COMPARATIVE BLOOD PRESSURE AND ELECTROCARDIOGRAPHIC CHANGES INDUCED BY PROSCILLARIDIN AND OUABAIN

1966 ◽  
Vol 44 (6) ◽  
pp. 887-892 ◽  
Author(s):  
K. I. Melville ◽  
H. E. Shister ◽  
B. Klingner
Keyword(s):  
Blood Pressure ◽  
Ventricular Fibrillation ◽  
Ventricular Arrhythmias ◽  
Pressor Response ◽  
The Other ◽  
Onset Of Action ◽  
Qualitative And Quantitative ◽  
Arterial Blood ◽  
Electrocardiographic Changes ◽  
Quantitative Changes

Femoral arterial blood pressure and electrocardiograms (ECG, lead II) were recorded concurrently in artificially respired cats anesthetized with pentobarbital, and responses to the new squill glycoside, proscillaridin (Talusin), and to ouabain were compared. All drugs were injected intravenously, in groups of five cats for each dose level. Following single injections, it was observed that doses of 150 μg of proscillaridin/kg produced only slight increases in blood pressure and slight bradycardia, but no change in the ECG pattern. In contrast, similar doses of ouabain or doses of 500 μg of proscillaridin/kg produced bradycardia, ventricular arrhythmias, and fibrillation in all experiments. Whereas striking pressor effects were noted with ouabain those due to proscillaridin were slight. With continuous infusions, proscillaridin and ouabain in doses of 5 μg/kg per minute led to similar qualitative and quantitative changes (bradycardia, arrhythmias, and ventricular fibrillation), but these developed more slowly with proscillaridin. Infusions of proscillaridin in doses of 2.5 μg/kg per minute also produced similar but still more delayed changes. Doses of 15 μg/kg per minute of proscillaridin, on the other hand, produced all the effects more rapidly than 5 μg/kg per minute of ouabain, but the pressor response was again less pronounced. It is concluded that (a) proscillaridin exerts characteristic digitalis-like effects; (b) when single intravenous doses are compared, proscillaridin is approximately one-third as toxic to the heart as ouabain; (c) when continuous intravenous infusions are compared, proscillaridin shows variable onset of action depending on dosage and is approximately one-half as toxic as ouabain; and (d) in all experiments proscillaridin exerts less marked pressor effects than ouabain. The drug is being further studied.

Augmented pressor response to vasopressin in awake dogs after cardiac denervation

1987 ◽  
Vol 252 (1) ◽  
pp. R145-R152
Author(s):  
B. C. Wang ◽  
G. F. Ginter ◽  
K. L. Goetz
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Pressor Response ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
The Other ◽  
Cardiac Denervation ◽  
Arterial Blood ◽  
Cardiac Receptors

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.

Changes in Seryl-tRNA Formative in Developing Chick Muscle

1974 ◽  
Vol 52 (10) ◽  
pp. 838-844 ◽  
Author(s):  
Mark Nwagwu ◽  
John Lianga
Keyword(s):  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Deae Cellulose ◽  
The Other ◽  
Embryonic Chick ◽  
Qualitative And Quantitative ◽  
Embryonic Muscle ◽  
Quantitative Changes ◽  
The One

As a prelude to an analysis of the dependence of muscle protein synthesis on aminoacyl tRNA's, we have investigated the rates of seryl-tRNA formation, in vitro, by aminoacylating systems isolated from 11-, 14-, and 17-day chick embryonic muscle. The results show that the combination of 14-day tRNA and 14-day aminoacyl synthetase is the most efficient in seryl-tRNA formation. We have also studied the qualitative and quantitative changes in seryl-tRNA prepared from 11-, 14-, and 17-day embryonic chick muscle by chromatography of seryl-tRNA on benzoylated DEAE-cellulose columns. The results show that, although there are no qualitative differences in the chromatographic patterns of seryl-tRNA from the different ages, there are significant quantitative differences between the patterns for 11-day and 17-day seryl-tRNA on the one hand, and the pattern for 14-day seryl-tRNA on the other.

The effect of lidocaine when used as a local anesthetic or by intravenous injection

2021 ◽  
Vol 1 (4) ◽  
pp. 234-237
Author(s):  
Hamza Khalifa , ,, , Ibrahim ◽  
Abdulfatah Saed ◽  
Naser Ramdan R. Amaizah ◽  
Aejeeliyah Yousuf ◽  
Malak Abdalh Akim Esdera
Keyword(s):  
Myocardial Infarction ◽  
Local Anesthetic ◽  
Ventricular Arrhythmias ◽  
Rapid Onset ◽  
The Other ◽  
Important Class ◽  
Onset Of Action ◽  
Digitalis Poisoning ◽  
Duration Of Efficacy ◽  
Efficacy Profile

The efficacy profile of lidocaine as a local anesthetic is characterized by a rapid onset of action and an intermediate duration of efficacy. Therefore, lidocaine is suitable for infiltration, block, and surface anesthesia. Longer-acting substances such as bupivacaine are sometimes given preference for spinal and peridural anesthesias, however, lidocaine, on the other hand, has the advantage of a rapid onset of action. Adrenaline supplements could delay the resorption and the duration of efficacy could be doubled. Lidocaine is the most important class 1B antiarrhythmic drug: it is used intravenously for the treatment of ventricular arrhythmias (for acute myocardial infarction, digitalis poisoning, cardioversion, or cardiac catheterization). However, a routine prophylactic administration is no longer recommended for acute cardiac infarction. The overall benefit of this measure is not convincing. Lidocaine has also been efficient in refractory cases of status epilepticus.

Blood pressure during routine activity, stress, and feeding in black racer snakes (Coluber constrictor)

1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Acute Stress ◽  
Pressor Response ◽  
Routine Activity ◽  
Plasma Norepinephrine ◽  
Arterial Blood ◽  
Coluber Constrictor ◽  
S Peak ◽  
Hematological Changes

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.

Interaction of bradykinin and prostaglandin E1 on cardiac pressor reflex and sympathetic afferents

1986 ◽  
Vol 250 (5) ◽  
pp. R815-R822 ◽  
Author(s):  
T. Nerdrum ◽  
D. G. Baker ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Blood Pressure ◽  
Prostaglandin E1 ◽  
Pressor Response ◽  
Interactive Effect ◽  
Small Reduction ◽  
Arterial Blood ◽  
Repeated Applications ◽  
Pressor Reflex ◽  
Cardiac Afferents ◽  
Afferent Response

Bradykinin applied to the epicardium stimulates cardiac sympathetic afferents and evokes a reflex increase in arterial blood pressure. In anesthetized cats we examined the potentiation of these effects by prostaglandin E1 (PGE1) applied to the ventricular epicardium. We recorded cardiac afferent impulses from the second to the fifth left thoracic sympathetic rami. PGE1 (0.1 microgram/ml) alone had little effect on blood pressure, but it significantly increased the pressor response to bradykinin, and it reduced or abolished tachyphylaxis to repeated applications of bradykinin. Both mechanosensitive and chemosensitive sympathetic cardiac afferents were stimulated by bradykinin. Indomethacin (intravenous) caused a small reduction in the afferent response to bradykinin. Epicardial application of PGE1 significantly increased the response (magnitude and duration) of chemosensitive endings to bradykinin but not that of mechanosensitive endings; however, PGE1 abolished the tachyphylaxis of both chemosensitive and mechanosensitive endings to repeated applications of bradykinin. Because both bradykinin and prostaglandins are released in the ischemic myocardium, their interactive effect on cardiac sympathetic afferents could play a part in the sensory and reflex responses to myocardial ischemia.

Mechanism of circulatory responses to systemic hypoxia in the anesthetized dog

1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
The Other ◽  
Arterial Flow ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.

Abnormalities of peripheral venous tone in women with pregnancy-induced hypertension

1986 ◽  
Vol 70 (2) ◽  
pp. 155-157 ◽  
Author(s):  
Karen Stainer ◽  
Rachel Morrison ◽  
C. Pickles ◽  
A. J. Cowley
Keyword(s):  
Blood Pressure ◽  
Pregnant Women ◽  
Inverse Correlation ◽  
The Other ◽  
Normal Blood ◽  
Pregnancy Induced Hypertension ◽  
Normal Blood Pressure ◽  
Venous Tone ◽  
Arterial Blood ◽  
Induced Hypertension

1. Forearm venous tone was measured in two groups of pregnant women: one group with pregnancy-induced hypertension and the other group with normal blood pressure. 2. The women with pregnancy-induced hypertension were venoconstricted in the forearm (P < 0.01) compared with the pregnant women with normal blood pressure. However, there was no difference in venous tone between the women with pregnancy-induced hypertension and nonpregnant women. 3. There was an inverse correlation between mean arterial blood pressure and forearm venous tone (r = −0.581, P < 0.001) for all the pregnant women studied. Further evaluation of peripheral venous tone may provide valuable information about the pathophysiology and treatment of women with pregnancy-induced hypertension.

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Interleukin 1 ◽  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Interleukin 1 Beta ◽  
Pronounced Increase ◽  
Arterial Blood

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

In vitro and in vivo inhibition of renin by fatty acids.

1978 ◽  
Vol 234 (6) ◽  
pp. E593 ◽  
Author(s):  
T A Kotchen ◽  
W J Welch ◽  
R T Talwalkar
Keyword(s):  
Blood Pressure ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Angiotensin Ii ◽  
Neutral Lipids ◽  
Pressor Response ◽  
Arterial Blood ◽  
Arachidonic Acids

Circulating neutral lipids inhibit the in vitro renin reaction. To identify the inhibitor(s), free fatty acids were added to human renin and homologous substrate. Capric, lauric, palmitoleic, linoleic, and arachidonic acids each inhibited the rate of angiotensin I production in vitro (P less than 0.01). Inhibition by polysaturated fatty acids (linoleic and arachidonic) was less (P less than 0.01) after catalytic hydrogenation of the double bonds. To evaluate an in vivo effect of renin inhibition intra-arterial blood pressure responses to infusions of renin and angiotensin II (5.0 microgram) were measured in anephric rats (n = 6) before and after infusion of linoleic acid (10 mg iv). Mean increase of blood pressure to angiotensin II before (75 mmHg +/- 9) and after (90 +/- 12) linoleic acid did not differ (P greater than 0.05). However, the pressor response to renin after linoleic acid (18 +/- 3) was less (P less than 0.00)) than that before (102 +/- 13). In summary, several fatty acids inhibit the in vitro renin reaction, and in part inhibition is dependent on unsaturation. Linoleic acid also inhibits the in vivo pressor response to renin. These results suggest that fatty acids may modify the measurement of plasma renin activity and may also affect angiotensin production in vivo.

Muscle chemoreflex alters vascular conductance in nonischemic exercising skeletal muscle

1994 ◽  
Vol 77 (6) ◽  
pp. 2761-2766 ◽  
Author(s):  
S. W. Mittelstadt ◽  
L. B. Bell ◽  
K. P. O'Hagan ◽  
P. S. Clifford
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Response To Exercise ◽  
Muscle Chemoreflex

Previous studies have shown that the muscle chemoreflex causes an augmented blood pressure response to exercise and partially restores blood flow to ischemic muscle. The purpose of this study was to investigate the effects of the muscle chemoreflex on blood flow to nonischemic exercising skeletal muscle. During each experiment, dogs ran at 10 kph for 8–16 min and the muscle chemoreflex was evoked by reducing hindlimb blood flow at 4-min intervals (0–80%). Arterial blood pressure, hindlimb blood flow, forelimb blood flow, and forelimb vascular conductance were averaged over the last minute at each level of occlusion. Stimulation of the muscle chemoreflex caused increases in arterial blood pressure and forelimb blood flow and decreases in forelimb vascular conductance. The decrease in forelimb vascular conductance demonstrates that the muscle chemoreflex causes vasoconstriction in the nonischemic exercising forelimb. Despite the decrease in vascular conductance, the increased driving pressure caused by the pressor response was large enough to produce an increased forelimb blood flow.

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