PubMed Health⌕ Search

Biomedical subjects

A de Jonge

Publications and source records attributed to A de Jonge.

At least 19 recordsLinked to original sources
PubMed2007

Increased blood loss in upright birthing positions originates from perineal damage.

OBJECTIVE: To assess whether the risk of severe blood loss is increased in semi-sitting and sitting position, and if so, to which extent blood loss from perineal damage is responsible for this finding. DESIGN: Secondary analysis of data from a large trial. SETTING: Primary care midwifery practices in the Netherlands. POPULATION: About 1646 low-risk women who had a spontaneous vaginal delivery. METHODS: Blood loss was measured using a weighing scale and measuring jug. Logistic regression analysis was used to examine the net effects of birthing position and perineal damage on blood loss greater than 500 ml. MAIN OUTCOME MEASURES: Mean total blood loss and incidence of blood loss greater than 500 ml and 1000 ml. RESULTS: Mean total blood loss and the incidence of blood loss greater than 500 ml and 1000 ml were increased in semi-sitting and sitting position. In logistic regression analysis, the interaction between birthing position and perineal damage was almost significantly associated with an increased risk of blood loss greater than 500 ml. Semi-sitting and sitting position were only significant risk factors among women with perineal damage (OR 1.30, 95% CI 1.00-1.69 and OR 2.25, 95% CI 1.37-3.71, respectively). Among women with intact perineum, no association was found. CONCLUSIONS: Semi-sitting and sitting birthing positions only lead to increased blood loss among women with perineal damage.

Adult↗
PubMed2004

Treating urinary incontinence in the elderly--conservative therapies that work: a systematic review.

OBJECTIVE: To evaluate the effectiveness of conservative treatment in the community-based elderly (aged > or = 55 years) with stress, urge, and mixed urinary incontinence. DESIGN: Systematic review of before-after studies or randomized controlled trials on the effect of exercise and drug therapy in urinary incontinence. MAIN OUTCOMES MEASURED: Reduction of urinary accidents, patient's perception, cystometric measurement, perineometry, and side effects. SEARCH STRATEGY: MEDLINE (1966-2001), EMBASE (1986-2001), Science Citation Index (1988-2001), The Cochrane Library, and PiCarta were searched. RESULTS Four before-after studies and 4 randomized controlled trials were identified. Drug therapy alone: no study of sufficient quality. Drug therapy compared with behavioral therapy, 3 studies: bladder-sphincter biofeedback reduced urinary accidents in cases of urge or mixed incontinence by 80.7%, significantly better than oxybutynin (68.5%) or placebo (39.4%). Adding drug to behavioral treatment or behavioral to drug treatment also resulted in significant reduction in urodynamic urge incontinence (57.5%-88.5% vs 72.7-84.3%). Pelvic floor exercises alone reduced urinary accidents by 48% (compared with 53% for phenylpropanolamine) in patients with mixed or stress incontinence. Behavioral therapy, 5 studies: bladder-sphincter biofeedback in case of urge or mixed incontinence, bladder training in case of urge incontinence and pelvic floor exercises in case of stress incontinence reduced the urinary accidents with 68% to 94%. CONCLUSION: There are only a few studies of sufficient methodological quality on the effect of conservative treatment of urinary incontinence in the elderly. Behavioral therapy reduced urinary accidents; the effect of drug therapy is unclear. We recommend behavioral therapy as first choice.

Aged↗
PubMed2001

Support for teenage mothers: a qualitative study into the views of women about the support they received as teenage mothers.

AIM OF THE STUDY: To gain insight into the support teenage mothers received during pregnancy, birth and their child's pre-school years and young women's perceptions of the usefulness of a support group for teenage mothers. BACKGROUND: Most qualitative studies have focused on teenage mothers around the time of the birth of their first child. For this study, women were recruited several years after the birth (median 8.5 years), so that they would have had time to reflect on the support they had received. DESIGN: The qualitative method of semi-structured interviews was chosen to obtain in-depth information and to allow teenage mothers' own views to be heard. Ten individual interviews and one paired interview were undertaken. FINDINGS: Recruitment was difficult because taking part in research was not a priority for many of the women. The study confirmed the strong link between deprivation and teenage pregnancy found in other studies, and suggested that mental health problems in teenage mothers may be more difficult to detect. Teenage women need more information on mental health and on services available to them. The fear, expressed by some of the women in this study, of becoming different from other women in their social network should be considered by health workers when establishing intervention programmes. CONCLUSIONS: Professional bodies of health workers should lobby government to provide a minimum standard of living and sufficient child-care to combat deprivation. Former teenage mothers should be involved in the recruitment, planning and implementation stages of research and interventions. Health professionals should be aware that mental health problems in teenage mothers may be particularly difficult to detect. Key community health workers or a support group may provide information on services, mental health and education facilities available that would benefit teenage mothers. A support group may also give emotional support.

Adolescent↗
PubMed1993

Development of high-affinity 5-HT3 receptor antagonists. Structure-affinity relationships of novel 1,7-annelated indole derivatives.

On the basis of the structures of ondansetron and GR 65,630, its ring-opened C-linked methylimidazole analogue, novel 1,7-annelated indole derivatives were synthesized as potential 5-HT3 antagonists. Receptor binding studies show that all compounds display a high affinity for the 5-HT3 receptors. In both series annelation results in compounds being 7 and 4 times more potent than the references ondansetron and GR 65,630, respectively. Similar to ondansetron, the 1,7-annelated indoles show little stereoselectivity. The (-)-isomers are only slightly more potent than the (+)-isomers. The receptor binding profile of l-10-[(2-methyl-1H-imidazol-1-yl)methyl]-5,6,8,9,10,11-hexahydro-4H-pyri do [3,2,1-jk]carbazol-11-one hydrochloride (24b) (INN cilansetron) shows that the compound displays, besides a high affinity for 5-HT3 receptors (Ki = 0.19 nM), a weak affinity for sigma-receptors (Ki = 340 nM), muscarine M1 receptors (Ki = 910 nM), and 5-HT4 receptors (Ki = 960 nM) and no affinity (Ki > or = 5000 nM) for all the other receptor types tested (n = 37). The new compounds fit the proposed necessary chemical template for binding: a heteroaromatic ring system, a coplanar carbonyl group, and a nitrogen center at well-defined distances. The enhanced potency of the annelated 1,7-indole derivatives indicates that the extra ring provides a favorable hydrophobic area for interaction with the 5-HT3 receptor site. In vivo cilansetron is more potent and induces less central side effects than ondansetron. At present cilansetron is in clinical trials.

Animals↗
PubMed1993

Hypofractionated radiation therapy in unresectable stage III non-small cell lung cancer.

BACKGROUND: Hypofractionation is the current choice for radiation therapy for patients with unresectable non-small cell lung cancer (NSCLC) at the authors' institute. METHODS: In this nonrandomized study, three hypofractionated radiation schedules (40-Gy split course; 30-32 Gy in 6 fractions and 24 Gy in 3 fractions) are evaluated in 301 patients with unresectable Stage III NSCLC: RESULTS: Patients with Stage IIIA disease treated with a 40-Gy split course had longer survival (P < 0.005) and a lower local relapse rate (P < 0.01), but a higher distant failure rate (P < 0.01) than those receiving 24-32 Gy. Survival for patients with Stage IIIA disease treated with 40 Gy at 1, 2, and 5 years was 47%, 22%, and 7%, respectively. For patients with Stage IIIB disease, the radiation scheme used did not correlate with survival and relapse rates. Survival at 1, 2, and 5 years was 30%, 9%, and 2%, respectively. The hypofractionated radiation schemes were well tolerated, and no severe complications were recorded. CONCLUSIONS: In patients with Stage IIIA disease, 40-Gy split-course radiation therapy yields survival rates comparable to those achieved with conventional radiation therapy. In patients with Stages IIIB and IV NSCLC, 24 Gy in 3 weekly fractions yields survival rates comparable to those achieved with higher total doses given in more fractions.

Adenocarcinoma↗
PubMed1993

Consolidative thoracic radiotherapy and prophylactic cranial irradiation in limited disease small cell lung cancer.

Between 1983 and 1990, 128 patients with limited disease small cell lung cancer (SCLC) received consolidative thoracic irradiation after reaching a complete (CR) or partial response (PR) to combination chemotherapy. Patients in CR (n = 85) received 35-36 Gy in 12-14 fractions and patients in PR (n = 43) 24-30 Gy in 3-6 fractions. Until 1989, prophylactic cranial irradiation (PCI) was given to patients in CR. There was no significant difference in survival between the CR and PR group. However, patients with residual tumor detected by radiology or bronchoscopy or cyto-/histology had significantly longer survival than those with residual tumor demonstrated by more than one of the above methods of investigation. Overall, local progression was observed in 22% and distant dissemination in 63% of patients. The rate of brain metastases was significantly lower in patients treated with methotrexate and nitrosurea containing schedules and PCI, compared to those who were treated with other schedules (irrespective of PCI).

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1991

Renal sensitivity to endothelium-derived-relaxing-factor-mediated vasodilatation in the spontaneously hypertensive rat.

1. The sensitivity of the kidney to endothelium-derived-relaxing-factor-mediated vasodilatation has been investigated in the spontaneously hypertensive rat and the Wistar-Kyoto normotensive rat using an isolated perfused rat kidney model. 2. No difference in the slope, ED50 or maximum of the concentration-response curves for the endothelial-dependent vasodilators A23187, a calcium ionophore, and acetylcholine could be demonstrated between kidneys obtained from the spontaneously hypertensive and the Wistar-Kyoto normotensive rats. 3. No difference in the slope or the ED50 of the concentration-response curve for the endothelial-independent vasodilators, atrial natriuretic factor and sodium nitroprusside, could be demonstrated between kidneys obtained from the spontaneously hypertensive and the Wistar-Kyoto normotensive rats. However, in the spontaneously hypertensive rats, the maximum vasodilator response to atrial natriuretic factor, but not to sodium nitroprusside, was increased. 4. The perfused kidney from the spontaneously hypertensive rat also showed an increase in the maximum but not in the slope or ED50 of the concentration-response curve for vasoconstriction induced by the alpha 1-adrenoceptor agonist methoxamine. 5. The involvement of endothelium-derived relaxing factor in mediating the renal vasodilator response to A23187 and acetylcholine was confirmed in experiments performed in perfused kidneys obtained from normotensive Wistar rats. 6. It is concluded that the sensitivity of the kidney to endothelium-derived-relaxing-factor-mediated vasodilatation is not modified in the spontaneously hypertensive rat. This does not, however, exclude a role for the synthesis of endothelium-derived relaxing factor in the maintenance of blood pressure in the spontaneously hypertensive rat.

Acetylcholine↗
PubMed1990

Cyclic GMP release and vasodilatation induced by EDRF and atrial natriuretic factor in the isolated perfused kidney of the rat.

1. Guanosine 3':5'-cyclic monophosphate (cyclic GMP) release and vascular tone was measured in the isolated kidney of the rat perfused at constant flow with Krebs-Henseleit solution. The effects of 3 vasodilators, acetylcholine (ACh), atrial natriuretic factor (ANF) and sodium nitroprusside (SNP) on the renal release of cyclic GMP and vascular tone were examined. The ability of the endothelial-derived relaxing factor (EDRF) inhibitors, haemoglobin and gossypol, to modify vasodilatation and vasodilator-induced changes in cyclic GMP releases from the kidney was also investigated. 2. Renal cyclic GMP release was elevated 8 fold by ANF (0.01 microM), 5 fold by SNP (1 microM) and 3 fold by ACh (0.3 microM). 3. For ACh, both the increase in renal cyclic GMP release and the vasodilatation were reduced by the EDRF inhibitors, haemoglobin (1 microM) and gossypol (15 microM). For SNP, neither the increase in renal cyclic GMP release nor vasodilatation were inhibited by gossypol (15 microM). 4. For ANF, neither the increase in cyclic GMP release from the kidney nor its vasodilator activity were affected by haemoglobin (1 microM). 5. EDRF inhibitors reduced the basal release of cyclic GMP from 0.32 +/- 0.06 pmol min-1 to 0.18 +/- 0.03 pmol min-1, gossypol being more effective than haemoglobin. 6. The results are consistent with the ability of ACh to induce EDRF-mediated vasodilatation in the isolated perfused kidney of the rat. Basal EDRF release appears to contribute approximately 50% to the basal release of cyclic GMP from this preparation. The renal vasodilator action of ANF however, is independent of EDRF, although the renal vascular endothelium cannot be discounted as a site at which ANF stimulates cyclic GMP production.

Acetylcholine↗
PubMed1987

Selectivity of muscarinic antagonists in radioligand and in vivo experiments for the putative M1, M2 and M3 receptors.

In the present study we investigated the nature of the muscarinic receptors present in the hippocampus, sympathetic ganglia, atria and salivary glands of the rat. The heterogeneity of the muscarinic receptors was examined both in vivo and in radioligand binding experiments. To study whether the receptors present in the investigated tissues are indeed distinct subtypes we determined the potencies of antagonists in both systems. It is proposed that there are three different binding sites present in hippocampal, atrial and submandibular membranes and we suggest to classify them as M1, M2 and M3, respectively. Both in vivo and in vitro pirenzepine appears to possess high affinity for M1 receptors, whereas 4-diphenylacetoxy-N-methylpiperidine methobromide and dicyclomine show high affinity for both M1 and M3 receptors. AF-DX 116 (11-2[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5, 11-dihydro-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one) displayed high affinity for M2 receptors.

Animals↗
PubMed1986

Discrimination by N-ethylmaleimide between the chronotropic and inotropic response to muscarinic receptor stimulation in rat atrium.

N-ethylmaleimide (NEM) rapidly blocked the negative chronotropic effect of carbachol on rat right atrium. In contrast, NEM did not reduce the negative inotropic response to muscarinic (M) receptor stimulation. Carbachol inhibited the specific binding of [3H]-N-methylscopolamine [( 3H]-NMS) to membranes of rat atria as reflected by a shallow inhibition curve. Both guanosine triphosphate (GTP) and NEM shifted the [3H]-NMS inhibition curves of carbachol to the right. Pretreatment of the atrial membranes with NEM abolished the GTP-induced rightward shift. However, when instead of the membranes the intact atria were pre-incubated with NEM, no interaction between NEM and GTP in the membranal preparation was observed. The results indicate that NEM sharply discriminated between the inotropic and chronotropic effects to M-receptor stimulation in rat atria. The inhibitory effect of NEM on the M-receptor-mediated negative chronotropic effect in rat atrium cannot be explained by an interaction of the sulfhydryl reagent with GTP-binding proteins, like Ni or No.

Animals↗
PubMed1986

Inhibitory effect of alpha-1 adrenoceptor stimulation on cardiac sympathetic neurotransmission in pithed normotensive rats.

In the present study we investigated the inhibitory effect of the selective alpha-1 adrenoceptor agonists cirazoline, amidephrine and St 587 on the cardiac sympathetic neurotransmission in pithed normotensive rats. Increases in heart rate were elicited by electrical stimulation of the cardiac sympathetic nerves or by i.v. administration of norepinephrine, isoproterenol or tyramine. Intravenous pretreatment of the animals with cirazoline, amidephrine or St 587 diminished the heart rate response to sympathetic stimulation significantly. However, the tachycardia produced by norepinephrine, isoproterenol or tyramine was also inhibited significantly by the selective alpha-1 adrenoceptor agonists. The selective alpha-1 antagonist prazosin blocked the sympathoinhibitory effect to alpha-1 adrenoceptor stimulation significantly. However, the inhibitory effect of cirazoline and St 587 was not suppressed completely by a maximally effective dose of prazosin. In contrast, the sympathoinhibitory action of amidephrine was antagonized completely by prazosin. However, the selective alpha-2 antagonist rauwolscine also produced a significant, albeit modest, attenuation of the sympathoinhibitory effect to amidephrine. The results of the present study indicate that alpha-1 adrenoceptor agonists, at relatively high doses, inhibit the sympathetic neurotransmission in rat heart. This sympathoinhibitory effect is mediated largely by alpha-1 adrenoceptors which are localized postjunctionally rather than prejunctionally.

Adrenergic alpha-Agonists↗
PubMed1986

Central and peripheral effects of S 3341 [(N-dicyclopropylmethyl)-amino-2-oxazoline] in animal models.

The effects on blood pressure and heart rate of S 3341 [(N-dicyclopropylmethyl)-amino-2-oxazoline] were investigated in rats and cats. Upon i.v. injection in pithed rats, S 3341 produced pressor responses which were antagonized by prazosin as well as by yohimbine. In pentobarbitone-anesthetized rats S 3341 produced a short-lasting increase in mean arterial pressure, followed by a long-lasting reduction. During a 12-day, continuous subcutaneous infusion in conscious spontaneously hypertensive rats, S 3341 reduced blood pressure and heart rate. Upon cessation of treatment, an overshoot of heart rate and blood pressure lability occurred. The hypotensive effect was abolished by reserpinization of the rats. S 3341 was more potent in reducing mean arterial pressure upon infusion via the vertebral artery than after infusion via the femoral artery of chloralose-anesthetized cats. S 3341 did not prolong the hexobarbitone-induced loss of righting reflex in mice. S 3341 was more potent in displacing [3H]clonidine than [3H]prazosin from their specific binding sites in rat brain membranes. These data characterize S 3341 as a clonidine-like, centrally acting antihypertensive drug. The lack of sedative effect, as assessed by the prolongation of hexobarbitone-induced sleeping in mice, remains to be clarified.

Adrenergic alpha-Agonists↗
PubMed1986

Interaction between the adrenergic and renin-angiotensin-aldosterone-systems.

In congestive heart failure (CHF) both the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone-system (RAAS) are activated. Both phenomena are only of short-term benefit and inevitably detrimental with prolonged activation. There are many possibilities for interaction between the systems, in particular when they are both in the activated state as in CHF. Renin release from the renal juxtaglomerular cells is stimulated by the SNS via beta 1-adrenoceptors. At a higher level of renal nerve stimulation there is recruitment of antinatriuretic and finally vasoconstrictor activity, mediated by alpha 1-adrenoceptors. The vasoconstrictor potency of angiotensin II (AII) involves both postsynaptic angiotensin II-receptors and also various processes stimulating sympathetic activity and its sequelae. The following sympathetic components may contribute to the effect of angiotensin II:ganglionic stimulation; enhanced release of noradrenaline (tyramine-like effect); inhibited noradrenaline re-uptake; facilitation of noradrenaline release via presynaptic AII-receptors; sensitization of postsynaptic alpha-adrenoceptors. The presynaptic AII-mechanism is probably the most sensitive and relevant process, which is also involved in the vasodilator activity of ACE-inhibitors.

Angiotensin II↗
PubMed1985

Effects of the irreversible alpha-adrenoceptor antagonists phenoxybenzamine and benextramine on the effectiveness of nifedipine in inhibiting alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in pithed rats.

In pithed normotensive rats, i.v. injection of the selective alpha 1-adrenoceptor agonist cirazoline produced vasoconstriction which was largely resistant to inhibition by nifedipine. On the other hand, the pressor effects of the selective alpha 1-adrenoceptor agonists St 587 and Sgd 101/75 were much more effectively blocked by nifedipine, although not as effectively as the pressor effects to the selective alpha 2-adrenoceptor agonist B-HT 920. The sensitivity to inhibition of vasoconstriction in pithed rats to the different agonists increased in the order cirazoline much less than St 587 less than Sgd 101/75 less than B-HT 920. Phenoxybenzamine (3-300 micrograms/kg, i.v., -60 min) irreversibly antagonized the vasoconstriction to cirazoline, St 587, Sgd 101/75 and B-HT 920. After treatment of the rats with phenoxybenzamine the potency and efficacy of nifedipine in antagonizing vasoconstriction to alpha 1-, but not to alpha 2-adrenoceptor activation was dose-dependently enhanced. The potency of nifedipine to inhibit alpha 1-adrenoceptor-mediated vasoconstriction by cirazoline, St 587 and Sgd 101/75 was increased maximally to the level of efficacy at which nifedipine antagonized B-HT 920-induced vasoconstriction. The dose of phenoxybenzamine required to maximally increase the potency and efficacy of nifedipine to antagonize vasoconstriction of the alpha 1-adrenoceptor agonists was inversely related to the level of sensitivity to blockade by nifedipine of the vasoconstriction they produced. In contrast, pretreatment of rats with the irreversible antagonist, benextramine (10 mg/kg, i.v., -100 to -60 min) did not increase the potency or efficacy of nifedipine to antagonize vasoconstriction to cirazoline, St 587, Sgd 101/75 or B-HT 920, despite irreversible blockade of alpha 1- and alpha 2-adrenoceptors. These data suggest that phenoxybenzamine, but not benextramine, selectively inhibits the alpha 1-adrenoceptor mediated vasoconstrictor mechanism that is independent of influx of extracellular calcium. Moreover, the results show that the existence of receptor reserve or the number of alpha 1-adrenoceptors activated does not determine the relative contribution of calcium influx-independent mechanisms in alpha 1-adrenoceptor-mediated vasoconstriction.

Animals↗
PubMed1985

Subclassification of muscarinic receptors in the heart, urinary bladder and sympathetic ganglia in the pithed rat. Selectivity of some classical agonists.

In pithed normotensive rats muscarinic receptors were characterized in heart, urinary bladder and sympathetic ganglia; the selectivity of some classical muscarinic agents for these subtypes was investigated. The potencies in decreasing heart rate, increasing bladder pressure and increasing diastolic blood pressure were measured for the following, intraarterially administered cholinergic agonists: McN-A-343 ([4-m-chlorophenylcarbamoyloxy]-2-butynyltrimethylammonium), pilocarpine, carbachol, oxotremorine, arecoline, acetyl-beta-methylcholine and acetylcholine. The selective M1-antagonist pirenzepine, the mixed M1/M2-antagonist dexetimide and the cardioselective M2-antagonist gallamine were used as tools for identification of the receptors. All data were obtained after intravenous pretreatment with a high dose of atenolol to eliminate tachycardia induced by stimulating sympathetic ganglionic muscarinic receptors. Dexetimide strongly antagonized the bradycardia as well as the increase in bladder pressure induced by pilocarpine, carbachol, oxotremorine, arecoline, acetyl-beta-methylcholine and acetylcholine, whereas pirenzepine was much less effective. Gallamine antagonized the bradycardia, whereas no influence was found on the bladder contraction. Pilocarpine acted as a partial agonist in reducing heart rate as well as in increasing bladder pressure, whereas McN-A-343 was almost ineffective in doses up to 1 mg/kg. The hypertensive response to pilocarpine and carbachol was less pronounced than that produced by McN-A-343. Pirenzepine and dexetimide significantly antagonized the hypertensive response to McN-A-343 and pilocarpine, whereas gallamine was much less effective. The hypertensive response induced by carbachol was totally blocked by hexamethonium. The other agonists used in this study did not produce a significant increase in diastolic blood pressure in doses that produced a maximal effect on heart rate and urinary bladder pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Influence of respiratory acidosis or alkalosis on pressor responses mediated by alpha 1- and alpha 2-adrenoceptors in pithed normotensive rats.

The effect of respiratory acidosis and alkalosis on the vasoconstriction to alpha 1- and alpha 2-adrenoceptor stimulation was studied in pithed normotensive rats. The selective alpha 1-adrenoceptor agonists (-)amidephrine, cirazoline, (+/-)erythro methoxamine, (-)phenylephrine, Sgd 101/75 and St 587 were used, as well as the selective alpha 2-adrenoceptor agonists B-HT 920, B-HT 933, DP-6,7-ADTN, M-7 and UK 14,304. The non-selective alpha-adrenoceptor agonists xylazine, noradrenaline and adrenaline were included as well. The latter two were also studied under selective doses of the antagonists rauwolscine and prazosin, thus yielding the respective alpha 1- and alpha 2-adrenoceptor components of the vasoconstriction to these agonists. The effect of acid-base balance disturbances on presynaptically released noradrenaline elicited by electrical stimulation of preganglionic nerves was studied as well. Dose response curves for the agonists were generated under various conditions of ventilation, yielding either alkalotic, normal or acidotic values of arterial blood pH. Pressor responses to all agonists were maximally affected by changes in acid-base status at the low doses of the agonists. Acidosis was found to inhibit increases in diastolic pressure mediated by the alpha 1-as well as the alpha 2-adrenoceptor agonists studied, although not to the same extent. Alkalosis exerted either an obvious potentiation or did not significantly influence alpha 1-adrenoceptor mediated pressor responses. On the basis of acid-base sensitivity the following groups of agonists were distinguished: Cirazoline, phenylephrine, methoxyamine, electrically released noradrenaline from presynaptic sites, of which pressor responses are obviously potentiated and attenuated by alkalosis and acidosis, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗