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Biomedical subjects

G Feuerstein

Publications and source records attributed to G Feuerstein.

At least 235 records · Page 13Linked to original sources
PubMed1982

Delta versus mu receptors: cardiovascular and respiratory effects of opiate agonists microinjected into nucleus tractus solitarius of cats.

The cardiovascular and respiratory responses to relatively specific mu or delta agonists microinjected (0.5 microliter/kg) into the region of the nucleus of tractus solitarius (NTS) were examined in anesthetized cats. Blood pressure, heart rate, and respiratory rate were monitored for 30 min after the microinjection of opioid compounds or saline vehicle. The delta agonist, (D-Ala2,D-Leu5)-enkephalin (10-100 nmol/kg) elicited dose-dependent decreases in blood pressure, heart rate, and respiratory rate which were naloxone reversible. In contrast the mu agonists, morphine (10-54 nmol/kg) and morphiceptin (100-320 nmol/kg) had no effect on blood pressure or respiratory rate; yet, naloxone elicited pressor responses in animals pretreated with these mu agonists. A receptor-binding assay demonstrated a predominance of mu sites in the NTS. These data show that the delta opiate agonist is more effective than mu agonists in modifying cardiovascular variables in the NTS; we suggest caution in relating specific cardiovascular function to receptor subtypes defined by binding assays.

Animals↗
PubMed1982

Mechanisms involved in central cardiovascular effects of prostaglandin F2 alpha.

Prostaglandin F2 alpha (PGF2 alpha) injected into the cerebroventricular system (icv) of halothane-anesthetized rats increased the arterial blood pressure, heart rate, and rectal temperature. These effects were accompanied by a preferential increase in plasma norepinephrine concentration. Plasma levels of epinephrine, renin, and vasopressin were not changed in the PGF2 alpha-icv-treated rats. Bilateral vagotomy did not affect the PGF2 alpha-induced hypertension and tachycardia nor was there any change in the selective increase in plasma norepinephrine concentration. Hexamethonium pretreatment suppressed, in a dose-response manner, the increases in blood pressure, heart rate, and rectal temperature in response to PGF2 alpha-icv. Plasma norepinephrine and epinephrine levels were not altered by PGF2 alpha-icv in hexamethonium-treated rats, but plasma vasopressin concentration was markedly elevated in all hexamethonium-infused rats. These results suggest that selective central activation of the sympathetic nervous system underlies the profound cardiovascular and temperature responses elicited by central administration of PGF2 alpha.

Animals↗
PubMed1982

Cardiovascular, sympathetic, and renin-angiotensin system responses to hemorrhage in vasopressin-deficient rats.

To determine if the subnormal blood pressure recovery after hemorrhage in Brattleboro rats is due to secondary abnormalities in the renin-angiotensin or sympathetic nervous systems, we measured the hemodynamic, catecholamine, and renin activity responses to moderate acute hemorrhage in anesthetized Brattleboro rats. Results were compared to responses in groups of animals matched for either age or weight. Blood pressure recovery was significantly blunted (P less than 0.01) in Brattleboro rats compared to that in either control group, but heart rate responses were similar. Basal plasma norepinephrine was significantly higher in Brattleboro rats than in controls (P less than 0.001), but the response to hemorrhage was not significantly different. Both plasma epinephrine levels and renin activity were significantly higher before hemorrhage and increased more after hemorrhage in vasopressin-deficient animals. Plasma vasopressin in controls increased approximately 10-fold, reaching levels of 790 +/- 140 pg/ml in age-matched controls and 425 +/- 60 pg/ml in weight-matched controls. Vasopressin levels in Brattleboro rats were undetectable both before and after hemorrhage. We conclude from these data that the subnormal blood pressure recovery observed in vasopressin-deficient rats is not due to secondary abnormalities of the renin-angiotensin or sympathetic nervous systems, but, instead, is related more directly to the vasopressin deficiency.

Animals↗
PubMed1982

Cardiovascular and sympathetic effects of l-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine in conscious SHR and WKY rats.

Injections of 1-)-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (alkylacetyl-GPC, 0.2-5.0 nmol/300 g body weight) induced dose-related hypotension and tachycardia in spontaneous hypertensive (SHR) and normotensive control (WKY) rats. The hypotension that developed was more pronounced in SHR than in WKY rats and was unchanged by indomethacin pretreatment. Plasma norepinephrine (NE) and epinephrine (EPI) levels were markedly increased at the time of maximal hypotension (2 min after injection of alkylacetyl-GPC); plasma EPI (but not NE) was higher in the SHR than in WKY animals. Plasma levels of TXB2, but not 6-keto-PGF 1 alpha, increased in both groups; the increase was more pronounced in SHR than in WKY rats. In pithed SHR rats, alkylacetyl-GPC caused only short lasting hypotension without any effect on heart rate or circulating levels of NE or EPI. These data suggest that there is an increased vascular sensitivity to alkylacetyl-GPC in SHR rats and activation of thromboxane-generating elements in both SHR and WKY rats.

Animals↗
PubMed1982

Leukotriene D4: cardiovascular and sympathetic effects in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats.

Leukotriene D4 (1--20 micrograms/kg i.a.) administered to conscious spontaneously hypertensive rats (SHR) and WKY rats caused acute elevation of blood pressure in both groups, but only in SHR a prolonged hypotensive period followed the hypertensive event. SHR rats had tachycardia during the hypertensive phase and relative bradycardia during the hypotensive phase which was more pronounced and prolonged than in WKY rats. In SHR rats only, plasma epinephrine and norepinephrine were elevated (6- and 3-fold, respectively) at the peak of the hypertensive period. Pretreatment of SHR rats with indomethacin (5 mg/kg) potentiated the LTD4-induced pressor response and shortened the hypotensive-bradycardic effect of LTD4. This same biphasic, dose-dependent response to LTD4 (1--20 micrograms/kg i.v.) was present in pithed SHR rats. Therefore, a direct action of LTD4 on vascular smooth muscle and heart is suggested. In all WKY rats and some SHR rats, a bradycardic effect of LTD4 resulted from sinus bradycardia, whereas in pithed SHR rats impaired conduction varying from transient second degree atrioventricular block to complete heart block was observed. Electrocardiographic signs of ischemia were seen only in LTD4-injected, pithed SHR rats. These results suggest fundamental differences between SHR and WKY rats in regard to their sensitivity to lipoxygenase products.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Cardiovascular effects of leukotriene D4 in SHR and WKY rats.

Leukotriene D4 (LTD4, 0.8-4 micrograms/kg i.a.) increased blood pressure and heart rate of conscious SHR and WKY rats. LTD4, 20 micrograms/kg (i.a.), caused a short lasting increase in blood pressure and heart rate in WKY. In SHR, LTD4, 20 micrograms/kg (i.a.) caused a triphasic effect: hypotension and bradycardia (0.5-1 min), hypertension and tachycardia (2-5 min) and prolonged hypotension and bradycardia (5-180 min). Leukopenia was observed after LTD4, 20 micrograms/kg in both groups of rats but platelets count was unaffected. These results show that SHR are mor sensitive than WKY to the hypotension-bradycardia effect of LTD4.

Animals↗
PubMed1981

Dopamine partially mediates the cardiovascular effects of naloxone after spinal injury.

Following spinal injury, the opiate antagonist naloxone selectively elevates plasma dopamine levels, with the dopamine changes significantly correlated with improved cardiovascular function. Moreover, the cardiovascular effects of naloxone are significantly attenuated by pretreatment with the dopamine antagonist domperidone. From these data, it is concluded that the cardiovascular effects of naloxone after spinal injury are in part dopamine mediated.

Animals↗
PubMed1981

Effect of PGD2, PGE2 PGF2 alpha and PGI on blood pressure, heart rate and plasma catecholamine responses to spinal cord stimulation in the rat.

The following experiments were designed in order to examine the inter-relationships of various prostaglandins (PG's) and the adrenergic nervous system, in conjunction with blood pressure and heart rate responses, in vivo. Stimulation of the entire spinal cord (50v, 0.3-3 Hz, 1.0 msec) of the pithed rat increased blood pressure, heart rate and plasma epinephrine (EPI) and norepinephrine (NE) concentration (radioenzymatic-thin layer chromatographic assay). Infusion of PGE2 (10-30 microgram/kg. min, i.v.) suppressed blood pressure and heart rate responses to spinal cord stimulation while plasma EPI (but not NE) was augmented over levels found in control animals. PGI2 (0.03-3.0 microgram/kg. min, i.v.) suppressed the blood pressure response to spinal cord stimulation without any effect on heart rate or the plasma catecholamine levels, PGE2 and PGF2 alpha (10-30 microgram/kg. min, i.v.) did not change the blood pressure, heart rate or plasma EPI and Ne responses to the spinal cord stimulation although PGF2 alpha disclosed an overall vasopressor effect during the pre-stimulation period. At the pre-stimulation period it was also observed that PGE2, PGF2 alpha and PGI2, had a positive chronotropic effect on the heart rate, the cardiac accelerating effect of PGE2 was not abolished by propranolol. These in vivo studies suggest that in the rat, PGE2 and PGI2 modulate sympathetic responses, primarily by interaction with the post-synaptic elements - PGE2 on both blood vessels and the heart and PGI2 by acting principally on blood vessels.

Animals↗
PubMed1981

Catecholamines and vasopressin in forebrain nuclei of hypertension prone and resistant rats.

Catecholamine and vasopressin content were studied in discrete brain nuclei of the Sabra strain of hypertension prone (SBH) and resistant (SBN) rats. Higher concentrations of dopamine, norepinephrine and epinephrine were observed in the median eminence of SBN compared to SBH or controls (SB) rats. Dopamine and epinephrine levels were higher in the lateral septal nucleus of SBH rats as compared to SBN or SB. Vasopressin content in discrete regions along the hypothalamo-pituitary axis was elevated in both SBH and SBN as compared to SB, but were especially elevated in the SBH group. The catecholamine and vasopressin changes found in SBH are different than those described in other genetically hypertensive rats indicating a difference in either the pathogenesis or central response to hypertension of this strain.

Animals↗
PubMed1981

Cardiovascular and sympathetic responses to PGF2 alpha injection into hypothalamic nuclei.

Injection of prostaglandin F2 alpha (1 nmol/rat) into the paraventricular, dorsomedial and posterior hypothalamic nuclei of halothane anesthetized rats elicited rapid increases of heart rate and blood pressure. The injection of this same dose of prostaglandin F2 alpha into the cerebroventricular system or intravenously had no effect on these parameters. The cardiovascular responses observed following prostaglandin F2 alpha injection into these hypothalamic nuclei were accompanied by increases in plasma levels of norepinephrine and epinephrine, with peak levels at the maximal cardiovascular response. This study suggests a possible role for prostaglandin F2 alpha in modulation of the cardiovascular system via specific hypothalamic nuclei.

Animals↗
PubMed1981

Effect of indomethacin on the blood pressure and plasma catecholamine responses to acute endotoxaemia.

Injection of E. coli endotoxin (7 mg kg-1 i.v.) to pentobarbitone anaesthetized cats resulted in prolonged decrease of systemic blood pressure and increases in plasma concentrations of adrenaline, noradrenaline and 6-ketoprostaglandin (PG) F 1 alpha. Indomethacin pretreatment (10 mg kg-1 i.v.) attenuated the decrease in blood pressure following endotoxin injection. Plasma adrenaline, noradrenaline and 6-keto-PG F1 alpha were significantly lower in the indomethacin-treated cats. These data indicate that the superior haemodynamic status of the indomethacin pretreated animals exposed to endotoxic shock is not the result of potentiation of the peripheral sympathetic response.

Animals↗
PubMed1981

Prostaglandins, catecholamines, and cardiovascular responses to hemorrhage.

The effects of prostaglandins (PGE2 and 16,16-dimethyl-PGE1) on epinephrine (E) and norepinephrine (NE) release, in response to a hypotensive stimulus (bleeding 5 ml/300 g), were studied in relation to blood pressure and heart rate responses in the rat. PGE2 (10 micrograms/kg-1 . min-1) and 16,16-dimethyl-PGE1 (1 microgram . kg-1 . min-1) accelerated blood pressure and heart rate recovery rate following acute hemorrhage and increased plasma E and NE levels. Plasma levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) were not affected by PG infusion. In bilaterally nephrectomized rats, PGE2 increased plasma levels of E, NE, and DHPG but failed to enhance the blood pressure and had only a mild effect on heart rate recovery following bleeding. In hexamethonium-treated rats, infusion of PGE2 had a small and transient effect on blood pressure recovery, but its effect on the heart rate was not affected; NE and E levels in the plasma of the hexamethonium-treated rats were still higher in the PGE2-infused rats. These studies indicate that in the intact rat, administered PGE potentiate the release of E and NE and facilitate blood pressure and heart rate recovery following acute hemorrhage. The hemodynamic effects of the PGE appear to be mediated by a renal factor whereas the effects of PGE on E and NE response to hemorrhage are independent of the presence of intact kidneys.

Animals↗
PubMed1981

Attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride in rats.

The effect of amiloride on lithium-induced polydipsia and polyuria and on the lithium concentration in the plasma, brain, kidney, thyroid and red blood cells was investigated in rats, chronically treated with LiCl. Amiloride reduced the drinking and urine volume of rats in an acute (6 or 12 h) and a subacute (3 days) experiment. 6 h after the administration of amiloride, a reduction was observed in the lithium content of the renal medulla but not in the other organs studied. At 12 h, all the tissues showed a slight increase in lithium levels. After 3 days of combined treatment, a marked elevation in plasma and tissue lithium levels accompanied a reduction in water intake. In all the experiments, the attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride was accompanied by a reduction of the ratio between the lithium concentration in the renal medulla and its levels in the blood and an elevation in the plasma potassium level. It is concluded that acute amiloride administration to lithium-treated patients suffering from polydipsia and polyuria might relieve these patients but prolonged amiloride supplementation would result in elevated lithium levels and might be hazardous.

Amiloride↗
PubMed1981

Prostacyclin reversal of lethal endotoxemia in dogs.

Severe endotoxemia, a condition where microembolization and intravascular coagulation are thought to play important roles, was treated experimentally with prostacyclin (PGI(2)). In a study of 24 dogs, 8 control animals injected with 1.75 mg.kg(-1) of endotoxin died within 24 h. Six animals given intravenous aspirin 100 mg/kg, 30 min after endotoxin died. 9 of 10 dogs infused with 100 ng PGI(2).kg(-1).min(-1) for 3 h, given 30 min after the injection of endotoxin survived 24 h (P < 0.025). Injection of endotoxin resulted in a: (a) maximal 62% fall in mean arterial pressure (P < 0.001); (b) transient doubling of mean pulmonary arterial pressure (P < 0.001); (c) initial 70% drop in cardiac index (P < 0.001); (d) decline in blood platelets from 213,700 to 13,700/mm(3) (P < 0.001), and leukocytes from 7,719 to < 750/mm(3) (P < 0.001); (e) depressed urine output (P < 0.001); (f) 34% decrease in blood fibrinogen (P < 0.01) and an increase in fibrin degradation products > 50 mug/ml (P < 0.001); (g) fivefold increase in circulating cathepsin D titer (P < 0.005) and (h) increase in blood norepinephrine (P < 0.005), dopamine (P < 0.005), and epinephrine (P < 0.001). Aspirin treatment led to an increase in mean arterial pressure (P < 0.001) and mean pulmonary arterial pressure (P < 0.005), but cardiac index, urine flow, platelets, leukocytes, fibrin degradation products, and cathepsin D levels remained similar to untreated controls. After infusion of PGI(2) there was a: (a) prompt increase of cardiac index to base-line levels; (b) late increase in mean arterial pressure (P < 0.005) after the discontinuation of PGI(2) treatment (c) restoration of urine output; (d) increase in circulating platelets to levels still below base line but above untreated control animals (P < 0.05); (e) no effect on circulating leukocyte levels; (f) fall in fibrin degradation products to 11.2 mug/ml (P < 0.05); (g) decline in cathepsin D levels to values 60% lower than the untreated controls (P < 0.025); and (h) reduction in plasma norepinephrine levels to base line at 4 h (P < 0.005). Although the mode of PGI(2) action is not clear, it is effective in the treatment of experimental endotoxemia.

Animals↗
PubMed1981

Effect of GABA agonist and antagonists on cardiovascular and sympathetic responses in SHR and WKY rats.

Injection of muscimol (4 mg/kg, i.a.) to unanesthetized SHR rats reduced the arterial blood pressure and heart rate more than in WKY rats. These cardiovascular responses were accompanied by a moderate increase in plasma norepinephrine level and a marked increase in plasma epinephrine level, in the SHR rats. In the WKY rats, only a moderate increase in plasma epinephrine level was seen. Injection of subconvulsive doses of picrotoxin (2 mg/kg, i.a.) or bicuculline (1 mg/kg, i.a.) to SHR rats, elicited a higher and a more prolonged increase of the arterial blood pressure than in WKY rats. Plasma norepinephrine and epinephrine levels increased to the same extent in both the SHR and WKY rats following picrotoxin injection. These results suggest that the SHR rats differ from the WKY rats in the reactivity of GABAergic responses in cardiovascular centers which also modulate the peripheral sympathetic tone.

Animals↗