Effects of central osmotic stimulation on vasopressin and enkephalin release into the blood and cerebrospinal fluid and blood pressure

1990 ◽  
Vol 122 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Kozo Ota ◽  
Tokihisa Kimura ◽  
Kuniaki Matsui ◽  
Kazuhiro Iitake ◽  
Masaru Shoji ◽  
...  

Abstract To assess the central effect of hypertonic NaCl on the release of vasopressin (AVP) and methionine enkephalin-like substances into the blood and cerebrospinal fluid, and on blood pressure, ventriculocisternal perfusion (0.25 ml/min, 60 min) was performed in anesthetized dogs with artificial cerebrospinal fluid (CSF), either isotonic (300 mosmol/kg) or hypertonic (600 and 1200 mosmol/kg). The effect of central administration of a V1-AVP antagonist on the central osmotic challenge was also studied. In dogs, given 600 mosmol/kg, CSF osmolality increased with a concomitant rise in mean arterial pressure and plasma AVP concentrations. Plasma osmolality, heart rate, CSF AVP and plasma and CSF methionine enkephalin-like substances showed no significant change. In dogs, given 1200 mosmol/kg, the CSF osmolality increase was accompanied by a rise in mean arterial pressure, heart rate, plasma AVP and CSF AVP. Plasma osmolality and plasma and CSF methionine-enkephalinlike substances did not change significantly. A V1-AVP antagonist given centrally attenuated the rise in mean arterial pressure induced by osmotic challenge. In dogs, given 300 mosmol/kg, no parameters changed significantly except for a gradual fall in heart rate. These results suggest that central osmotic stimulation by hypertonic NaCl increases blood pressure, heart rate and the release of AVP, but not methionine enkepholin-like substances, into the blood and CSF, and a V1-blocker given centrally attenuates the pressor response.

1998 ◽  
Vol 94 (1) ◽  
pp. 49-55 ◽  
Author(s):  
Sharmini Puvi-Rajasingham ◽  
Gareth D. P. Smith ◽  
Adeola Akinola ◽  
Christopher J. Mathias

1. In human sympathetic denervation due to primary autonomic failure, food and exercise in combination may produce a cumulative blood pressure lowering effect due to simultaneous splanchnic and skeletal muscle dilatation unopposed by corrective cardiovascular reflexes. We studied 12 patients with autonomic failure during and after 9 min of supine exercise, when fasted and after a liquid meal. Standing blood pressure was also measured before and after exercise. 2. When fasted, blood pressure fell during exercise from 162 ± 7/92 ± 4 to 129 ± 9/70 ± 5 mmHg (mean arterial pressure by 22 ± 5%), P < 0.0005. After the meal, blood pressure fell from 159 ± 8/88 ± 6 to 129 ± 6/70 ± 4 mmHg (mean arterial pressure by 22 ± 3%), P < 0.0001, and further during exercise to 123 ± 6/61 ± 3 mmHg (mean arterial pressure by 9 ± 3%), P < 0.01. The stroke distance—heart rate product, an index of cardiac output, did not change after the meal. During exercise, changes in the stroke distance—heart rate product were greater when fasted. 3. Resting forearm and calf vascular resistance were higher when fasted. Calf vascular resistance fell further after exercise when fasted. Resting superior mesenteric artery vascular resistance was lower when fed; 0.19 ± 0.02 compared with 032 ± 0.06, P < 0.05. After exercise, superior mesenteric artery vascular resistance had risen by 82%, to 0.53 ± 0.12, P < 0.05 (fasted) and by 47%, to 0.29 ± 0.05, P < 0.05 (fed). 4. On standing, absolute levels of blood pressure were higher when fasted [83 ± 7/52 ± 7 compared with 71 ± 2/41 ± 3 (fed), each P < 0.05]. Subjects were more symptomatic on standing post-exercise when fed. 5. In human sympathetic denervation, exercise in the fed state lowered blood pressure further than when fasted and worsened symptoms of postural hypotension.


Author(s):  
Sidharth Sraban Routray ◽  
Ramakanta Mohanty

ABSTRACTObjective: During laparoscopic surgeries, pneumoperitoneum can lead to various pathophysiologic changes in the cardiovascular system resulting inhypertension and tachycardia. Search for ideal drug to prevent this hemodynamic response goes on. The aim of our study was to evaluate the effect oforally administered moxonidine in attenuating the hemodynamic responses that occur during the laparoscopic surgeries.Methods: A total of 50 adult acetylsalicylic acid I and II patients scheduled for elective laparoscopic surgeries were selected for this prospectiverandomized double-blinded study. They were randomly allocated into two groups: moxonidine group (M) and placebo group (P). M group receivedoral moxonidine 0.3 mg at 8 pm on the day before surgery and at 8 am on the day of surgery. P group received a placebo at the same timing as that ofthe M group.Results: Following pneumoperitoneum rise in systolic blood pressure (SBP), diastolic BP (DBP), mean arterial pressure (MAP), and heart rate (HR)was higher in P group in comparison to M group which was statistically significant.Conclusion: Significant rise in HR, SBP, DBP, and mean BP was noted in the P group in comparison to moxonidine group. Moxonidine provided betterperioperative hemodynamic stability in patients undergoing laparoscopic surgeries.Keywords: Moxonidine, Stress response, Laparoscopic.


2020 ◽  
Vol 9 (1) ◽  
pp. 8-15
Author(s):  
Arya Justisia Sani ◽  
Ardhana Tri Arianto ◽  
Muhammad Husni Thamrin

Latar Belakang dan Tujuan: Peningkatan respon hemodinamik yang disebabkan oleh nyeri dapat menyebabkan peningkatan aliran darah otak dan tekanan intrakranial. Blok scalp pada kraniotomi menumpulkan respon hemodinamik karena rangsangan nyeri serta mengurangi penambahan analgesi lain. Penelitian ini bertujuan untuk mengetahui efektifitas blok scalp sebagai analgetik pada kraniotomi.Subjek dan Metode: Penelitian ini menggunakan uji klinik acak tersamar ganda pada 36 pasien dengan status fisik ASA 1–3 dilakukan operasi kraniotomi eksisi dan memenuhi kriteria inklusi. Sampel dibagi menjadi kelompok I (dengan blok scalp) dan kelompok II (tanpa blok scalp). Blok dilakukan sesaat setelah induksi anestesi. Digunakan levobupivakain 0,375% sebanyak 3 ml tiap insersi, pada masing-masing saraf. Tekanan darah, tekanan arteri rata-rata, detak jantung sebelum intubasi dan setelah intubasi, pemasangan pin, insisi kulit dan insisi duramater serta total kebutuhan fentanyl tambahan dicatat. Data yang diperoleh dianalisis dengan program komputer SPSS versi 17 lalu diuji menggunakan uji Kruskal-Wallis atau One-way ANOVA. Batas kemaknaan yang diambil adalah p < 0,05.Hasil: Selama kraniotomi, detak jantung, tekanan darah, tekanan arteri rata-rata secara signifikan lebih tinggi pada pasien tanpa blok scalp terutama pada saat pemasangan pin. Hasil uji statistik menunjukkan perbedaan signifikan, penambahan fentanyl pada pasien dengan blok scalp lebih sedikit dibandingkan tanpa blok scalp, p=0,000 (p<0,05).Simpulan: Blok scalp levobupivakain efektif dalam menurunkan respon hemodinamik terutama pada saat pemasangan pin. Pasien kraniotomi dengan blok scalp membutuhkan penambahan fentanyl lebih sedikit. Differences on Hemodynamic Response with Levobupivacaine Scalp Block in Craniotomy SurgeryAbstractBackground and Objective: Increased hemodynamic response caused by pain can lead to increased cerebral blood flow and intracranial pressure. Scalp block in craniotomy blunts hemodynamic response due to pain and reduce other analgesics addition. This study aims to determine effectiveness of scalp blocks as analgesic in craniotomy.Subject and Method: This study used a double-blind randomized clinical trial in 36 patients with physical status ASA 1-3 who underwent craniotomy and met inclusion criteria. Samples were divided into group I (with scalp block) and group II (without scalp block). Scalp Block was performed right after anesthesia induction. Using levobupivacaine 0.375% 3 ml for each insertion. Blood pressure, mean arterial pressure, heart rate before and after intubation, during pin placement, skin incision and duramater incision and total need for additional fentanyl were recorded. SPSS version 17 was used and data were analysed using Kruskal-Wallis or One-way ANOVA. Statistical significance was accepted at p < 0.05.Result: During craniotomy, heart rate, blood pressure, mean arterial pressure were significantly higher in patients without scalp block especially during pin placement. Statistical test showed significant difference, additional fentanyl in patients with scalp blocks was lesser, p = 0.000 (p <0.05). Conclusion: Levobupivacaine scalp block was effective to blunt hemodynamic response especially during pin placement. Scalp block also decreased additional fentanyl in craniotomy.


1995 ◽  
Vol 79 (5) ◽  
pp. 1546-1555 ◽  
Author(s):  
B. Pannier ◽  
M. A. Slama ◽  
G. M. London ◽  
M. E. Safar ◽  
J. L. Cuche

Pulsatile changes in blood pressure and arterial diameter were studied noninvasively with applanation tonometry and echo-tracking techniques at the sites of the common carotid artery (CCA) and the carotid arterial bulb (CAB) in 12 healthy volunteers. Determinations were performed before and during application of -10 and -40 mmHg lower body negative pressure (LBNP) to investigate noninvasively the tensile forces acting on the CAB. Together with significantly decreased mean arterial pressure, increased heart rate, forearm vascular resistance, and plasma norepinephrine, the -40 mmHg LBNP stimulus produced the following significant changes in CCA and CAB hemodynamics: 1) for the same decrease in mean arterial pressure, a greater decrease in carotid than in brachial pulse pressure was observed (P < 0.01) due to a significant change in pressure wave transmission and in the timing of the carotid backward pressure wave; and 2) a highly significant decrease in pulsatile changes in diameter and tangential tension occurred, with a greater decrease in systolic than in diastolic tangential tension. Subsequently, cyclic tangential tension decreased more substantially than mean tangential tension. The cyclic changes in tension were quite significant after -40 mmHg LBNP but were already observed for mild -10 mmHg LBNP in which mean systemic blood pressure and heart rate were not modified. During -10 and -40 mmHg LBNP, CCA and CAB compliance and distensibility were unchanged. This study provides evidence that the autonomic nervous system activation produced by the LBNP procedure is associated with significant changes in pressure-wave amplification and in cyclic tensile forces acting on the CAB. These changes, which may occur even for mild LBNP, should be taken into account when interpreting results of the LBNP procedure in humans.


1991 ◽  
Vol 260 (3) ◽  
pp. E333-E337 ◽  
Author(s):  
C. K. Klingbeil ◽  
V. L. Brooks ◽  
E. W. Quillen ◽  
I. A. Reid

Angiotensin II causes marked stimulation of drinking when it is injected centrally but is a relatively weak dipsogen when administered intravenously. However, it has been proposed that the dipsogenic action of systemically administered angiotensin II may be counteracted by the pressor action of the peptide. To test this hypothesis, the dipsogenic action of angiotensin II was investigated in dogs, in which low and high baroreceptor influences had been eliminated by denervation of the carotid sinus, aortic arch, and heart. In five sham-operated dogs, infusion of angiotensin II at 10 and 20 ng.kg-1.min-1 increased plasma angiotensin II concentration to 109.2 +/- 6.9 and 219.2 +/- 38.5 pg/ml and mean arterial pressure by 20 and 29 mmHg, respectively, but did not induce drinking. In four baroreceptor-denervated dogs, the angiotensin II infusions produced similar increases in plasma angiotensin II concentration and mean arterial pressure but, in contrast to the results in the sham-operated dogs, produced a dose-related stimulation of drinking. Water intake with the low and high doses of angiotensin II was 111 +/- 44 and 255 +/- 36 ml, respectively. The drinking responses to an increase in plasma osmolality produced by infusion of hypertonic sodium chloride were not different in the sham-operated and baroreceptor-denervated dogs. These results demonstrate that baroreceptor denervation increases the dipsogenic potency of intravenous angiotensin II and provides further support for the hypothesis that the dipsogenic action of intravenous angiotensin II is counteracted by the rise in blood pressure.


1982 ◽  
Vol 62 (2) ◽  
pp. 137-141 ◽  
Author(s):  
L. Andrén ◽  
G. Lindstedt ◽  
M. Björkman ◽  
K. O. Borg ◽  
L. Hansson

1. Noise stimulation (95 dBA) for 20 min caused a significant increase in diastolic (12%, P < 0.001) and mean arterial pressure (7%, P < 0.001) in 15 healthy normotensive male subjects. 2. There was no significant change in systolic blood pressure or heart rate during exposure to noise. 3. Adrenaline, noradrenaline, prolactin, cortisol and growth hormone concentrations in venous plasma were not affected during noise stimulation.


2007 ◽  
Vol 292 (2) ◽  
pp. R937-R945 ◽  
Author(s):  
Orville A. Smith ◽  
Cliff A. Astley

Hypertension is a prominent underlying factor in the genesis of cardiovascular-related morbidity and mortality. A major impediment to the investigation into the causes of the disease is the paucity of naturally occurring animal models of the disease. There is evidence that some species of New World primates spontaneously become hypertensive. We used chronically implanted pressure transducers to assess normally occurring blood pressure and heart rate levels at rest and during routine laboratory procedures in a group of one of these New World primates ( Aotus sp.). Resting mean arterial pressure ranged from 72 to 130 mmHg. Three animals were judged to have resting mean arterial pressure levels in the hypertensive range (≥110 mmHg). In all of the animals, pressor responses to routine laboratory events were exaggerated (average highest mean pressure during 1 min from any session was 97–196 mmHg). Subsequently, the region of the perifornical/lateral hypothalamus known to produce elevated blood pressure and heart rate responses to electrical stimulation was removed, and the blood pressure responses to the laboratory routines were significantly decreased and, in some cases, eliminated. Control lesions in nearby tissue had no effect on these responses. This region may play a critical role in initiating or exacerbating cardiovascular responses that contribute to the development of essential hypertension.


2016 ◽  
Vol 3 (1) ◽  
pp. 22-27 ◽  
Author(s):  
Manisha Pradhan ◽  
Brahma Dev Jha

Background: The ideal method to prevent hypotension due to intravenous propofol for induction of anesthesia is still debatable. The aim of the study was to compare the hemodynamic response of ephedrine and volume loading with ringer lactate in preventing the hypotension caused by propofol as inducing agent in patients scheduled for elective surgeries requiring general anesthesia with endotracheal intubation.Methods: This was prospective randomized study conducted in 40 patients of ASA physical status I, aged 20-50 years, scheduled for elective surgeries requiring general anesthesia with endotracheal intubation. Group I received intravenous ephedrine sulphate (70 mcg/kg) just before induction of anaesthesia, and patients assigned to Group II received preloading with Ringer's lactate (12 ml/kg) over the 10-15 minutes before the administration of propofol. The variables compared were heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure following induction of anesthesia till 10 minutes after intubation of trachea.Results: We found that there were increase in systolic blood pressure, diastolic blood pressure and mean arterial pressure after induction in both the groups but the difference between the groups was not significant. The increase in heart rate was found to be significantly higher in ephedrine group in comparison to volume loading group.Conclusion: Our study showed that both the methods used were equally effective in preventing hypotension induced by propofol in the adult ASA physical status I patients requiring general anesthesia with endotracheal intubation. However, the heart rate was significantly higher in patients receiving ephedrine in comparison to volume loading group.


1983 ◽  
Vol 244 (1) ◽  
pp. R74-R77 ◽  
Author(s):  
J. Schwartz ◽  
I. A. Reid

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.


1989 ◽  
Vol 257 (4) ◽  
pp. R762-R764 ◽  
Author(s):  
T. D. Williams ◽  
J. R. Seckl ◽  
S. L. Lightman

The act of drinking causes a fall in plasma arginine vasopressin (AVP) concentration that precedes changes in plasma osmolality. To investigate the specificity of this drinking stimulus on hormone secretion, six volunteers (5 male, 1 female, aged 22-39 yr) were water deprived for 36 h and then drank 15 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.5 +/- 0.5 min (mean +/- SE). This caused a fall in plasma AVP from 4.5 +/- 0.7 to 3.2 +/- 0.5 pmol/l (P less than 0.05) and in thirst (by 5.7 +/- 0.6 on a 10-cm linear analog scale) (P less than 0.05) 5 min after drinking. No significant changes occurred in mean arterial pressure, heart rate, or plasma atrial natriuretic peptide (ANP) concentration. A second study was undertaken to determine whether the reflex inhibition of AVP secretion is activated simply by the act of swallowing regardless of the volume of liquid consumed. The six volunteers were water deprived for 36 h and then sipped and swallowed 1 ml/kg water at 10-12 degrees C using 15-20 swallowing actions/min over 3.0 +/- 0.1 min. There was no change in plasma AVP concentration, although thirst was reduced by 2.3 +/- 0.6 (P less than 0.05) at 5 min. Plasma AVP 10 min after sipping and swallowing (4.2 +/- 0.8 pmol/l) was significantly greater than at 10 min after drinking 15 ml/kg (2.8 +/- 0.5 pmol/l) (P less than 0.05) despite the fact that plasma osmolality at this stage was similar in both studies. We conclude that the drinking-mediated reflex inhibition of AVP secretion in humans is dependent on swallowing an adequate volume and is not accompanied by changes in hemodynamics or in plasma ANP concentration.


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