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Biomedical subjects

G C Scroop

Publications and source records attributed to G C Scroop.

At least 37 records · Page 2Linked to original sources
PubMed1986

Age dependent heart rate responses to prostacyclin (PGI2) in unanaesthetized fetal and neonatal sheep.

Intravenous injections of PGI2 (1.5-12 X 10(-5) nmol/ml blood volume) caused hypotensive responses which increased with dose in both fetal and neonatal sheep. In the fetus, as gestation advanced and basal heart rate declined, the predominant heart rate response to PGI2 changed progressively from bradycardia to tachycardia. In the neonate, PGI2 always induced tachycardia and the effect was unrelated to postnatal age. The bradycardia induced by PGI2 in young fetal sheep (123-132 days) was converted to tachycardia following either bilateral vagotomy or cervical cord transection. Heart rate was unchanged by PGI2 in fetal sheep subjected to both procedures. The depressor response to PGI2 was enhanced by cervical cord transection but was essentially unchanged in fetal sheep subjected to either bilateral vagotomy alone or combined vagotomy and cord section. Despite increased plasma renin activity following PGI2, the cardiovascular response was not modified by bilateral nephrectomy. It is concluded that while intravenous PGI2 has a similar depressor effect in both fetal and neonatal sheep the heart rate response is age-dependent. Bradycardia is the principal response in young fetal sheep and is mediated by vagal pathways while tachycardia, which is the more usual response in older sheep, is probably sympathetic in nature.

Animals↗
PubMed1986

Angiotensin I and II in the assessment of baroreceptor function in fetal and neonatal sheep.

In fetal and neonatal sheep intravenous injections of angiotensin I, angiotensin II and noradrenaline each increased mean blood pressure and decreased heart rate in a dose-dependent manner. Blood pressure responses to given doses of angiotensin I and II were larger in neonatal than fetal animals while the reverse was true for noradrenaline. In both sheep groups angiotensin II was more pressor than angiotensin I. Baroreceptor function was assessed by correlating blood pressure response to angiotensin II with corresponding changes in either heart rate or heart period. A more sensitive baroreceptor reflex was found in the fetal group in that a given blood pressure response resulted in a significantly larger bradycardia and the calculated gain of the reflex was higher. In those fetuses subjected to either bilateral vagotomy or cervical cord transection pressor responses to both angiotensin II and noradrenaline were enhanced but a significant change was only seen in the cervical cord transection fetuses. Heart rate responses to these drugs were essentially unchanged in the cervical cord transected fetuses while in vagotomized fetuses the bradycardia with each drug was replaced by a tachycardia. It is concluded that the baroreflex is more active in the fetus than the neonate and is mediated by autonomic effector mechanisms similar to those found in the adult.

Angiotensin I↗
PubMed1985

Role of prostaglandins and the areas postrema in the central pressor action of bradykinin.

Vertebral and carotid artery infusions of bradykinin increased blood pressure and heart rate in anaesthetised greyhounds. Indomethacin pretreatment abolished the pressor response to vertebral infusion and reduced that to carotid infusion. Areas postrema ablation abolished the pressor response to bradykinin with both routes of administration. The tachycardia responses to cranial artery infusions and the entire cardiovascular response to intravenous infusion were unaffected by either treatment. It is concluded that intact areas postrema and normal prostaglandin synthesis are essential for the full expression of the central pressor action of bradykinin.

Angiotensin II↗
PubMed1982

Comparison of the effects of prostaglandin E2, prostacyclin and 1-24 adrenocorticotrophin on plasma cortisol levels of fetal sheep.

The changes in plasma cortisol levels in response to intravenous infusions of prostaglandin E2 (PGE2), prostacyclin and 1-24 ACTH have been studied in chronically catheterized fetal sheep during the last third of gestation. All three drugs increased plasma cortisol levels with prostacyclin being sigificantly more potent than either PGE2 or 1-24 ACTH. No interaction between the steroidogenic actions of 1-24 ACTH and either PGE2 or prostacyclin could be demonstrated. The steroidogenic action of PGE2 was not significantly modified by fetal hypophysectomy. It is concluded that neither PGE2 nor prostacyclin is likely to be involved in the enhanced adrenal responsiveness to 1-24 ACTH observed in fetal sheep in the period immediately before birth.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Measurement of blood volume in fetal and neonatal sheep using red blood cells labelled with 99m technetium.

Blood volume has been measured in fetal and neonatal sheep using red blood cells labelled with 99mTc. The calculated volumes were highly correlated with simultaneous measurements made using the standard 51Cr labelled red cell method, although in absolute terms the 99m Tc method provided volumes which on average exceeded by a small percentage those determined with the 51Cr method. Measurements using the 99mTc method were also made at different ages in fetal and neonatal sheep and, while no correlation could be demonstrated between blood volume and either fetal or neonatal age, neonatal blood volumes were highly correlated with body weight. The 99mTc method is considered to be a reliable technique for measuring perinatal blood volumes in sheep with the short half-life of the isotope offering additional advantages.

Animals↗
PubMed1980

Modulation of the baroreceptor reflex by angiotensin II and other vasoactive drugs in anaesthetized greyhounds.

1. The effects of vascular infusions of acetylcholine, angiotensin II, noradrenaline and prostaglandin F2 alpha on the baroreceptor reflex were studied in the anaesthetized greyhound. 2. Vertebral artery infusions of low doses of angiotensin II, but not of acetylcholine or prostaglandin F2 alpha, resulted in a significant reduction in the depressor response to carotid sinus nerve stimulation. 3. The increases in blood pressure and heart rate in response to bilateral carotid artery occlusion were not significantly changes during vertebral artery infusions of acetylcholine, angiotensin II or prostaglandin F2 alpha. 4. The increases in blood pressure in response to intravenous infusions of noradrenaline were significantly enhanced during vertebral artery infusions of acetylcholine and angiotensin II, but not of prostaglandin F2 alpha. The bradycardia during noradrenaline infusions was significantly enhanced by angiotensin II alone. 5. The depressor response to carotid sinus nerve stimulation was significantly reduced during intravenous infusions of both noradrenaline and angiotensin II. 6. It is considered that although angiotensin II can be shown to have a specific central action to attenuate the response to carotid sinus nerve stimulation, the role of this action in the complete baroreceptor reflex is unproven.

Acetylcholine↗
PubMed1980

Disappearance of angiotensin II and noradrenaline from the renal and femoral circulations of the dog.

1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds. 2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route. 3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77.8 +/- 4.1% (mean +/- SEM, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27.2 +/- 4.9% (n = 12). 4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28.9 +/- 6.8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99.0 +/- 1.0% (n = 7) reduction in the pressor responses. 5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions. 6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1977

Hypertension due to a renin-secreting tumour localised by segmental renal vein sampling.

An 18-year-old female was found to be hypertensive on routine medical examination. Further investigation disclosed persistent hypokalaemia and elevated plasma renin activity in peripheral venous blood. Segmental renal vein sampling with assay of blood samples located the source of excess renin secretion in the lower mid-zone of the left kidney. This localization was not confirmed by either angiography or by palpation of the exposed kidney before nephrectomy but macroscopic examination of the freshly sectioned kidney revealed a small tumour in the region suggested by renal vein sampling. The tumour had the morphologic pattern fo an haemangiopericytoma with abundant ultrastructural specific granules and very high renin activity by tissue assay. Plasma renin activity fell precipitously after nephrectomy and remained very low for the first week. Although the immediate post-operative blood pressure fell to normal, hypertension recurred temporarily and was associated with elevated plasma aldosteron, producing a syndrome similar to primary aldosteronism. All variables returned to normal without specific therapy and hypertension has not subsequently recurred.

Adolescent↗
PubMed1971

Importance of central vasomotor effects in angiotensin-induced hypertension.

Ablation of the areas postrema in 10 dogs caused a highly significant reduction in the pressor response to intravenous infusions of angiotensin yet was without significant effect on the pressor response to intravenous infusions of noradrenaline. The reduction in the pressor response to angiotensin is almost certainly due to abolition of the specific central autonomic effects of the hormone which are dependent on the integrity of the areas postrema. It is suggested that this central effect also contributes to the cardiovascular response to endogenous angiotensin.

Angiotensin II↗
PubMed1971

Central autonomic effects of prostaglandin F2 alpha on the cardiovascular system of the dog.

1. Prostaglandin F(2alpha) infused into the vertebral artery of the anaesthetized greyhound in doses which had no effect when given intravenously ((8-64 ng/kg)/min) caused an increase in blood pressure and heart rate.2. This response was not significantly altered by beta-adrenoceptor blockade with propranolol (10 mg i.v.) or by cervical cord section at C(4-6).3. The tachycardia was abolished and the pressor response greatly reduced by vagotomy or atropine (250 mug/kg i.v.).4. The pressor response which remained after vagotomy was abolished by subsequent sympathetic blockade with bethanidine (2-3 mg/kg i.v.) or bretylium (10 mg/kg i.v.).5. In contrast to the effects of propranolol or cervical cord section bethanidine (4-5 mg/kg i.v.) or bretylium (10 mg/kg i.v.) significantly reduced blood pressure and heart rate responses to intravertebral prostaglandin F(2alpha). This result suggests that bethanidine and bretylium have some central actions.6. It is concluded that the cardiovascular effects of intravertebral infusions of prostaglandin F(2alpha) are mediated by the autonomic nervous system and that the preferential pathway is withdrawal of vagal tone to the heart.

Animals↗
PubMed1970

Cardiovascular effects of prostaglandins mediated by the central nervous system of the dog.

1. Prostaglandins A(1), E(1), F(1alpha) and F(2alpha) were infused into the vertebral artery of the chloralose-anaesthetized greyhound and the resulting cardiovascular responses were compared with those obtained on intravenous and intracarotid infusions in the same dose range.2. Infusions of PGF(2alpha) intravertebrally (4-64 (ng/kg)/min) caused an increase of blood pressure, tachycardia and a fall of central venous pressure. Cardiac output was increased and peripheral resistance was essentially unchanged. There was never any response to intravenous or intracarotid PGF(2alpha) infusions in this dose range.3. PGF(1alpha) was found to have similar effects to PGF(2alpha) but it was much less potent.4. PGE(1) infusions (4-360 (ng/kg)/min) into the vertebral artery caused a tachycardia which was greater than that obtained with intracarotid or intravenous infusions, but there was no significant effect on blood pressure.5. Infusions of PGA(1) caused a small fall of blood pressure accompanied by an increase of heart rate and the dose response relationships were similar for all three routes of administration.6. It is concluded that some prostaglandins can activate cardioregulatory centres within the territory of distribution of the vertebral artery. Prostaglandin F(2alpha) is the most potent of these.

Animals↗