Electrical stimulation of the sinus nerve or excitation of the carotid baroceptors by increasing the intrasinus pressure significantly decreased the right ventricular contractile force, heart rate, and blood pressure in 19 anesthetized cats. The decreases in force and rate, but not blood pressure, were abolished by stellate ganglionectomy and by 3–6 mg/kg of dichloroisoproterenol (DCI). The decreases in cardiac contractility and rate were not secondary to the hypotension for they were still obtained when aortic pressure was kept constant. The reductions in contractile force and heart rate are the results of an inhibition of sympathetic control of the heart activity. The data indicates that 40 per cent of contractile force measured in the anesthetixed vagotomized preparation is dependent upon tonic sympathetic impulses. In experiments in which the stellate ganglia were decentralized, the force and rate were increased to predenervation levels by stimulating the isolated right stellate ganglion at a frequency of 1/sec. Seventy-five per cent of the maximum response in force and rate were obtained at stimulus frequencies of 3/sec. The sinus baroceptor reflex exercises its major effects on the heart and blood vessels within a relatively limited range of 40 mm Hg on either side of normal blood pressure for the cat.

Acta Anaesthesiologica ScandinavicaVolume 8, Issue s15 p. 34-35 NEUROTRANSMISSION AT THE CHOLINERGIC NERVE ENDINGS Percy Lindgren, Percy Lindgren StockholmSearch for more papers by this author Percy Lindgren, Percy Lindgren StockholmSearch for more papers by this author First published: December 1964 https://doi.org/10.1111/j.1399-6576.1964.tb00256.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume8, Issues15December 1964Pages 34-35 RelatedInformation

Acta Pharmacologica et ToxicologicaVolume 17, Issue 1 p. 69-83 Parasympatholytic Effects of TMB-4 [1,1-Trimethylene-bis (4-formylpyridinium Bromide)-dioximel and some related Oximes in the Cat *). Percy Lindgren, Percy Lindgren Department of Pharmacology (Professor Börje Uvnäs, M.D.), Karolinska Institutet, Stockholm 60; and the Research Institute of National Defence, Dept. 1 (Professor Gustaf Ljunggren, Ph.D., M. D.), Sundbyberg 4, Sweden.Search for more papers by this authorAnders Sundwall, Anders Sundwall Department of Pharmacology (Professor Börje Uvnäs, M.D.), Karolinska Institutet, Stockholm 60; and the Research Institute of National Defence, Dept. 1 (Professor Gustaf Ljunggren, Ph.D., M. D.), Sundbyberg 4, Sweden.Search for more papers by this author Percy Lindgren, Percy Lindgren Department of Pharmacology (Professor Börje Uvnäs, M.D.), Karolinska Institutet, Stockholm 60; and the Research Institute of National Defence, Dept. 1 (Professor Gustaf Ljunggren, Ph.D., M. D.), Sundbyberg 4, Sweden.Search for more papers by this authorAnders Sundwall, Anders Sundwall Department of Pharmacology (Professor Börje Uvnäs, M.D.), Karolinska Institutet, Stockholm 60; and the Research Institute of National Defence, Dept. 1 (Professor Gustaf Ljunggren, Ph.D., M. D.), Sundbyberg 4, Sweden.Search for more papers by this author First published: August 1960 https://doi.org/10.1111/j.1600-0773.1960.tb01231.xCitations: 20 * ) A preliminary report was presented at the Scandinavian Congress of Biochemistry, Physiology and Pharmacology in Åbo, Finland, August 27-29, 1959. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume17, Issue1August 1960Pages 69-83 RelatedInformation

In a previous investigation it was observed that activation of the sympathetic vasodilator outflow by hypothalamic stimulation was accompanied by a discharge of catechols from the adrenals, consisting mainly of adrenaline. The present experiments were undertaken in order to study the adrenal function during medullary stimulation of this pathway. The catechol output from one adrenal gland was observed to increase on activation of the sympathetic vasodilator outflow by bulbar stimulation. Adrenaline increased relatively more than noradrenaline. The mean values for the adrenaline output in the control samples and those taken during the stimulation periods were 0.05 and 0.22 μg/kg/min (increase 340 per cent). The corresponding figures for noradrenaline were 0.22 and 0.50 μag/kg/min (increase 130 per cent). The findings are in accordance with our previous results showing that intracerebral stimulation of the sympathetic vasodilator outflow is accompanied by a discharge of catechols – predominantly adrenaline – from the adrenals. The amounts secreted are of such a low magnitude as to have only minor vascular effects.

Summary. The amount of catechols secreted from the adrenal glands concomitant with activation of the sympathetic vasodilator outflow by hypothalamic stimulation was studied in 14 cats. Blood samples from the left adrenal vein were collected during control and stimulation periods, and were tested (rat uterus and rat colon) after separating adrenaline and noradrenaline by paper chromatography. The mean values for the adrenaline output in the control samples and those taken during hypothalamic stimulation of the sympathetic vasodilator area were 0.06 and 0.32 μg/kg/min (increase 433 per cent). The corresponding figures for noradrenaline were 0.19 and 0.35 μg/kg/min (increase 84 per cent). As will be seen from these values the increase of catechol output consisted predominantly of adrenaline. The conclusion is drawn that in most experiments the amounts of adrenaline released were of such a low magnitude as to have only minor vascular effects, they may have been sufficient to produce metabolic effects. The findings are discussed in view of our hypothesis that activation of the vasodilator outflow under physiologic conditions is an integral part of emergency reactions.

Summary. Vasodilatation in the skeletal muscles is produced by electric stimulation of a sinus nerve, a vagus nerve, the depressor area of the oblongate medulla or by activation of sympathetic vasodilator nerves. Destruction of the depressor area does not prevent the transmission of impulses in the bulbar sympathetic vasodilator tract. The depressor area and the bulbar part of the sympathetic vasodilator tract seem to be separate anatomical and functional entities. The writers have been unable to activate the two vasodilator mechanisms simultaneously, a fact that is regarded to support the conception that they form two independently operating mechanisms. The expenses of this investigation were partly defrayed by a grant from the Swedish Medical Research Council to one of us (B. U.) which is gratefully acknowledged.

Acta Physiologica ScandinavicaVolume 29, Issue 2-3 p. 137-144 Vasodilator Responses in the Skeletal Muscles of the Dog to Electrical Stimulation in the Oblongate Medulla PERCY LINDGREN, PERCY LINDGREN Department of Pharmacology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorBÖRJE UVNÄS, BÖRJE UVNÄS Department of Pharmacology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this author PERCY LINDGREN, PERCY LINDGREN Department of Pharmacology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this authorBÖRJE UVNÄS, BÖRJE UVNÄS Department of Pharmacology, Karolinska Institutet, Stockholm, SwedenSearch for more papers by this author First published: April 1953 https://doi.org/10.1111/j.1748-1716.1953.tb01012.xCitations: 12AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume29, Issue2-3April 1953Pages 137-144 RelatedInformation

Acta Physiologica ScandinavicaVolume 27, Issue 1 p. 17-37 Representation in the Hypothalamus and the Motor Cortex in the Dog of the Sympathetic Vasodilator Outflow to the Skeletal Muscles. SVEN ELIASSON, SVEN ELIASSON Department of Physiology, University of Lund.Search for more papers by this authorPERCY LINDGREN, PERCY LINDGREN Department of Physiology, University of Lund.Search for more papers by this authorBÖRJE UVNÄS., BÖRJE UVNÄS. Department of Physiology, University of Lund.Search for more papers by this author SVEN ELIASSON, SVEN ELIASSON Department of Physiology, University of Lund.Search for more papers by this authorPERCY LINDGREN, PERCY LINDGREN Department of Physiology, University of Lund.Search for more papers by this authorBÖRJE UVNÄS., BÖRJE UVNÄS. Department of Physiology, University of Lund.Search for more papers by this author First published: January 1953 https://doi.org/10.1111/j.1748-1716.1953.tb00921.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume27, Issue1January 1953Pages 17-37 RelatedInformation

Acta Physiologica ScandinavicaVolume 23, Issue 4 p. 333-351 Activation of Sympathetic Vasodilator Nerves to the Skeletal Muscles in the Cat by Hypothalamic Stimulation SVEN ELIASSON, SVEN ELIASSON Department of Physiology, University of LundSearch for more papers by this authorBJÖRN FOLKOW, BJÖRN FOLKOW Department of Physiology, University of LundSearch for more papers by this authorPERCY LINDGREN, PERCY LINDGREN Department of Physiology, University of LundSearch for more papers by this authorBÖRJE UVNÄS, BÖRJE UVNÄS Department of Physiology, University of LundSearch for more papers by this author SVEN ELIASSON, SVEN ELIASSON Department of Physiology, University of LundSearch for more papers by this authorBJÖRN FOLKOW, BJÖRN FOLKOW Department of Physiology, University of LundSearch for more papers by this authorPERCY LINDGREN, PERCY LINDGREN Department of Physiology, University of LundSearch for more papers by this authorBÖRJE UVNÄS, BÖRJE UVNÄS Department of Physiology, University of LundSearch for more papers by this author First published: December 1951 https://doi.org/10.1111/j.1748-1716.1951.tb00819.xCitations: 159AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume23, Issue4December 1951Pages 333-351 RelatedInformation