PubMed Health⌕ Search

Biomedical subjects

I A Reid

Publications and source records attributed to I A Reid.

At least 73 records · Page 4Linked to original sources
PubMed1984

Cardiovascular and metabolic sequelae of inducing anesthesia with ketamine or thiopental in hypovolemic swine.

If further sympathetic stimulation is neither possible nor desirable during moderate hypovolemia, anesthetic agents capable of sympathetic stimulation would not be advantageous for induction of anesthesia during hypovolemia. To test this hypothesis, 21 swine were studied during normovolemia and after 30% of their estimated blood volume was removed. Swine were divided randomly into three equal groups to receive no anesthetic or the minimal anesthetic dose of ketamine (6.65 +/- 0.38 mg/kg, iv) or thiopental (5.77 +/- 0.21 mg/kg, iv). After the initial response to hypovolemia, animals given no drug did not exhibit further changes during the hypovolemic period. Five minutes after induction of anesthesia in the hypovolemic state, ketamine, but not thiopental, caused large increases in plasma epinephrine, norepinephrine, and renin activity. Despite these differences, both anesthetics equally depressed systemic vascular resistance, mean systemic arterial blood pressure, heart rate, and cardiac output. Ketamine, but not thiopental, decreased stroke volume. Neither anesthetic affected oxygen consumption. Both anesthetics caused similar increases in blood lactate concentration. Thirty minutes after induction of anesthesia, plasma epinephrine, norepinephrine, and renin activity remained higher in animals given ketamine than in those given thiopental. Stroke volume, systemic vascular resistance, cardiac output, and oxygen consumption did not differ among groups; however, only the animals given ketamine showed further increase in blood lactate concentration and base-deficit. Thirty minutes after infusion of shed blood, cardiac output and blood lactate concentration were greater in the animals given ketamine than in those given thiopental or no anesthetic. Ninety minutes after infusion of shed blood, no differences existed among groups. The authors conclude that after moderate hemorrhage, further increase in circulating catecholamines is possible but that the levels achieved either exceed the maximal effective concentration at site(s) of action or their effects are overwhelmed by the depressant effects of ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1984

Actions of angiotensin II on the brain: mechanisms and physiologic role.

Angiotensin II acts on the brain to produce a variety of effects including elevation of arterial blood pressure, increased release of vasopressin and ACTH, stimulation of drinking and sodium appetite, and natriuresis. Many, and possibly all, of these effects can be produced by centrally administered angiotensin II or by circulating angiotensin II, which appear to act at common receptor sites located in the circumventricular organs. Whether these effects are normally produced by blood-borne angiotensin II formed by the renal renin-angiotensin system, by angiotensin II formed centrally by the putative brain renin-angiotensin system, or by both, remains to be determined. A large body of information concerning the site and mechanism of these different central actions of angiotensin II is available, and the physiologic significance of these actions is beginning to be understood. Nevertheless, much additional research will be required before the actions of angiotensin II on the brain are completely understood.

Adrenocorticotropic Hormone↗
PubMed1984

Effect of renal denervation on the suppression of renin secretion by vasopressin in conscious dogs.

Previous studies have shown that the inhibition of renin secretion by vasopressin (AVP) in conscious dogs is related to vasoconstrictor activity and may be a reflex response mediated by the renal nerves. The aim of the present experiments was to determine whether the suppression of plasma renin activity (PRA) by AVP is blocked by renal denervation. AVP and, for comparison, angiotensin II (ANG II) were infused intravenously for 45 min in seven conscious dogs before and after bilateral renal denervation. Before denervation, AVP infusion at 0.2 and 1.0 ng X kg-1 X min-1 suppressed PRA from 7.4 +/- 1.1 to 4.7 +/- 1.0 (P less than 0.01) and from 7.9 +/- 1.8 to 3.8 +/- 0.8 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. ANG II infusion at 5.0 and 10.0 ng X kg-1 X min-1 decreased PRA from 7.5 +/- 2.3 to 2.5 +/- 0.7 (P less than 0.01) and from 6.0 +/- 1.1 to 1.8 +/- 0.4 ng X ml-1 X 3 h-1 (P less than 0.01), respectively. One to three weeks following renal denervation, PRA had decreased from 6.7 +/- 1.3 to 2.9 +/- 0.5 ng X ml-1 X 3 h-1 (P less than 0.01), and renal norepinephrine was undetectable. After denervation, neither AVP infusion at 0.2 (3.0 +/- 0.5 to 2.4 +/- 0.4 ng X ml-1 X 3 h-1) nor 1.0 ng X kg-1 X min-1 (3.1 +/- 0.8 to 2.8 +/- 1.0 ng X ml-1 X 3 h-1) suppressed PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1984

Mechanism of suppression of vasopressin and adrenocorticotropic hormone secretion by clonidine in anesthetized dogs.

Studies were performed in anesthetized dogs to investigate the mechanism of the suppression of vasopressin and adrenocorticotropic hormone (ACTH) secretion by clonidine. Injection of clonidine (30 micrograms/kg i.v.) produced an initial increase in arterial pressure followed by hypotension, decreased heart rate, increased right atrial pressure and decreased plasma renin activity. Plasma vasopressin concentration decreased from 14.6 +/- 3.0 to 2.2 +/- 0.4 pg/ml (P less than .01), and this was accompanied by increases in urine volume and free water clearance from 0.15 +/- 0.02 to 1.03 +/- 0.28 and -0.50 +/- 0.05 to 0.30 +/- 0.27 ml/min, respectively (P less than .01), and a decrease in urinary osmolality from 1450 +/- 124 to 372 +/- 97 mOsmol/kg of H2O (P less than .01). Plasma corticosteroid concentration, used an an index of ACTH secretion, decreased from 8.9 +/- 1.6 to 2.2 +/- 0.3 micrograms/dl (P less than .01). Plasma osmolality did not change. Pretreatment of dogs with the alpha adrenoceptor antagonist yohimbine (2 mg/kg i.p.) blocked all cardiovascular, endocrine and renal responses to clonidine. Bilateral cervical vagotomy did not block the suppression of vasopressin or corticosteroid secretion by clonidine. Intraventricular injection of yohimbine blocked the hypotension and suppression of plasma corticosteroid concentration produced by clonidine but did not block the decrease in plasma vasopressin concentration or the associated renal effects of clonidine. Intracarotid infusion of clonidine caused small decreases in plasma vasopressin and corticosteroid concentrations even though blood pressure decreased by 22 mm Hg. Intraventricular and intravertebral clonidine had no significant effect on plasma vasopressin or corticosteroid concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1983

[Sar,Ala]angiotensin II in cerebrospinal fluid blocks the binding of blood-borne [125I]angiotensin II to the circumventricular organs.

There is a specific, high affinity uptake of angiotensin II in the circumventricular organs when the peptide is injected systemically. The question of whether angiotensin II in cerebrospinal fluid can reach angiotensin receptors in the circumventricular organs was investigated in rats by determining the effect of intraventricular administration of the angiotensin II receptor blocking peptide [Sar,Ala]angiotensin II (saralasin) on the binding of blood-borne [125I]angiotensin II. Other rats received intraventricular saline, intraventricular ACTH as a peptide control, or intravenous saralasin. The brains of the rats were then sectioned and subjected to radioautography. ACTH had no effect on angiotensin II uptake. Intraventricular saralasin reduced the uptake of blood-borne angiotensin II in the median eminence and organum vasculosum of the lamina terminalis to the same degree as intravenous saralasin, and reduced uptake in the subfornical organ and area postrema to a lesser extent. Uptake was reduced 40% in the anterior lobe of the pituitary by intraventricular saralasin and 73% by intravenous saralasin, indicating that some saralasin entered the portal vessels. Uptake in the posterior lobe was unaffected by intraventricular saralasin, but reduced by intravenous saralasin. The data indicate that saralasin, and so presumably angiotensin II, in the cerebrospinal fluid can reach angiotensin II receptors in the circumventricular organs which bind blood-borne angiotensin II. Consequently, the effects of intraventricular angiotensin II that are also produced by intravenous angiotensin II can probably be explained by the peptide acting on the circumventricular organs.

Angiotensin II↗
PubMed1983

Role of vasopressin in blood pressure regulation in conscious water-deprived dogs.

The role of vasopressin in the regulation of blood pressure during water deprivation was assessed in conscious dogs with two antagonists of the vasoconstrictor activity of vasopressin. In water-replete dogs, vasopressin blockade caused no significant changes in mean arterial pressure, heart rate, plasma renin activity (PRA), or plasma corticosteroid concentration. In the same dogs following 48-h water deprivation, vasopressin blockade increased heart rate from 85 +/- 6 to 134 +/- 15 beats/min (P less than 0.0001), increased cardiac output from 2.0 +/- 0.1 to 3.1 +/- 0.1 1/min (P less than 0.005), and decreased total peripheral resistance from 46.6 +/- 3.1 to 26.9 +/- 3.1 U (P less than 0.001). Plasma renin activity increased from 12.4 +/- 2.2 to 25.9 +/- 3.4 ng ANG I X ml-1 X 3 h-1 (P less than 0.0001) and plasma corticosteroid concentration increased from 3.2 +/- 0.7 to 4.9 +/- 1.2 micrograms/dl (P less than 0.05). Mean arterial pressure did not change significantly. When the same dogs were again deprived of water and pretreated with the beta-adrenoceptor antagonist propranolol, the heart rate and PRA responses to the antagonists were attenuated and mean arterial pressure decreased from 103 +/- 2 to 91 +/- 3 mmHg (P less than 0.001). These data demonstrate that vasopressin plays an important role in blood pressure regulation during water deprivation in conscious dogs.

11-Hydroxycorticosteroids↗
PubMed1983

Effects of blockade of brain angiotensin II receptors in conscious, sodium-deprived dogs.

The present studies were designed to evaluate the physiological significance of the actions of angiotensin II (ANG II) on the brain. The effects of blockade of brain ANG II receptors by intracarotid or intravertebral infusions of saralasin were studied in conscious dogs with high circulating ANG II levels (142 +/- 16 pg/ml) due to a low-sodium diet. Three doses of saralasin were infused into each pair of arteries and intravenously: 0.1, 0.3, and 1.0 micrograms X kg-1 X min-1. Saralasin produced dose-related decreases in arterial pressure during infusion into the carotid or vertebral arteries, confirming that ANG II maintains arterial pressure during sodium deficiency. However, intravenous saralasin administration decreased pressure to a similar degree, suggesting that the hypotensive effect was due to recirculation of saralasin, rather than to blockade of a central action of circulating ANG II. Heart rate was not altered by infusion of saralasin by any route. Saralasin administration also caused a dose-dependent increase in plasma renin activity and plasma ANG II concentration. However, because the increases produced by intracarotid or intravertebral saralasin did not differ from the increase produced by intravenous infusion, these results do not provide evidence that renin release is modulated by a central action of ANG II during sodium deficiency. Plasma corticosteroid levels were reduced (2.4 +/- 0.5 to 1.4 +/- 0.2 micrograms/dl, P less than 0.05) by intravenous infusion of the highest dose of saralasin, but neither intracarotid nor intravertebral saralasin infusion altered plasma corticosteroid concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗
PubMed1983

Role of vasopressin in blood pressure regulation during adrenal insufficiency.

The effect of adrenal insufficiency on the plasma concentrations of two vasoactive hormones, vasopressin and angiotensin II, was studied in conscious dogs. In addition the role of vasopressin in the maintenance of blood pressure during adrenal insufficiency was studied using [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]arginine vasopressin, a specific antagonist of the vasoconstrictor action of vasopressin. Dogs were bilaterally adrenalectomized and maintained on daily cortisol and deoxycorticosterone acetate injections. Withdrawal of steroids for 4 days resulted in a 4-fold increase in plasma vasopressin concentration (P less than 0.05) and a 3-fold increase in plasma angiotensin II concentration (P less than 0.001); mean arterial pressure did not change significantly. Administration of the vasopressin antagonist in adrenalectomized dogs maintained on steroids had no effect on blood pressure. In marked contrast, vasopressin blockade in dogs with adrenal insufficiency decreased mean arterial pressure by 22 +/- 5 mm Hg (P less than 0.001). These results demonstrate the plasma angiotensin II and vasopressin concentrations increase during adrenal insufficiency in conscious dogs, and that vasopressin plays an important role in blood pressure regulation in this hypovolemic state.

Adrenal Insufficiency↗
PubMed1982

Effects of a nonpressor analogue of vasopressin on plasma renin activity and salt and water excretion in water-loaded, anesthetized dogs.

The object of this study was to determine the importance of vasoconstrictor activity in the suppression of renin secretion by vasopressin. Arginine vasopressin (AVP) (0.05 and 0.1 ng/kg/min) and a nonpressor analogue of vasopressin, 1-deamino-[4-threonine, 8-D-arginine]-vasopressin (dTDAVP) (0.01 and 0.05 ng/kg/min), were infused intravenously in anesthetized hypophysectomized dogs. Neither dTDAVP nor AVP influenced arterial pressure or heart rate but both suppressed plasma renin activity. Infusion of dTDAVP at 0.01 and 0.05 ng/kg/min suppressed plasma renin activity to 86 +/- 4% (p less than 0.05) and 63 +/- 6% (p less than 0.01) of the control values respectively. Infusion of AVP at 0.05 and 0.1 ng/kg/min suppressed plasma renin activity to 60 +/- 8% (p less than 0.01) and 59 +/- 12% (p less than 0.05) of the control values respectively. dTDAVP and AVP both produced significant increases in sodium excretion. These data demonstrate that vasoconstrictor activity is not required for the effects of vasopressin on renin secretion and sodium excretion.

Anesthesia↗
PubMed1982

Measurement and localization of angiotensin-like immunoreactivity in juxtaglomerular cells of the rat.

The existence and distribution of angiotensin I (A I) and angiotensin II (A II) in rat kidney were examined in immunocytochemical studies using the peroxidase-antiperoxidase technique and in biochemical studies using rat kidney homogenates extracted with acid-ethanol and purified by Sephadex G-25 gel chromatography. Immunopositive A II-like staining was observed in the juxtaglomerular cells of the afferent arteriole, but no histochemical evidence for A I was found. On the other hand, renal homogenates were found to contain both A I and A II immunoreactivities which coeluted on gel chromatography with synthetic A I and A II. These results indicate that A I as well as A II immunoreactivities are present in the kidney and that A II immunoreactivity can be localized to the juxtaglomerular cells. The origin of the immunoreactive A II in the juxtaglomerular cells remains to be determined.

Angiotensin I↗
PubMed1982

Differential distribution of immunoreactive angiotensin and angiotensin-converting enzyme in rat brain.

To help resolve the controversy about the brain renin-angiotensin system, the distribution of immunoreactive angiotensin in the brains of male rats was analyzed using twelve different antibodies to angiotensin II, two of which had previously been reported to stain nerve fibers in the central nervous system. The distribution of angiotensin-converting enzyme immunoreactivity was also examined using an antibody to rabbit lung converting enzyme, and the distribution of this immunoreactivity was compared to that of immunoreactive angiotensin. Weak angiotensin-like immunoreactivity was found in cell bodies of the hypothalamic magnocellular nuclei of colchicine-treated rats and in nerve terminals of the median eminence, neurohypophysis, central nucleus of the amygdala, bed nucleus of the stria terminalis and various other sites in the brain and spinal cord of untreated rats. Staining could be demonstrated with only three antisera. Antigenic specificity was carefully studied in these antisera. Each was similar in that staining could be blocked with angiotensins I, II or III and tetradecapeptide renin substrate, although angiotensins II and III were most potent. Because of the relatively few angiotensin II antisera which could stain brain and because they are blockable with angiotensin I and tetradecapeptide renin substrate, the precise nature of immunoreactive angiotensin remains an open question. Intense converting enzyme-like activity was localized in endothelial cells of capillaries throughout the brain, in the subfornical organ and in the 'brush border' of choroidal epithelial cells in contact with cerebrospinal fluid. No activity was detected in neural tissue other than the subfornical organ and occasional weak activity in some ependymal elements elsewhere. These findings indicate that angiotensin and converting enzyme immunoreactivities are not co-distributed and raises several questions regarding the nature of, and pathway for, formation of immunoreactive angiotensin in the brain.

Angiotensin II↗
PubMed1982

Analysis of the actions of angiotensin on the central nervous system of conscious dogs.

Angiotensin II (ANG II) acts on the brain to elevate blood pressure (BP), stimulate drinking, increase the secretion of vasopressin and corticotropin (ACTH), and inhibit the secretion of renin. The present studies were designed to evaluate the possible physiological significance of these effects. The experiments were performed in conscious dogs with small catheters chronically implanted in both carotid and both vertebral arteries. ANG II was infused into both carotid or both vertebral arteries in doses of 0.1, 0.33, 1.0, and 2.5 ng.kg-1.min-1. Intravertebral ANG II produced dose-related increases in BP that were generally accompanied by increases in heart rate. Intracarotid angiotensin also increased BP but did not change heart rate. Intracarotid ANG II stimulated drinking and, at the highest dose only, increased the secretion of vasopressin, ACTH, and corticosteroids. Intravertebral and intracarotid ANG II suppressed plasma renin activity (PRA). In a parallel series of experiments, the effects of intravenous ANG II, in doses of 2, 5, 10, and 20 ng.kg-1.min-1, were studied. These infusions produced dose-related increases in BP and water intake and suppressed PRA. Only the highest dose of ANG II increased vasopressin or corticosteroid secretion. Analysis of these results in terms of calculated or measured changes in plasma ANG II concentration indicate that the central cardiovascular and dipsogenic actions of angiotensin, as well as the suppression of PRA, can be elicited by concentrations of the peptide that are within the physiological range. On the other hand high, probably supraphysiological, levels of ANG II are required to increase vasopressin or ACTH secretion.

Adrenal Cortex Hormones↗
PubMed1982

Stimulation of renin secretion by vasoactive intestinal peptide.

Vasoactive intestinal peptide (VIP) increased plasma renin activity (PRA) in pentobarbital-anesthetized dogs. A 15-min infusion of VIP directly into the renal artery at a dose of 33 ng . kg-1 min-1 increased renin secretion rate from 1,461 +/- 393 to 5,769 +/- 1,794 ng ANG I . ml-1 . 3 h-1 . min-1, and increased PRA from 19.2 +/- 2.3 to 29.2 +/- 4.7 ng ANG I . ml-1 . 3 h-1. Renal blood flow and creatinine clearance were also increased, whereas plasma potassium concentration and diastolic blood pressure decreased. There was no change in sodium or potassium excretion. When administered intravenously, 33 and 13 ng . kg-1 . min-1 VIP increased PRA. A dose of 3.3 ng . kg-1 . min-1 failed to increased PRA when given intravenously but produced a significant increase in PRA from 22.8 +/- 8.1 to 40.5 +/- 19.4 ng ANG I . ml-1 . 3 h-1 when infused into the renal artery. This increase occurred without any change in plasma potassium concentration or blood pressure. Renin secretion was increased by a two- to threefold increase in plasma VIP; comparable increases in plasma VIP have been reported to be produced by various experimental procedures. The data indicate that VIP increases renin secretion. The peptide appears to act directly on the kidney and may act directly on the juxtaglomerular cells.

Animals↗
PubMed1981

Effect of vasopressin blockade on blood pressure regulation during hemorrhage in conscious dogs.

The role of vasopressin in the regulation of blood pressure during nonhypotensive hemorrhage was assessed in conscious dogs. An antagonist of the vasoconstrictor activity of vasopressin was administered (10 microgram/kg) to four normal dogs five min prior to the commencement of a 15 min arterial hemorrhage (1 ml/kg/min). The withdrawn blood was reinfused 15 min after completion of the hemorrhage. In the absence of vasopressin blockade, blood pressure and heart rate did not change significantly, while plasma renin activity increased from 3.8 +/- 0.9 to 10.8 +/- 3.1 ng/ml/3h (P less than 0.005), and plasma corticosteroid concentration increased from 1.5 +/- 0.8 to 8.6 +/- 2.0 microgram/dl (P less than 0.001). Following vasopressin blockade, the same hemorrhage decreased mean arterial pressure from 96 +/- 264 +/- 7 mmHg (P less than 0.001), increased heart rate from 71 +/- 10 to 130 +/- 23 beats/min (P less than 0.05), increased plasma renin activity from 7.1 +/- 0.8 to 30.3 +/- 6.7 ng/ml/3h (P less than 0.005) and increased plasma corticosteroid concentration from 1.9 +/- 0.7 to 11.4 +/- 1.2 microgram/dl (P less than 0.001). These data indicate that vasopressin plays an important role in blood pressure regulation during mild hemorrhage in conscious dogs.

Adrenal Cortex Hormones↗