Biomedical subjects

J Kucharczyk

Publications and source records attributed to J Kucharczyk.

At least 73 records · Page 4Linked to original sources

PubMed1988

Altered drinking responses in dogs with chronic metabolic alkalosis.

Chronic chloride depletion alkalosis in dogs causes a lowered osmotic threshold and increased sensitivity for vasopressin (AVP) release. Since AVP release and drinking behavior normally are closely associated over a narrow range of changes in plasma osmolality (Posm), we investigated whether alkalotic dogs would also show an altered responsiveness to the dipsogenic effects of angiotensin II (ANG II) and osmotic stimuli. Dogs made chronically alkalotic by a combination of chloride-free diet and furosemide injections developed polydipsia in the absence of any increase in solute intake and in the presence of a significant reduction in Posm. The animals were chronically hypochloremic, hyponatremic and hypokalemic, and appeared to be extracellular fluid (ECF) contracted. Plasma renin activity (PRA) was 10-fold higher in alkalotic dogs than controls. When Posm was increased by a slow 2 hr infusion of hypertonic sodium sulfate, alkalotic dogs were found to have a significantly lower osmotic threshold for inducing drinking (289.8 +/- 1.1 mOsm/kg/H2O vs. 305.1 +/- 1.3 mOsm/kg/H2O in controls), but the slope or sensitivity of the water intake/Posm relationship was not significantly different. Finally, compared to normal animals, alkalotic dogs were unresponsive to the dipsogenic effects of IV ANG II. These data indicate that the central mechanisms which mediate drinking in response to cellular and extracellular thirst stimuli are altered in chronic metabolic alkalosis.

Alkalosis↗

PubMed1988

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs.

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8-1 g.kg-1.day-1NH4Cl over 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 +/- 0.013, 7.40 +/- 0.024, and 7.51 +/- 0.015 in normal dogs, and 7.22 +/- 0.025, 7.42 +/- 0.009, and 7.49 +/- 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 +/- 0.88, 22.0 +/- 0.80, and 32.4 +/- 1.88 mequiv. in normal dogs, and 12.3 +/- 1.30, 22.6 +/- 0.66, and 35.0 +/- 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid-base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH (r = 0.69, p less than 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid-base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid-base status.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1988

Plasma AVP and renal concentrating defect in chloride depletion metabolic alkalosis.

These studies were undertaken to determine the effect of chronic chloride depletion metabolic alkalosis (Cl-DEP-MALK) on water intake, plasma arginine vasopressin (AVP) levels, and renal concentrating ability. Cl-DEP-MALK was induced by feeding a chloride-free diet to rats subjected to gastric drainage and to dogs treated with furosemide. All of the animals developed a urine concentrating defect, polydipsia, and a persistent reduction in plasma osmolality. However, AVP release was not suppressed. The results of osmotic loading experiments in dogs analyzed using either linear or log-linear models have shown that chronic Cl-DEP-MALK significantly alters the relation between plasma osmolality and plasma AVP. In the classic linear analysis the results suggest that Cl-DEP-MALK reduces the plasma osmolality at which plasma AVP can be detected, i.e., reduced "threshold," and increases the slope of the plasma osmolality-to-plasma AVP relation nearly twofold, i.e., increased "sensitivity." Finally, we provide evidence that the concentrating defect is not related to high water turnover or deficient endogenous AVP and is therefore nephrogenic.

Alkalosis↗

PubMed1987

Central mechanisms for apomorphine-induced emesis in the dog.

In order to investigate whether different receptor populations mediate emesis induced by intracerebroventricular (i.c.v.) and intravenous (i.v.) apomorphine, adult beagle dogs were tested with various doses of the drug with and without central and peripheral pretreatment with the dopamine antagonist sulpiride. The threshold dose of apomorphine to induce emesis by i.c.v. injections was 30-50 times lower than via the i.v. route, while the response latencies after i.c.v. administration were typically longer and the number of bouts of vomiting greater. I.v. pretreatment with sulpiride was more effective than i.c.v. pretreatment in blocking emesis induced by i.v. apomorphine, whereas both i.v. and i.c.v. sulpiride effectively blocked vomiting after i.c.v. apomorphine. Finally, in separate experiments, surgical interruption of blood flow in the region of the area postrema permanently abolished the emetic response to i.c.v. apomorphine, but only transiently disrupted emesis induced by i.v. apomorphine. These data suggest the possibility that i.v. and i.c.v. apomorphine-induced emesis may be mediated by separate dopamine receptors on the cerebrospinal fluid-side and blood-side of the area postrema.

Animals↗

PubMed1987

Pressor inhibition of angiotensin-induced ACTH secretion.

We investigated whether the pressor effects of systemically administered angiotensin II (AII) influence ACTH secretion. Adrenalectomized barbiturate-anesthetized mongrel dogs with constant low resting cortisol concentrations due to slow constant cortisol infusion received either bolus injections (2.5 micrograms kg-1) or 15-min i.v. infusions of a low dose (12.5 ng kg-1min-1) of AII during which blood samples were taken for ACTH and cortisol determinations. In sequential continuous experiments in each dog, blood pressure was allowed to increase in response to AII administration or was controlled by means of concurrent i.v. injections or infusions of the hypotensive drug papaverine, or by blood withdrawal from the vena cava. When the arterial pressure rise induced by AII was substantially attenuated or prevented by papaverine administration or blood withdrawal, mean ACTH secretion rates increased 400-800% and mean ACTH concentrations increased by 280-500%. On the other hand, AII administration alone caused large increases in mean arterial blood pressure but did not increase ACTH secretion significantly above control levels. These data suggest that when endogenous AII levels are elevated without a concurrent increase in blood pressure, as occurs during hypovolemia or sodium depletion, AII may have a significant influence on ACTH secretion.

Adrenalectomy↗

PubMed1987

Posterior pituitary gland: appearance on MR images in normal and pathologic states.

T1-weighted magnetic resonance (MR) images of the pituitary gland and sella turcica routinely demonstrate a region of high signal intensity in the neurohypophysis. High-resolution MR imaging studies of the sella turcica in 200 subjects with a normal or abnormal sella were analyzed. The hyperintensity was found in the images of about 90% of healthy subjects and patients with microadenoma, in only 43% of patients with macroadenoma, and in 12% of patients with empty sellae. The signal was absent in several patients with functional or anatomic abnormalities of the hypothalamic-hypophyseal axis. It is concluded that the high signal intensity in the posterior lobe of the pituitary gland is present in most healthy individuals and that its absence in many patients with large intrasellar masses and empty sellae is due to compression of posterior lobe tissue. Its absence in diabetes insipidus further suggests a relationship between hyperintensity and the functional status of the hypothalamic-hypophyseal axis.

Adenoma↗

PubMed1986

Cerebral renin-angiotensin mediation of isoproterenol-induced thirst in the dog.

Pretreatment of dogs with s.c. isoproterenol (10 micrograms/kg) caused a significant increase in drinking when 100 ng renin substrate was administered 3 min later to the lateral cerebral ventricles or subfornical organ. Isoproterenol itself was a potent peripheral (10 micrograms/kg), but unreliable central (0.01-1 microgram) dipsogen. The increased drinking after combined s.c. isoproterenol and intracerebroventricular (i.c.v.) renin substrate injections was significantly attenuated by i.c.v. captopril (20 micrograms), but was not influenced by s.c. captopril (500 micrograms/kg). However, combined i.c.v./s.c. pretreatment with captopril nearly abolished drinking to peripheral isoproterenol, or the combination of s.c. isoproterenol and i.c.v. renin substrate. Finally, single intracranial injections of the components of the renin-angiotensin system elicited dose-dependent and site-specific drinking. Renin substrate, angiotensin I and angiotensin III produced greater intakes at forebrain tissue sites than after i.c.v. or subfornical organ injections. Renin, on the other hand, was more potent i.c.v. than at forebrain loci. These results suggest that the cerebral renin-angiotensin system may participate in beta-adrenergic thirst mechanisms by increasing local angiotensin II biosynthesis in specific areas of the brain.

Animals↗

PubMed1986

Neuroendocrine factors mediating polydipsia induced by dietary Na, Cl, and K depletion.

We investigated whether the increased intake of water during dietary electrolyte depletion is related to activation of the renin-angiotensin system. Young adult male rats were fed a low Na-, Cl-, K-free (low-salt) diet for 2 wk during which measurements were made of daily water intake and urine volume, plasma osmolality (Posm) and electrolytes, and plasma renin activity (PRA) and angiotensin I (ANG I) concentration. Water intake and urine output increased on day 3 of the low-salt diet, reached a maximum on day 4, and remained elevated, paralleling the time course of increases in PRA and ANG I plasma concentrations. Posm was normal after 2 days on the low-salt, although it was significantly lower by day 11. Renal concentrating ability was not different from controls after 6 days, but was significantly reduced after 11 days of treatment. Electrolytic lesions of the subfornical organ (SFO) abolished the low-salt diet-induced polydipsia, but had no effect on the diet-induced increases in PRA and plasma ANG I concentration. These data demonstrate that polydipsia induced by feeding a low-salt diet can develop in the presence of a normal or reduced Posm and precedes the development of a renal concentrating defect. The primary polydipsia is associated with elevated PRA and ANG I and appears to be mediated by angiotensin receptors in the SFO.

Animals↗

PubMed1985

Discrete lesions of the area postrema abolish radiation-induced emesis in the dog.

Studies carried out in several mammalian species during the 1950's led to the concept of a 'vomiting center' located in the dorsolateral reticular formation and a 'chemoreceptor trigger zone' (CTZ) within or near the area postrema (AP). This early work suggested that the AP was essential for vomiting induced by a variety of chemical emetics and by ionizing radiation. However, the lesion techniques used often produced significant damage to neural tissue underlying the AP, as well as to the AP itself, making localization of function very difficult. In the present study, electrolytic lesions confined to the AP abolished both radiation- and apomorphine-induced emesis in dogs. Thus, in addition to its postulated function in osmoreception and central cardiovascular regulation, the AP also appears to have a key role in vomiting initiated by chemical emetics and by ionizing irradiation.

Animals↗

PubMed1985

Emetic effects of centrally administered angiotensin II, arginine vasopressin and neurotensin in the dog.

Short-latency emetic responses were induced in dogs by injecting angiotensin II (AII), arginine vasopressin (AVP), and neurotensin (NTN) into cerebroventricular (ICV) and cisternal (ICT) sites also responsive to the emetic effects of apomorphine (APO). Angiotensin III, bradykinin, bombesin, oxytocin, adrenocorticotropic hormone, substance P, gastrin-related peptide and cholecystokinin were ineffective. The results suggest a possible dopaminergic mediation of peptide-induced emesis by receptors in the area postrema (AP).

Angiotensin II↗

PubMed1985

Fluid regulation and reproductive cyclicity in female rats treated neonatally with testosterone and methandrostenolone.

Female rats injected with 1 mg of testosterone propionate on day 5 after birth weighed significantly more during the immediate postpubertal period than methandrostenolone-treated (1 mg) or vehicle-injected control females. There were no differences between groups in 24-hour intakes of food or water, when expressed on a per unit body weight basis. Testosterone- and methandrostenolone-treated rats ingested less water than controls in response to acute extracellular dehydration but not after cellular dehydration. The volume of the 'sexually dimorphic nucleus' of the preoptic area was significantly greater in brains taken from the two steroid-injected groups compared to control females. Testosterone had a stronger androgenic effect than methandrostenolone in terms of disrupting the estrous cycle.

Animals↗

PubMed1984

Central angiotensin-induced water intake and salt appetite in the pig.

Single intracranial injections of the peptide analogues of angiotensin and the enzyme renin induced drinking of water and 1.8% NaCl solution in prepubertal female pigs maintained ad libitum on a sodium-free diet with unrestricted access to both fluids. Over the dose range 10(-12)-10(-9) mol angiotensin (AI), angiotensin II (AII), angiotensin III (AIII), and renin substrate (RS), the volumes of water and salt solution ingested were dose-dependent. As in other vertebrates, AII was the most potent and rapidly acting dipsogen. However, unlike in the rat, dog and pigeon, AIII was highly effective in stimulating both water intake and salt appetite, whereas AI and RS were relatively weak. Pretreatment of intracranial sites with 10(-9) mol of the AII competitive antagonist, Sar1-Ala8-angiotensin, had no effect on the volume of water or 1.8% NaCl ingested after 10(-10) mol AIII, suggesting that in the pig AIII can exert its dipsogenic effects without acting on central AII receptors. Single microinjections of 1 and 10 mU of renin also elicited dose-dependent drinking of water and 1.8% NaCl, but compared with the peptide analogues of angiotensin the responses had a longer latency and duration and were more variable between individual animals.

Angiotensins↗

PubMed1984

Neuroendocrine mechanisms mediating fluid intake during the estrous cycle.

Gonadal steroids appear to influence fluid-electrolyte homeostasis through behavioral as well as renal mechanisms. The marked fluctuations in drinking behavior observed during the estrous cycle of the female rat may be due to an interaction between estrogen and the dipsogenic peptide hormone, angiotensin II, at the level of basal forebrain receptors. The preoptic region in particular may play an important integrative role in the maintenance of extracellular fluid balance in synchrony with the estrous cycle, since it contains receptors for angiotensin and estrogen. Prolactin may also directly participate in mechanisms of extracellular thirst, while an exact role for vasopressin has yet to be established. Recent studies also suggest that estrogens may influence body fluid regulation by interacting with several neurotransmitters, including serotonin, dopamine and noradrenaline.

Angiotensin II↗

PubMed1984

Localization of central nervous system structures mediating extracellular thirst in the female rat.

Water intake elicited by microinjection of the hormone angiotensin-II into the preoptic region of cyclic female rats was significantly less on days of vaginal oestrus than at dioestrus or metoestrus, whereas the drinking of 2.7% NaCl solution, to which rats also had access, did not vary with the cycle. Administration of the same dose of angiotensin-II to the subfornical organ and the lateral cerebral ventricles induced drinking at all stages of the oestrous cycle, but the volumes of water or 2.7% NaCl ingested did not vary with the cycle. Water intake after subcutaneous injection of isoprenaline, a beta-adrenergic agonist which causes increased angiotensin biosynthesis, varied cyclically with the stage of the oestrous cycle. On the other hand, water and 2.7% NaCl intakes induced by intraperitoneal injection of hypertonic NaCl (a cellular stimulus of thirst) or by 24-h water deprivation (which dehydrates both the extracellular and cellular body fluid compartments) did not differ significantly at the various stages of the oestrous cycle. The finding that fluctuations in angiotensin- and isoprenaline-induced water intake parallel the changes in spontaneous 24-h drinking suggests that the preoptic region may play an important role in the maintenance of extracellular fluid balance in synchrony with the oestrous cycle.

Angiotensin II↗

PubMed1983

Drinking behavior following electrical stimulation of the subfornical organ in the rat.

Electrical stimulation of the subfornical organ (SFO) through implanted stainless-steel electrodes produced drinking in water-sated rats. Drinking was elicited primarily during the interstimulation (OFF) periods. Water intake in rats with hippocampal electrode placements occurred during both ON and OFF periods at current intensities (24-100 microA) similar to rats with SFO placements. These findings support the hypothesis that the SFO is involved in the central control of fluid balance.

Animals↗

PubMed1983

Solar activity and myocardial infarction.

The correlation between the incidence of myocardial infarction, sudden cardiac death, the solar activity and geomagnetism in the period 1969-1976 was studied, basing on Wrocław hospitals material registered according to WHO standards; sudden death was assumed when a person died within 24 hours after the onset of the disease. The highest number of infarctions and sudden deaths was detected for 1975, which coincided with the lowest solar activity, and the lowest one for the years 1969-1970 coinciding with the highest solar activity. Such an inverse, statistically significant correlation was not found to exist between the studied biological phenomena and geomagnetism.

Adult↗

PubMed1979

Dependence of spontaneous and angiotensin-induced drinking in the rat upon the oestrous cycle and ovarian hormones.

The influence of the oestrous cycle on spontaneous and dipsogen-induced drinking was studied in female rats. Spontaneous fluid intake was lowest on the day of oestrus. Drinking induced by subcutaneous isoprenaline, and by angiotensin II (injected into the preoptic area), also showed marked cyclical variation, being lower at pro-oestrus and oestrus than at other stages of the cycle. Drinking induced by subcutaneous hypertonic NaCl or by intracranial carbachol did not vary with the oestrous cycle. Cyclicity of spontaneous and of angiotensin-induced water intake was not apparent in rats before puberty or after ovariectomy. Ovariectomy reduced drinking in response to isoprenaline. Treatment with oestradiol benzoate (20 micrograms) caused a reduction in spontaneous water intake, but a marked increase in the drinking response to isoprenaline. Treatment with oestradiol benzoate and progesterone (2.5 mg) caused a larger decrease in spontaneous water intake and an insignificant increase in isoprenaline-induced drinking. Water intake induced by subcutaneous hypertonic saline was unaffected by gonadal steroids. The results provide further evidence for the view that the thirst of extracellular origin, in which the renin-angiotensin system is involved, is brought about by mechanisms different from those that respond to cellular dehydration. Only drinking caused by activation of extracellular mechanisms appeared to be sensitive to the ovarian cycle and to ovarian hormones.

Angiotensin II↗

PubMed1978

Autoradiographic evidence for pathways from the medial preoptic area to the midbrain involved in the drinking response to angiotensin II.

The 3H-amino acid autoradiographic method was used to localize intracerebral sites from which angiotensin II (AII) elicits drinking and to identify their efferent neural pathways. Small injections (0.02-0.1 mul) of AII and 3H-amino acid mixtures were injected together or separately into widespread regions of the forebrain of adult rats in normal food and water balance. From an analysis of 39 positive and negative injection sites it was concluded that the caudal half of the medial preoptic area and the adjacent rostral part of the anterior hypothalamic area are sensitive to AII. Two anatomically defined pathways arising from neurons within this region were identified. One descends through the medial forebrain bundle and appears to terminate in the lateral hypothalamic area, the ventromedial nucleus, the mammillary body, and the ventral tegmental area. The other descends through the periventricular region and posterior hypothalamic area to end in the midbrain central gray. Additional widespread connections with the amygdala, septum, habenula, and pons appear to arise in the lateral preoptic area (Swanson, '76). Combined AII-3H-amino acid injections centered in the subfornical organ only elicited drinking in those cases in which injected label diffuse through the third ventricle to the medial preoptic area. No efferent pathways were identified in experiments in which a small injection (0.02 mul) heavily labeled cells strictly confined to the subfornical organ and there was no ventricular spread of label.

Angiotensin II↗