Effect of sinoaortic denervation on pressor responses in pregnant rats

1992 ◽  
Vol 262 (6) ◽  
pp. R1100-R1105 ◽  
Author(s):  
T. Hines ◽  
W. M. Barron

We tested the hypothesis that augmented arterial baroreflex activity contributes to attenuation of pressor responses in intact pregnant animals by comparing changes in blood pressure and heart rate during infusions of angiotensin II, phenylephrine, and vasopressin in chronically instrumented pregnant and virgin rats approximately 5 wk after sinoaortic denervation (SAD) or sham surgery. Baseline mean arterial pressure was significantly lower in pregnant animals in both the sham-operated (pregnant 91.7 +/- 1.7 mmHg, virgin 103.7 +/- 2.5 mmHg) and SAD states (pregnant 107.3 +/- 4.0 mmHg, virgin 114.1 +/- 4.0 mmHg). Pressor responses to all three agents were significantly blunted in pregnant animals compared with similarly treated virgins, with the magnitude of attenuation similar in both sham and SAD states. Heart rate decreased similarly in reflex-intact pregnant and virgin animals during pressor infusions. These findings suggest that attenuated pressor responses in the pregnant rat are due primarily to mechanisms other than augmentation of arterial baroreflex activity and are consistent with a generalized reduction in vascular sensitivity during gestation.

1995 ◽  
Vol 268 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
G. Weichert ◽  
C. A. Courneya

We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.


1993 ◽  
Vol 265 (5) ◽  
pp. E690-E698 ◽  
Author(s):  
R. R. Magness ◽  
C. R. Parker ◽  
C. R. Rosenfeld

Human and ovine pregnancies are associated with increases in plasma levels of estrogens and angiotensin II (ANG II), cardiac output (CO), blood volume (BV), and uterine blood flow (UBF), as well as attenuated ANG II pressor responses. We hypothesized that, in nonpregnant animals, prolonged estradiol-17 beta (E2 beta) treatment would reproduce these endocrine and hemodynamic alterations. Nonpregnant ovariectomized ewes (n = 5) received 5 microgram E2 beta/kg iv followed by 220 micrograms/day for 14 days. Plasma E2 beta increased from 36 +/- 6 to 269 +/- 79 (SE) pg/ml (P < 0.05) during E2 beta treatment, returning to control values 4 days posttreatment. By 3 days of E2 beta, mean arterial pressure (MAP) and systemic vascular resistance (SVR) fell 9 +/- 1 and 29 +/- 1%, whereas heart rate (HR) and CO increased 20 +/- 5 and 26 +/- 1% (P < 0.05). Stroke volume (SV), BV, and plasma volume were unchanged until 7 days of E2 beta, with values rising 17 +/- 5, 13 +/- 3, and 14 +/- 4, respectively (P < 0.05). Although MAP remained similarly depressed (-11 +/- 1%) during week 2 of E2 beta, SVR decreased further (-37 +/- 3%) and was associated with additional increases (P < 0.05) in CO to 44 +/- 5%, reflecting rises in SV (21 +/- 2%) but not HR. Increases in BV correlated with rises in CO (r = 0.55) and SV (r = 0.64) but not HR (r = -0.04).(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 83 (5) ◽  
pp. 549-556 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid

1. The blood pressure, heart rate, hormonal and pressor responses to constant rate infusion of various doses of the angiotensin (type 1) receptor antagonist Losartan (DuP 753/MK 954) were studied in the conscious salt-deplete dog. 2. Doses in the range 0.1–3 μmin−1 kg−1 caused no change in blood pressure, heart rate or pressor response to angiotensin II (54 ng min−1kg−1), and a dose of 10 μgmin−1 kg−1 had no effect on blood pressure, but caused a small fall in the pressor response to angiotensin II. Infusion of Losartan at 30 μmin−1 kg−1 for 3 h caused a fall in mean blood arterial pressure from baseline (110.9 ± 11.2 to 95.0 ± 12.8 mmHg) and a rise in heart rate (from 84.6 ± 15.1 to 103 ± 15.2 beats/min). Baseline plasma angiotensin II (42.5 ± 11.8 pg/ml) and renin (64.5 ± 92.7 μ-units/ml) concentrations were already elevated in response to salt depletion and rose significantly after Losartan infusion to reach a plateau by 70 min. The rise in mean arterial blood pressure after a test infusion of angiotensin II (35.3 ± 11.6 mmHg) was reduced at 15 min (11.8 ± 6.8 mmHg) by Losartan and fell progressively with continued infusion (3 h, 4.3 ± 3.3 mmHg). The peak plasma angiotensin II concentration during infusion of angiotensin II was unaffected by Losartan, but the rise in plasma angiotensin II concentration during infusion was reduced because of the elevated background concentration. Noradrenaline infusion caused a dose-related rise in mean blood arterial pressure (1000 ngmin−1kg−1, +19.9 ± 8 mmHg; 2000ngmin−1 kg−1, +52.8 ± 13.9 mmHg) with a fall in heart rate (1000 ng min−1 kg−1, −27.9 ± 11.5 beats/min; 2000 ng min−1 kg−1, −31.2 ± 17.3 beats/min). During Losartan infusion the 1000 but not the 2000 ng min−1 kg−1 noradrenaline infusion caused a greater rise in mean arterial blood pressure and a greater fall in heart rate. The fall in heart rate tended to decrease with continued infusion of Losartan. Plasma catecholamine concentrations were unaffected by Losartan. In a further study, higher doses of Losartan (100, 300 and 1000 μg min−1 kg−1; 30 min) produced greater falls in mean arterial blood pressure also with a rise in heart rate and complete blockade of the pressor effect of infused angiotensin II. Some animals became disturbed at the highest dose. 3. Losartan produces rapid dose-related falls in blood pressure and a rise in heart rate and renin release with elevation of plasma angiotensin II. Pressor responses to angiotensin II are reduced at intermediate doses and are eliminated at high doses. Losartan does not appear to inhibit angiotensin II clearance from the plasma and may in some way increase it.


1989 ◽  
Vol 257 (6) ◽  
pp. R1457-R1461 ◽  
Author(s):  
T. Hines ◽  
J. P. Porter

It is known that the pressor response to intravenous angiotensin II (ANG II) is blunted in pregnancy. In the present study we examined the pressor response to intracerebroventricular ANG II to determine whether central ANG II effects are also attenuated in conscious pregnant rats. Two to three days before experimentation, animals were instrumented with arterial and venous catheters and a ventricular guide cannula. Pressor responses to 10, 50, and 100 ng iv of ANG II, and 30, 100, and 300 ng iv of norepinephrine were significantly reduced in pregnant animals. The pressor response to 5, 20, and 50 ng iv of vasopressin was not attenuated in pregnant rats. The pressor response to intracerebroventricular 100 ng ANG II was significantly increased in pregnancy. Blockade of the vasopressin V1 receptor and the sympathetic ganglia indicated that the greater pressor response to intracerebroventricular ANG II in pregnancy may be the result of a larger contribution by the sympathetic nervous system. We conclude that the central effects of ANG II are augmented in pregnancy, suggesting a significant role for central ANG II in blood pressure regulation.


1997 ◽  
Vol 272 (1) ◽  
pp. R377-R385 ◽  
Author(s):  
M. Pecins-Thompson ◽  
M. Keller-Wood

Gonadal steroids have been implicated in the control of blood pressure and fluid homeostasis. These experiments test the effect of progesterone in ovariectomized ewes on blood pressure, volume, and hormone responses to hypotension. Eight ewes were each studied in four conditions: ovariectomized, progesterone and estrogen replaced, progesterone replaced, or sham treated. During each treatment mean arterial pressure (MAP), plasma volume (PV), baroreflex responsiveness, and adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hypotension were determined. Progesterone treatment significantly reduced resting MAP and increased PV compared with ovariectomy or sham treatments. Heart period at 85 mmHg was reduced with progesterone treatment. There was no effect of progesterone treatment on ACTH, AVP, or renin or heart rate responses to hypotension. Basal AVP levels were increased, and angiotensin II concentrations were decreased, by estrogen and progesterone and by sham treatments; plasma Na+ also tended to be increased during these treatments. These results suggest that a small increase in progesterone can reset resting MAP and PV without altering reflex heart rate or endocrine responses to hypotension.


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.


1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.


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.


2017 ◽  
Vol 26 (2) ◽  
pp. 116-21
Author(s):  
Arif H.M. Marsaban ◽  
Aldy Heriwardito ◽  
I G.N.A.D. Yundha

Background: Increased blood pressure and heart rate are the most frequent response to laryngoscopy which sometimes causes serious complications. Laryngoscopy technique and tools modification lessen the nociceptive stimulation, thus preventing hemodynamic response. BURP maneuver is used to lower Cormack-Lehane level, but it can cause additional pain stimulation during laryngoscopy. The aim of this study was to compare the cardiovascular response and the need of BURP maneuver during laryngoscopy between CMAC® and conventional Macintosh.Methods: A randomized, single blinded, control trial was performed to 139 subjects who underwent general anesthesia with endotracheal tube. Subjects were randomised into a control group (conventional Macintosh) and an intervention group (CMAC®). The cardiovascular parameters (systolic, dyastolic, mean arterial pressure, and heart rate) were measured prior to induction (T1). Midazolam 0.05 mg/kg and Fentanyl 2 micrograms/kg were given 2 minutes before the induction. Moreover, they were given propofol 1 mg/kg followed by propofol infusion of 10 mg/kg/hour and Atracurium 0.8–1 mg/kg. After TOF-0 cardiovascular parameters (T2) were remeasured, it was proceeded to laryngoscopy. When Cormack-Lehane 1–2 was reached (with or without BURP maneuver), cardiovascular parameters were measured again (T3).Results: Unpaired T-test showed that cardiovascular response during laryngoscopy were significantly lower in the intervention group compared to the control group (p<0.05). The need of BURP maneuver was significantly lower in the CMAC® group compared to the Convensional Macintosh group (13.9% vs 40.3%; p<0.05).Conclusion: Cardiovascular response and BURP maneuver during laryngoscopy with CMAC® were significantly lower compared to conventional Macintosh.


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.


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