenous treatment with a novel peptide, submandibular gland peptide-T (SGP-T; 100 micrograms/kg), 30 min before endotoxin injection did not affect the early fever response, but significantly suppressed by 0.37 +/- 0.10 degrees C the late-phase fever provoked by 150 micrograms/kg of endotoxin. These results suggest that the submandibular glands modulate thermogenic responses to inflammatory stimuli possibly through the endocrine release of hormones, such as SGP-T.

Animals↗
PubMed1994

Effect of potassium-induced cortical spreading depression on prostaglandin-induced fever in conscious and urethane-anesthetized rats.

Potassium-induced cortical spreading depression (CSD) on prostaglandin E1 (PGE1) induced fever has been investigated in a dose-responsive experimental design in both conscious and urethane-anesthetized adult male Sprague-Dawley rats. While CSD in itself had no effect on nonfebrile body temperature even under cold ambient conditions, CSD significantly suppressed small but not large fevers induced by intracerebroventricular PGE1. The increased oxygen consumption during fever was also reduced. We also explored the possible involvement of the antipyretic peptide arginine vasopressin, in the CSD-induced suppression of fever. Long term castrated rats have significantly reduced ventral septal levels of this peptide, yet CSD was effective in suppressing the initial 40 min of PGE1 fever in these animals. Thus we conclude that increased release of ventral septal arginine vasopressin is probably not involved in the action of CSD on fever.

Anesthesia↗
PubMed1994

Some responses of the cardiovascular system to heat and fever.

This review outlines the mechanisms of body temperature control and the validity of various sites of measurement of core temperature. The mechanism of fever in response to circulating endotoxins are discussed, and the roles of various peripherally generated pyrogenic cytokines are outlined together with the loci of their action in the brain. The cardiovascular consequences of exposure to heat, particularly the pooling of blood in the skin and the increase of heart rate due to heating of the sinoatrial node, are discussed. The consequences of blood pooling, such as syncope or diminished G tolerance, are very important. Heat exposure and exercise lead to complex circulatory interactions, such as a higher heart rate for a given exercise load in the heat compared with a cool environment. At high work loads there may be a relatively lower cardiac output in hot conditions. Blood lactate levels and rectal temperature tend to be higher in exercise in the heat than exercise in the cold. Fever causes a large renal vasodilation and hepatic vasodilation, which are humorally mediated and which effectively cause a splanchnic vascular shunt of some consequence if there is already heart failure or shock. Syncope during fever, endotoxin shock and the role of pyrogens in heat stroke are discussed.

Animals↗
PubMed1993

Regulation of a voltage-dependent, calcium-activated K conductance by cyclic GMP in dissociated flounder enterocytes.

Enterocytes from the winter flounder (Pseudopleuronectes americanus) were isolated by collagenase digestion and maintained in flounder Ringer's solution. Whole cell currents were studied using the amphotericin-perforated whole-cell patch clamp technique. The mean resting membrane potential and capacitance values or dissociated cells were -45 +/- 7 mV and 5 +/- 0.4 pF, respectively. Enterocytes held at -20 mV and treated with 1 mumol.l-1 ionomycin exhibited outward currents when cells were stepped through a series of voltages from -60 to +110 mV. The reversal potential of this current in flounder Ringer's solution was -55 mV and the voltage at which half-maximal activation occurred was +20 mV. Voltage-dependent inhibition of outward current was observed at +60 mV and above. When cells were bathed in symmetric K Ringer's solution the reversal potential shifted to zero mV and no inhibition of current was observed at voltages between -60 and 140 mV. When the holding potential of the cell was changed from -20 to -80 mV and stepped from -60 to +110 mV, a second [previously characterized, O'Grady et al. (1991)] K current with delayed-rectifier properties was identified. This observation demonstrated that the delayed rectifier K channel and the Ca(2+)-activated K channel described in this study exist in the same cell. Extracellular addition of 2 mmol.l-1 Ba2+ to cells bathed in symmetric K Ringer's solution resulted in nearly complete inhibition of outward current. Charybdotoxin produced only minor effects on this current.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

A method for continuous blood sampling during cold water immersion.

A technique, consisting of a pre-calibrated, catheter-peristaltic pump combination, for continuous blood sampling was tested using six volunteers during a 20 min immersion in cold water at 14.7 +/- 0.9 degrees C. The device offered the advantage of continued collection of blood samples from an antecubital vein during the experiment with little discomfort for the subjects and in sufficient volume for assay of plasma constituents eg. catecholamines.

Blood Specimen Collection↗
PubMed1993

Lupus anticoagulant testing: effect of the platelet count on the activated partial thromboplastin time.

The activated partial thromboplastin time (APTT) is often used as a test to diagnose patients with lupus anticoagulants. It is recommended that platelet-poor plasma be used in the APTT test. In this study the effects of residual platelet contamination on lupus anticoagulant and antiphospholipid antibody testing are described. In fresh samples the residual platelet contamination has no significant effect whereas in frozen samples the effect of residual platelet contamination can have a significant effect on the APTT testing.

Antibodies, Antiphospholipid↗
PubMed1993

Experimental characterization and applications of an anesthetized animal model for thermoregulatory investigations.

In the study of mechanisms of thermoregulation conscious animals are used and in most cases the conscious animal is the preferred choice. In some investigations however an anesthetized animal may be the model necessary for the practical purposes of the experimental design. We have developed, tested, and used an urethane anesthetized animal as a model in thermoregulatory investigations. Experiments have been completed in which we have shown that the adult male rat when anesthetized to a surgical level with urethane (1.5 gm/kg) cannot maintain its body temperature and becomes "poikilothermic-like". By providing a steady level of heat to the animal, body temperature can be stabilized for long periods of time at any basal level. This unique feature is not possible in conscious animals. Although apparently poikilothermic, these anesthetized animals respond with a dose-dependent fever to pyrogenic agents such as bacterial pyrogen, interleukin, and prostaglandin. Accompanying these fevers are physiological changes characteristic of fever including increases in arterial and central venous blood pressure, heart rate, oxygen consumption and shivering all of which are similar to the changes which occur in conscious animals. We have used this model for investigations on intracranial pressure, fever suppression and enhancement, application and recovery (for assay) of neuro-transmitters to and from specific brain loci, microdialysis, osmotic stimulation, and electrophysiological stimulation and recording.

Alprostadil↗
PubMed1992

Vasopressin perfusion within the medial amygdaloid nucleus attenuates prostaglandin fever in the urethane-anaesthetized rat.

The antipyretic effect of arginine vasopressin (AVP) introduced into the ventral septal area (VSA) by push-pull perfusion was investigated in the urethane-anaesthetized rat. In addition, experiments were carried out to determine whether AVP could suppress fever when similarly perfused within the medial amygdaloid nucleus (meA). During push-pull perfusion of artificial cerebrospinal fluid within the VSA or meA, PGE1 injected intracerebroventricularly evoked fevers with respective magnitudes of 1.3 +/- 0.2 degrees C and 1.4 +/- 0.3 degrees C above baseline. Perfusion of AVP (6.5 micrograms/ml) within the VSA had significantly reduced the magnitude of PGE1 fever to 0.3 +/- 0.3 degrees C above baseline, while having no significant effect on afebrile colonic temperature. Perfusion of AVP (6.5 micrograms/ml) within the meA had significantly attenuated the magnitude of PGE1 fever to 0.7 +/- 0.2 degrees C above baseline, while having no significant effect on afebrile colonic temperature. These results support further the utility of the urethane-anaesthetized rat model for future investigations of the central control of fever and antipyresis. In addition, these data are consistent with the hypothesis that AVP may act within the meA as an endogenous antipyretic.

Alprostadil↗
PubMed1992

Fever response of sheep in the peripartum period to gram-negative and gram-positive pyrogens.

We have measured body temperatures and serum iron concentrations of sheep in the peripartum period following administration of endotoxin and Staphylococcus aureus cell walls. Both the rise in rectal temperature and the fall in serum iron concentration following intravenous injection of S. aureus were the same immediately pre- and postpartum as they were 5 weeks after parturition. The rise in rectal temperature following intravenous endotoxin injection immediately pre- and postpartum was significantly less than that of the same ewes 5 weeks later. However, the fall in serum iron concentration following endotoxin injection was significantly suppressed only prepartum. We conclude that fever is not suppressed in sheep in the peripartum period, but the response to endotoxin is suppressed, through complex processes incidental to the mechanism responsible for the maintenance of gestation and induction of labour.

Animals↗
PubMed1991

Modulation of brown adipose tissue-mediated thermogenesis by lesions to the nucleus tractus solitarius in the rat.

Given that relatively little is known regarding the central control of brown adipose tissue (BAT)-mediated thermogenesis the present study assessed whether the direct pharmacological stimulation of beta- or alpha-adrenergic receptors located on the brown adipocytes would result in a typical thermogenic response following electrolytic lesions to the nucleus tractus solitarius (NTS). Bilateral electrolytic lesions to the NTS in the rat effectively disrupted the baroreceptor reflex arc. It was observed that the metabolic and temperature responses to either norepinephrine (1, 5, or 25 micrograms/kg/min) or to the beta-agonist isoproterenol (0.5 micrograms/kg/min) were significantly attenuated in the NTS-lesioned rats relative to the control animals with an intact baroreflex. Conversely, the cardiovascular effects of norepinephrine or of the alpha-agonist phenylephrine (10 micrograms/kg/min) were enhanced in the NTS-lesioned animals. The results suggest that the functional capacity of the brown adipocytes was reduced following NTS lesions and points to an alteration in the ability of beta-receptors to respond to pharmacological stimulation with a typical thermogenic response.

Adipose Tissue, Brown↗
PubMed1991

Cyclic GMP regulation of a voltage-activated K channel in dissociated enterocytes.

Enterocytes from the intestinal epithelium of the winter flounder were isolated by collagenase digestion and incubated in flounder Ringer solution. Conventional whole-cell and amphotericin-perforated whole-cell recording techniques were used to characterize the properties of a voltage-activated K current present in dissociated cells. Resting membrane potentials and series resistances were significantly lower (from -23 to -39 mV and 29 to 13 M omega, respectively) when amphotericin was used to achieve the whole-cell configuration. When cells were placed in flounder Ringer solution, held at -80 mV and subsequently stepped to a series of depolarizing voltages (from -70 to 0 mV), an outward current was observed that exhibited inactivation at voltages above -20 mV. This current was sensitive to holding potential and was not activated when the cells were held at -40 mV or above. When cells were bathed in symmetric K Ringer solution and the same voltage protocol was applied to the cell, inward currents were observed in response to the negative intracellular potentials. Reversal potentials at two different extracellular K concentrations were consistent with K as the current-carrying ion. BaCl2 (2 mM) and CsCl (0.5 mM) both produced voltage-dependent blockade of the current when added to the bathing solution. Charybdotoxin (300 nM extracellular concentration) completely blocked the current. The IC50 for charybdotoxin was 50 nM. Cyclic GMP inhibited the voltage-activated current in flounder Ringer and in symmetric K Ringer solution. The cyclic GMP analog, 8-Br cGMP, lowered the threshold for voltage activation and potentiated inactivation of the current at voltages above -40 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphotericin B↗
PubMed1991

Nucleus tractus solitarii lesions alter the metabolic and hyperthermic response to central prostaglandin E1 in the rat.

1. Given that the nucleus tractus solitarii (NTS) may regulate the ability of brown adipose tissue to evoke non-shivering thermogenesis and that brown fat may mediate the rise in whole-body metabolism observed following central pyrogen administration, we assessed whether interruption of baroreceptor afferents coursing though the NTS would interfere with the ability of prostaglandin E1 to evoke a normal fever response profile. 2. Infusion of 150-600 ng of prostaglandin E1 (PGE1) into a lateral cerebral ventricle of the conscious rat resulted in a rise in core temperature, and also an increase in whole-body metabolic rate, brown adipose tissue temperature, arterial blood pressure and heart rate. 3. Following bilateral electrolytic lesions to the NTS, resting core and brown fat temperatures, metabolic rates, blood pressures and heart rates in the NTS-lesioned animals were comparable to control rats. However, the PGE1-evoked increase in metabolic rate, along with the rise in core and brown adipose tissue temperatures and heart rate were attenuated. The pressor response was, however, enhanced, possibly due to the demonstrated interference by the lesions with normal baroreflex control. 4. The findings suggest that the nucleus tractus solitarii region of the rats' brain may be important in mediating the thermogenesis evoked by central PGE1.

Adipose Tissue, Brown↗
PubMed1991

Contribution of brown adipose tissue to central PGE1-evoked hyperthermia in rats.

The relative contribution of several effector systems to a prostaglandin E1-(PGE1) evoked hyperthermia was examined. Infusion of 150 ng of PGE1 into a lateral cerebral ventricle increased core temperature and whole body metabolic rate, brown adipose tissue temperature, systolic blood pressure, and heart rate. Pretreating the animals with a nonselective beta-antagonist propranolol (1 mg/kg iv in 0.3 ml followed by 3 mg.kg-1.h-1 in 0.3 ml/h) not only attenuated the rise in metabolism observed after the central administration of 150 ng PGE1 but also diminished the elevation in both core and brown fat tissue temperatures as well as the increase in heart rate. Pretreating the animals with the alpha-antagonist prazosin (2 mg/kg im followed by 50 micrograms.kg-1.h-1 iv in 0.3 ml/h) somewhat reduced the rise in whole body metabolism, suppressed the elevation in core temperature, but failed to alter the rise in brown adipose tissue temperature normally seen after the central administration of PGE1. Moreover, both the rise in systolic blood pressure and heart rate were attenuated when the PGE1 administration was preceded by prazosin. These results suggest that brown adipose tissue is an important effector organ responsible for mediating the hyperthermic response observed after the intracerebral injection of PGE1. In addition, the results indicate that alterations in vasomotor tone may also be important in producing or sustaining the elevated core temperature found after a pyrogen administration.

Adipose Tissue↗
PubMed1990

The effectiveness of arginine vasopressin and sodium salicylate as antipyretics in the Brattleboro rat.

The infusion of either 30 micrograms/microliters (approx. 100 micrograms/kg/h) of sodium salicylate or 10 ng/microliters (10(-5) M) arginine vasopressin within the ventral septal area of the Brattleboro rat brain reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. Conversely, the infusion of a related peptide, oxytocin (10 ng/microliters (10(-5) M), or 33 ng/kg/h) failed to alter the rise in core temperature following the PGE1 injection. These results suggest that the vasopressin receptors reported to be present in the Brattleboro rat may respond normally to exogenously administered vasopressin, thus allowing for the antipyretic action. Moreover, the antipyretic effects of sodium salicylate suggest that aspirin-like drugs may induce the release of alpha-melanocyte-stimulating hormone which, in turn, attenuates the PGE1-evoked fever. Given recent evidence, however, which suggests that the Brattleboro rat may contain vasopressin both peripherally and within the brain, the antipyretic action of sodium salicylate may be alternatively explained through the endogenous release of vasopressin.

Alprostadil↗
PubMed1990

Cerebrospinal fluid pressure in conscious rats during prostaglandin E1 fever.

Intraperitoneal body temperature was monitored from groups of 10 conscious adult male Wistar rats. The daily body temperature rhythm was determined, and an intraperitoneal body temperature dose response relationship was established for prostaglandin E1 (PGE1) delivered into a lateral cerebral ventricle (LCV). Cerebrospinal fluid pressure was measured by direct cannulation of a LCV. Heart rate, arterial and central venous blood pressure, and blood gases were also measured in groups of 10 animals. It was found that there was a daily rhythm in intraperitoneal body temperature that was higher at night than during the day but stable between 0800 and 1600 h. A significant temperature dose (20-2,000 ng)-response relationship was established for administration of PGE1 into the LCV. Cerebrospinal fluid pressure when measured from the LCV increased significantly during the "chill" phase of the PGE1-induced fever. Carotid arterial blood pressure also significantly increased at this time as did central venous pressure, particularly so with vigorous shivering. There was a significant fall in arterial CO2 partial pressure, a slight rise in pH, and no change in arterial O2 partial pressure. These data support the hypothesis that a significant increase in cerebrospinal fluid pressure occurs during the chill phase of a PGE1-induced fever in the conscious rat.

Alprostadil↗
PubMed1989

Indomethacin-induced antipyresis in the rat: role of vasopressin receptors.

Infusion of 15 micrograms/microliters (approximately 120 micrograms/kg/h) of indomethacin within the ventral septal area of the rat brain significantly reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. A bolus injection of a V1 receptor antagonist, d(CH2)5Try(Me)AVP, (200, 2000, or 20,000 pmol) within the ventral septal area had no effect of body temperature alone but did suppress the PGE1-induced fever. Similar bolus injections of the V1 receptor antagonist within the ventral septal area failed to alter the antipyretic action of indomethacin on the hyperthermia resulting from centrally administered PGE1. Central injections of a V2 receptor antagonist failed to alter either the PGE1-induced fever or the indomethacin-evoked antipyresis. The results suggest that the V1 receptor antagonist may exert non-specific neurodepressant effects which may interfere with the expression or production of PGE1 hyperthermia and may further mask any contribution of arginine vasopressin to the antipyretic effects of indomethacin.

Angiotensin Receptor Antagonists↗