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Biomedical subjects

K E Cooper

Publications and source records attributed to K E Cooper.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1989

Sodium salicylate: alternate mechanism of central antipyretic action in the rat.

Infusion of sodium salicylate (50.0 or 100.0 micrograms/microliters) into the ventral septal area (VSA) of the rat brain suppressed Prostaglandin-E1-induced hyperthermia. Infusion of artificial cerebrospinal fluid (aCSF) or 10.0 micrograms doses of salicylate did not. The suppression of intracerebroventricularly-induced (icv) Prostaglandin E1 (PGE1) hyperthermia was not due to a hypothermic action of salicylate since salicylate infusions given during cold exposure (10.0 degrees C) did not lower core body temperatures. A possible interaction between salicylate and endogenous arginine vasopressin (AVP) was investigated. Infusion of both salicylate (50.0 micrograms/microliters) and either AVP antiserum or AVP antagonist into the VSA resulted in PGE hyperthermias occurring at levels which were not different from control levels as opposed to enhanced hyperthermia (antiserum or antagonist alone) or suppressed hyperthermia (salicylate alone). These results are consistent with the notion that sodium salicylate infusions within the VSA enhance AVP action and thus bring about the attenuation of PGE-induced hyperthermia.

Alprostadil↗
PubMed1989

Potassium channels in chick lens epithelium change with maturation.

Before hatching, chick embryos show a high incidence of inwardly rectifying potassium channels and calcium-activated potassium channels in the apical membrane of their lens epithelium. Subsequent to hatching, these channel types disappear while, at about the same time, a new calcium insensitive maxi potassium channel appears. This new channel shows several properties in common with the calcium-activated maxi potassium channels but is different in its conductive and gating properties.

Analog-Digital Conversion↗
PubMed1988

Changes in body temperature and vasopressin content of brain neurons, in pregnant and non-pregnant guinea pigs, during fevers produced by Poly I:Poly C.

The synthetic polyribonucleotide pyrogen Poly I:Poly C (800 micrograms.kg-1) was injected intramuscularly on alternate days into pregnant and non-pregnant female guinea pigs. Pregnant animals, close to term, had smaller fevers in response to the pyrogen than did non-pregnant animals. Repeated injections of the pyrogen caused sequentially smaller fevers for the first 3-4 injections, particularly in non-pregnant animals, and this appeared to be like the tolerance usually developed to repeated injections of endotoxin. Continued pyrogen injections then caused, in non-pregnant animals, fevers of increasing magnitude until the original fever levels were reached, whereas in pregnant guinea pigs the fever responses remained reduced until parturition. The development of tolerance was associated with an increase in immunoreactivity for arginine vasopressin (AVP) in some neurons in the medial part of the paraventricular nucleus, and in terminals in the lateral septum and amygdala similar to changes found in these areas at term of pregnancy. These observations raise the possibility that AVP in these regions may have a role in the development of tolerance to pyrogens, and further quantitative studies of the AVP content of, and release from, nerve terminals projecting to the limbic system seem warranted.

Animals↗
PubMed1988

Acute changes in forearm venous volume and tone using radionuclide plethysmography.

In this investigation blood pool scintigraphy was validated as a method to study acute changes in human forearm veins. Changes in regional forearm vascular volume (capacity) and the occluding pressure-volume (P-V) relationship induced by sublingual nifedipine (NIF) and nitroglycerin (GTN) were recorded in 16 patients with simultaneous data collection by the radionuclide and the mercury-in-rubber strain-gauge techniques. The standard error of estimate (Syx) between successive control measurements using the radionuclide method was 3.1% compared with 3.2% for the strain-gauge method. The venous P-V curves were highly reproducible using both techniques. Strain gauge and radionuclide measurements of acute changes in forearm venous volume correlated well (r = 0.86; Syx = 7%, n = 156). After 20 mg of NIF or 0.6 mg of GTN, mean heart rate increased from 71 +/- 10 to 77 +/- 9 and from 68 +/- 10 to 75 +/- 11 beats/min, respectively, and group systolic blood pressure decreased from 128 +/- 22 to 120 +/- 19 and from 136 +/- 18 to 126 +/- 23 mmHg, respectively (P less than 0.05). At venous occluding pressures of 0 and 30 mmHg, the forearm vascular volume did not change after NIF (2 +/- 4 and -1 +/- 4%; P greater than 0.05), whereas it increased after GTN (8 +/- 5 and 12 +/- 7%; P less than 0.001). The forearm venous P-V relationship did not change after NIF, whereas a significant rightward shift (venodilation, with an increase in unstressed volume) occurred after GTN.(ABSTRACT TRUNCATED AT 250 WORDS)

Forearm↗
PubMed1988

Physiological changes during thermoregulation and fever in urethan-anesthetized rats.

Adult male Wistar rats were anesthetized with urethan (1.5 g/kg). They were unable to maintain body temperature (Tb) in a warm (32 degrees C) or cool (9 degrees C) environment or at a laboratory room temperature of 22 degrees C. Tb was allowed to fall to 35.8, 34.5, or 33.3 degrees C, and prostaglandin E1 (PGE1, 400 ng) was delivered into a lateral cerebral ventricle. An immediate feverlike rise in Tb resulted, accompanied by vigorous shivering. Animals were vasoconstricted throughout. When Tb was raised to and maintained at 38.3 or 39.5 degrees C, animals also responded with a fever; however, the magnitude of the fever diminished as the starting Tb increased. In a series of experiments in which Tb was maintained (36.8-37.4 degrees C) by means of a heating pad, PGE1 delivered into a lateral cerebral ventricle or into the anterior hypothalamus caused a dose-dependent change in Tb, which was similar in time of onset, magnitude, and duration to that observed in conscious animals. This fever was accompanied by shivering and increased O2 uptake, heart rate, arterial blood pressure, respiratory rate, and intracranial pressure during the rising phase of the fever, and vasodilation of the paws occurred during defeveresence. Animals were also able to develop a dose-dependent rise in Tb in response to purified human interleukin 1.

Alprostadil↗
PubMed1987

The effect of venous blood stream cooling on survival of bacterially infected rabbits.

The effect of physical cooling on the mortality rate of rabbits infected with Pasteurella multocida was investigated. Rabbits were cooled for 48 hours after bacterial injection by passing cold fluid through small hollow metal cuffs which had been surgically implanted around the abdominal vena cavae of rabbits. The average body temperatures of the rabbits during the 24-hour period after the intravenous injection of live Pasteurella multocida was 40.92 +/- 0.20 degrees C in control rabbits and 38.98 +/- 0.71 degrees C in cooled rabbits. 90% of physically cooled rabbits survived compared with 46% of control rabbits 48 hours after bacterial injection, suggesting that thermoregulatory effector mechanisms involved in cold defense may enhance survival.

Animals↗
PubMed1987

Blockade of prostaglandin E1 hyperthermia by sodium salicylate given into the ventral septal area of the rat brain.

1. Sodium salicylate (30.0 micrograms microliter-1) or artificial cerebrospinal fluid (ACSF) was infused bilaterally into the ventral septal area (v.s.a.) of the unrestrained rat for 1 h before and 1 h after the injection of prostaglandin E1 at a concentration of 20.0 ng microliter-1 into a lateral cerebral ventricle. 2. During control (ACSF) infusions, 200.0 ng of prostaglandin E1 evoked a hyperthermic response (0.95 +/- 0.16 degrees C). During sodium salicylate infusions, the prostaglandin E1-evoked hyperthermia was significantly reduced (P less than 0.025) to 0.31 +/- 0.16 degrees C. 3. The fever index (degrees C h for 1.0 h) during the infusion of sodium salicylate was reduced 66% below that of control infusions (P less than 0.01). 4. These data indicate that sodium salicylate infused in the v.s.a. of rats can antagonize a prostaglandin E-evoked hyperthermia. This suggests that there may be an additional mechanism of action for sodium salicylate antipyresis other than inhibition of prostaglandin E synthesis.

Alprostadil↗
PubMed1987

Evidence supporting a role for endogenous vasopressin in fever suppression in the rat.

1. Infusion of human purified interleukin-1 into a lateral cerebral ventricle of the rat evoked a rise in core temperature which was abolished by heating the interleukin-1. 2. When the intracerebroventricular infusion of interleukin-1 was preceded by a bilateral injection of saline into the ventral septal area, the resulting febrile response was not different from that induced by interleukin-1 alone. However, when the vasopressin V1 antagonist, d(CH2)5Tyr(Me)AVP, was injected into the ventral septal area prior to interleukin-1, a fever was evoked which was significantly greater in magnitude and duration. This enhancement of fever by the V1 antagonist was dose related. 3. Injection of either saline or the V1 antagonist into the ventral septal area, in the absence of interleukin-1, did not evoke any consistent alteration in the core temperature of the rats. 4. The vasopressin V2 antagonist, d(CH2)5-D-ValVAVP, was injected into the ventral septal area to determine the effect of another vasopressin analogue on the fever evoked by interleukin-1. The V2 antagonist did not alter the time course of interleukin-1-induced fever or alter core temperature in the afebrile rat. 5. These data are consistent with the hypothesis that endogenous vasopressin, released in the ventral septal area, may be involved in limiting fever. In addition, these results indicate that the central receptor mediating the antipyretic action of vasopressin may resemble the V1 subtype of peripheral vasopressin receptor.

Animals↗
PubMed1987

Vasopressin and fever: evidence supporting the existence of an endogenous antipyretic system in the brain.

Vasopressin administered into the ventral septum exerts a dose-related antipyresis. This site of action is similar in a number of species. The fever-reducing properties of vasopressin are both site and neuropeptide specific. Evidence supporting a role for endogenous vasopressin in fever suppression is the demonstration that the release of the peptide from the ventral septal area is altered during fever: the amount released correlates negatively with febrile changes in body temperature. In addition, changes in the concentration of vasopressin in the septum and amygdala have been demonstrated immunocytochemically during fever: an activation of vasopressinergic neurons occurs which is similar to that observed in pregnant animals at term when fever is absent. Specific antibodies directed against vasopressin or specific vasopressin antagonist analogues (e.g., d(CH2)5Tyr(Me)AVP) enhanced the febrile response to a pyrogen challenge when injected into the ventral septum. The same antagonist also can antagonize the antipyretic effect of exogenously administered vasopressin. The use of relatively specific antagonists and agonists of vasopressin, directed against the V1 and V2 subtypes of the peripheral vasopressin receptor, suggests that the central receptor responsible for the antipyretic effect of vasopressin may resemble the V1 subtype. Recent experiments using electrophysiological techniques have demonstrated the existence of thermoresponsive units in the ventral septal area whose activity may be altered by vasopressin which is possibly derived from the paraventricular nucleus and bed nucleus of the stria terminalis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

A cation channel in frog lens epithelia responsive to pressure and calcium.

Patch-clamp recording from the apical surface of the epithelium of frog lens reveals a cation-selective channel after pressure (about +/- 30 mm Hg) is applied to the pipette. The open state of this channel has a conductance of some 50 pS near the resting potential (-56.1 +/- 2.3 mV) when 107 mM NaCl and 10 HEPES (pH 7.3) is outside the channel. The probability of the channel being open depends strongly on pressure but the current-voltage relation of the open state does not. With minimal Ca2+ (55 +/- 2 microM) outside the channel, the current-voltage relation is nonlinear even in symmetrical salt solutions, allowing more current to flow into the cell than out. The channel, in minimal Ca2+ solution, is selective among the monovalent cations in the following sequence K+ greater than Rb+ greater than Cs+ greater than Na+ greater than Li+. The conductance depends monotonically on the mole fraction of K+ when the other ion present is Li+ or Na+. The single-channel current is a saturating function of [K+] when K+ is the permeant ion, for [K+] less than or equal to 214 mM. When [Ca2+] = 2 mM, the current-voltage relation is linearized and the channel cannot distinguish Na+ and K+.

Animals↗
PubMed1985

Neurotransmitter effects on body temperature are modified with increasing age.

This study reports effects on body temperature, in two different age groups of Sprague Dawley rats, of intracerebroventricular (ICV) administration of prostaglandin E2, noradrenaline, serotonin, dopamine, and carbachol. Young animals (3-5 months) developed fevers in response to administration of prostaglandin E2 (+ 1.02 +/- 0.26 degrees C), while no significant changes in colonic temperature were observed in the older (15-18 months) group of rats. Noradrenaline (10.0 micrograms), caused a decrease in colonic temperature in the younger group of animals (-2.02 +/- 0.70 degrees C), but had no significant effects on the body temperature of the older group. Similarly, differences between the temperature responses of the young as compared with the older group of animals were observed following ICV administration of carbachol, dopamine and serotonin. These data suggest that the roles of these substances in the hypothalamic control of body temperature may be modified with increasing age.

Aging↗
PubMed1985

Fever and intracranial pressures.

The effect of fever upon intracranial pressures was determined in the rabbit and cat. In the unanesthetized rabbit and cat, cerebrospinal fluid (CSF) pressure was measured via direct cannulation of the lateral cerebral ventricle. Intracranial pressure (ICP) was measured in the rabbit by a subarachnoid screw technique. In all cases, intravenous administration of bacterial pyrogen extracted from Salmonella abortus equi resulted in significant differences from controls in physiological variables measured during the initial "chill" phase of the fever. There was an increase in body temperature, a fall in CSF or ICP pulse rate, an increase in pulse pressure amplitude, and a small increase in mean CSF or ICP. In addition, venous and arterial blood pressures increased significantly and, consistent with heat conservation, there was a fall in respiratory rate as well as cutaneous vasoconstriction in the ears. The arterial carbon dioxide tension was unchanged during the prodrome but fell significantly during the chill and flush phases and rose again during defervescence. The results suggest that in these animals there is a slight increase in pressures within the cranium during the "chill" phase of a pyrogen induced fever, resulting from changes occurring in many body systems during this phase of the fever.

Animals↗
PubMed1985

Induced changes in intracranial pressure in the anesthetized rat and rabbit.

Intracranial pressure (ICP) was measured continuously in anesthetized, free-breathing, adult, male Sprague-Dawley rats and New Zealand White rabbits by means of a subarachnoid screw technique. The effect upon ICP of changing the volumes within the cranium by infusion of artificial cerebrospinal fluid into the lateral cerebral ventricle at various rates was examined. Results obtained demonstrated some of the elastic and compensatory aspects of cerebrospinal fluid dynamics. The effects upon ICP of the intravenous administration of urea, mannitol, acetazolamide, dimethyl sulfoxide, norepinephrine, epinephrine, isoproterenol, nitroglycerin, papaverine, histamine, angiotension II, pitressin, sodium nitroprusside, diazoxide, lidocaine, sodium pentobarbitone, as well as inhalation of amyl nitrate and carbon dioxide were examined in anesthetized rats. The effect upon ICP of the intravenous infusion of urea, as well as the bolus intravenous administration of epinephrine and pitressin was examined in the anesthetized rabbit. Results obtained from these animals demonstrate the action of these experimental interventions upon ICP as measured by means of the subarachnoid screw technique.

Anesthetics↗
PubMed1985

Peripheral blood flow during rewarming from mild hypothermia in humans.

During the initial stages of rewarming from hypothermia, there is a continued cooling of the core, or after-drop in temperature, that has been attributed to the return of cold blood due to peripheral vasodilatation, thus causing a further decrease of deep body temperature. To examine this possibility more carefully, subjects were immersed in cold water (17 degrees C), and then rewarmed from a mildly hypothermic state in a warm bath (40 degrees C). Measurements of hand blood flow were made by calorimetry and of forearm, calf, and foot blood flows by straingauge venous occlusion plethysmography at rest (Ta = 22 degrees C) and during rewarming. There was a small increase in skin blood flow during the falling phase of core temperature upon rewarming in the warm bath, but none in foot blood flow upon rewarming at room air, suggesting that skin blood flow seems to contribute to the after-drop, but only minimally. Limb blood flow changes during this phase suggest that a small muscle blood flow could also have contributed to the after-drop. It was concluded that the after-drop of core temperature during rewarming from mild hypothermia does not result from a large vasodilatation in the superficial parts of the periphery, as postulated. The possible contribution of mechanisms of heat conduction, heat convection, and cessation of shivering thermogenesis were discussed.

Adult↗