Vasodilators in critical illness

2016 ◽  
Author(s):  
A. B. J. Groeneveld ◽  
Alexandre Lima
Keyword(s):  
Smooth Muscles ◽  
Renin Angiotensin System ◽  
Phosphodiesterase Inhibitors ◽  
Peripheral Vessel ◽  
Venous Capacitance ◽  
Vasodilator Drugs ◽  
Arterial Blood ◽  
Resistance Vessels ◽  
Capacitance Vessels ◽  
The Right

Vasodilators are commonly used in the intensive care unit (ICU) to control arterial blood pressure, unload the left or the right heart, control pulmonary artery pressure, and improve microcirculatory blood flow. Vasodilator refers to drugs acting directly on the smooth muscles of peripheral vessel walls and drugs are usually classified based on their mechanism (acting directly or indirectly) or site of action (arterial or venous vasodilator). Drugs that have a predominant effect on resistance vessels are arterial dilators and drugs that primarily affect venous capacitance vessels are venous dilators. Drugs that interfere with sympathetic nervous system, block renin-angiotensin system, phosphodiesterase inhibitors, and nitrates are some examples of drugs with indirect effect. Vasodilator drugs play a major therapeutic role in hypertensive emergencies, primary and secondary pulmonary hypertension, acute left heart, and circulatory shock. This review discusses the main types of vasodilators drugs commonly used in the ICU.

scholarly journals Captopril Partially Decreases the Effect of H2S on Rat Blood Pressure and Inhibits H2S-Induced Nitric Oxide Release From S-Nitrosoglutathione

2015 ◽  
pp. 479-486 ◽  
Author(s):  
M. DROBNÁ ◽  
A. MISAK ◽  
T. HOLLAND ◽  
F. KRISTEK ◽  
M. GRMAN ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Biological Activities ◽  
Renin Angiotensin System ◽  
Bolus Administration ◽  
Angiotensin System ◽  
Nitric Oxide Release ◽  
Arterial Blood ◽  
Biphasic Effect ◽  
The Mean ◽  
The Right

We studied the effects of the H2S donor Na2S on the mean arterial blood pressure (MAP) and heart and breathing rates of anesthetized Wistar rats in the presence and absence of captopril. Bolus administration of Na2S (1-4 µmol/kg) into the right jugular vein transiently decreased heart and increased breathing rates; at 8-30 µmol/kg, Na2S had a biphasic effect, transiently decreasing and increasing MAP, while transiently decreasing heart rate and increasing and decreasing breathing rate. These results may indicate independent mechanisms by which H2S influences MAP and heart and breathing rates. The effect of Na2S in decreasing MAP was less pronounced in the presence of captopril (2 µmol/l), which may indicate that the renin-angiotensin system is partially involved in the Na2S effect. Captopril decreased H2S-induced NO release from S-nitrosoglutathione, which may be related to some biological activities of H2S. These results contribute to the understanding of the effects of H2S on the cardiovascular system.

Effect of Morphine on Limb Capacitance and Resistance Vessels

1981 ◽  
Vol 60 (1) ◽  
pp. 5-9 ◽  
Author(s):  
R. A. Cohen ◽  
J. D. Coffman
Keyword(s):  
Vascular Resistance ◽  
Venous Occlusion ◽  
Important Change ◽  
Venous Tone ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Intravenous Morphine ◽  
Capacitance Vessels ◽  
Venous Volume ◽  
Cutaneous Vascular Resistance

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intra-arterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.

scholarly journals Cardiovascular effects of vasopressin following V1 receptor blockade compared to effects of nitroglycerin

2001 ◽  
Vol 281 (3) ◽  
pp. R887-R893 ◽  
Author(s):  
C. R. Cooke ◽  
B. M. Wall ◽  
K. M. Huch ◽  
T. Mangold
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiovascular Effects ◽  
Normal Subjects ◽  
Receptor Blockade ◽  
Hemodynamic Effects ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Studies to more clearly determine the mechanisms associated with arginine vasopressin (AVP)-induced vasodilation were performed in normal subjects and in quadriplegic subjects with impaired efferent sympathetic responses. Studies to compare the effects of AVP with the hemodynamic effects of nitroglycerin, an agent that primarily affects venous capacitance vessels, were also performed in normal subjects. Incremental infusions of AVP following V1-receptor blockade resulted in equivalent reductions in systemic vascular resistance (SVRI) in normal and in quadriplegic subjects. However, there were major differences in the effect on mean arterial pressure (MAP), which was reduced in quadriplegic subjects but did not change in normal subjects. This difference in MAP can be attributed to a difference in the magnitude of increase in cardiac output (CI), which was twofold greater in normal than in quadriplegic subjects. These observations are consistent with AVP-induced vasodilation of arterial resistance vessels with reflex sympathetic enhancement of CI and are clearly different from the hemodynamic effects of nitroglycerin, i.e., reductions in MAP, CI, and indexes of cardiac preload, with only minor changes in SVRI.

Effect of adenosine and glucagon on hepatic blood volume responses to sympathetic nerves

1991 ◽  
Vol 69 (1) ◽  
pp. 43-48 ◽  
Author(s):  
W. Wayne Lautt ◽  
Joshua Schafer ◽  
Dallas J. Legare
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerves ◽  
Liver Weight ◽  
Maximal Response ◽  
Venous Capacitance ◽  
Resistance Vessels ◽  
Capacitance Vessels

Hepatic blood volume responses were studied in cats using in vivo plethysmography. The maximal response (Rmax) to sympathetic nerve stimulation and to infusions of norepinephrine into the hepatic artery or portal vein was similar (12–14 mL expelled per liver in 2.9-kg cats; average liver weight, 76.8 ± 6.8 g). The ED50 for norepinephrine intraportal (0.44 ± 0.13) and intrahepatic arterial infusions (0.33 ± 0.08 μg∙kg−1∙min−1) were similar indicating equal access of both blood supplies to the capacitance vessels. Adenosine (2.0 mg∙kg−1∙min−1) did not cause significant volume changes but produced a mild (27%) suppression of Rmax due to nerve stimulation with no change in the frequency (3.4 Hz) needed to produce 50% of Rmax. Rmax tended (not statistically significant) to decrease during glucagon (1.0 μg∙kg−1∙min−1) infusion but the nerve frequency needed to produce 50% of Rmax rose to 5.6 Hz. Thus both adenosine and glucagon produced modulation of sympathetic nerve-induced capacitance responses without having significant effects on basal blood volume. Adenosine, by virtue of its marked effects on arterial resistance vessels (at substantially lower doses than those used here) and the relative lack of effect on venous capacitance vessels, may be useful for producing clinical afterload reduction without venous pooling.Key words: blood volume, capacitance, sympathetic nerves, adenosine, glucagon.

scholarly journals The branches of the descending palatine artery and their relation to the vomeronasal organ inAngoragoats

2012 ◽  
Vol 51 (No. 2) ◽  
pp. 55-59 ◽  
Author(s):  
K. Besoluk ◽  
E. Eken ◽  
S. Bahar
Keyword(s):  
Vomeronasal Organ ◽  
Sphenopalatine Artery ◽  
Arterial Blood ◽  
The Right ◽  
Palatine Artery ◽  
Fine Branch

The aim of this study was to reveal the branches of the descending palatine artery, and its relation to the vomeronasal organ inAngoragoats. For this purpose, ten heads of adultAngoragoats obtained from a slaughterhouse were used. The ramifications of the latex enjected descending palatine artery and their vomeronasal organ-related findings were revealed by fine dissection and transverse sections. Arterial blood reached the caudally vomeronasal organ primarily via the sphenopalatine artery, and also cranially via a fine branch of the major palatine artery by crossing the palatine fissure. The average diameters of both the descending palatine artery and its branches were thicker on the left side than on the right, and its ramifications were not variable in this species.

Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.

Role of cGMP in relaxation of vascular and other smooth muscle

1989 ◽  
Vol 67 (4) ◽  
pp. 251-262 ◽  
Author(s):  
Kanji Nakatsu ◽  
Jack Diamond
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxation ◽  
Smooth Muscles ◽  
Phosphodiesterase Inhibitors ◽  
Current Evidence ◽  
Smooth Muscle Relaxation ◽  
Drug Induced ◽  
Intracellular Cgmp ◽  
Tissue Content

The hypothesis that the relaxant action of many drugs on vascular and other smooth muscle is mediated by increases in intracellular cGMP, the "cGMP hypothesis," is gaining wide acceptance. While much information supporting this idea can be found in the literature, there is also a significant amount of information indicating that an elevation in the tissue content of cGMP is by itself insufficient to cause smooth muscle relaxation. The literature is reviewed with reference to the criteria that need to be fulfilled to consider cGMP as the second messenger mediating relaxation of smooth muscle by a drug; i.e., activation of guanylate cyclase, elevation of tissue content of cGMP, potentiation by phosphodiesterase inhibitors, antagonism by inhibitors of cGMP synthesis, and production of relaxation by cGMP analogues. For each criterion, key observations supporting the hypothesis are considered, followed by examples of important observations not consistent with the hypothesis. It is concluded that in some smooth muscles, for example, rat myometrium and vas deferens, cGMP is not a mediator of drug-induced relaxation. In other smooth muscles, including vascular smooth muscle, cGMP appears to play an important role in the relaxation process; but current evidence suggests that other factors are also important and that the cGMP hypothesis may need to be modified.Key words: cGMP, vascular relaxation, smooth muscle relaxation, vasodilators.

Histamine-induced pulmonary edema distal to pulmonary arterial occlusion

1985 ◽  
Vol 58 (4) ◽  
pp. 1092-1098 ◽  
Author(s):  
M. D. Walkenstein ◽  
B. T. Peterson ◽  
J. E. Gerber ◽  
R. W. Hyde
Keyword(s):  
Pulmonary Edema ◽  
Pulmonary Circulation ◽  
Arterial Occlusion ◽  
Arterial Blood Flow ◽  
Water Volume ◽  
Lung Water ◽  
Arterial Blood ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
The Right

Histological studies provide evidence that the bronchial veins are a site of leakage in histamine-induced pulmonary edema, but the physiological importance of this finding is not known. To determine if a lung perfused by only the bronchial arteries could develop pulmonary edema, we infused histamine for 2 h in anesthetized sheep with no pulmonary arterial blood flow to the right lung. In control sheep the postmortem extravascular lung water volume (EVLW) in both the right (occluded) and left (perfused) lung was 3.7 +/- 0.4 ml X g dry lung wt-1. Following histamine infusion, EVLW increased to 4.4 +/- 0.7 ml X g dry lung wt-1 in the right (occluded) lung (P less than 0.01) and to 5.3 +/- 1.0 ml X g dry wt-1 in the left (perfused) lung (P less than 0.01). Biopsies from the right (occluded) lungs scored for the presence of edema showed a significantly higher score in the lungs that received histamine (P less than 0.02). Some leakage from the pulmonary circulation of the right lung, perfused via anastomoses from the bronchial circulation, cannot be excluded but should be modest considering the low pressures in the pulmonary circulation following occlusion of the right pulmonary artery. These data show that perfusion via the pulmonary arteries is not a requirement for the production of histamine-induced pulmonary edema.

Active, passive, and motor imagery paradigms: component analysis to assess neurovascular coupling

2013 ◽  
Vol 114 (10) ◽  
pp. 1406-1412 ◽  
Author(s):  
Angela S. M. Salinet ◽  
Thompson G. Robinson ◽  
Ronney B. Panerai
Keyword(s):  
Motor Imagery ◽  
Moving Average ◽  
Neurovascular Coupling ◽  
Neural Activation ◽  
Autoregressive Moving Average Model ◽  
Arterial Blood ◽  
Moving Average Model ◽  
End Tidal ◽  
The Right ◽  
Cognitive Paradigms

The association between neural activity and cerebral blood flow (CBF) has been used to assess neurovascular coupling (NVC) in health and diseases states, but little attention has been given to the contribution of simultaneous changes in peripheral covariates. We used an innovative approach to assess the contributions of arterial blood pressure (BP), PaCO2, and the stimulus itself to changes in CBF velocities (CBFv) during active (MA), passive (MP), and motor imagery (MI) paradigms. Continuous recordings of CBFv, beat-to-beat BP, heart rate, and breath-by-breath end-tidal CO2 (EtCO2) were performed in 17 right-handed subjects before, during, and after motor-cognitive paradigms performed with the right arm. A multivariate autoregressive-moving average model was used to calculate the separate contributions of BP, EtCO2, and the neural activation stimulus (represented by a metronome on-off signal) to the CBFv response during paradigms. Differences were found in the bilateral CBFv responses to MI compared with MA and MP, due to the contributions of stimulation ( P < 0.05). BP was the dominant contributor to the initial peaked CBFv response in all paradigms with no significant differences between paradigms, while the contribution of the stimulus explained the plateau phase and extended duration of the CBFv responses. Separating the neural activation contribution from the influences of other covariates, it was possible to detect differences between three paradigms often used to assess disease-related NVC. Apparently similar CBFv responses to different motor-cognitive paradigms can be misleading due to the contributions from peripheral covariates and could lead to inaccurate assessment of NVC, particularly during MI.

scholarly journals Fountain’s Sign as a Diagnostic Key in Acute Idiopathic Scrotal Edema: Case Report and Review of the Literature

2018 ◽  
Vol 61 (1) ◽  
pp. 37-39 ◽  
Author(s):  
Dimitrios Patoulias ◽  
Vasileios Rafailidis ◽  
Thomas Feidantsis ◽  
Maria Kalogirou ◽  
Dimitrios Rafailidis ◽  
...  
Keyword(s):  
Physical Examination ◽  
Color Doppler ◽  
Unknown Etiology ◽  
Acute Scrotum ◽  
Conservative Strategy ◽  
Ultrasonographic Examination ◽  
Arterial Blood ◽  
Scrotal Edema ◽  
Diagnostic Key ◽  
The Right

The acute idiopathic scrotal edema (AISE) is a self-limited disease of unknown etiology, characterized by edema and erythema of the scrotum and the dartos, without expansion to the underlying layers of scrotum’s wall or to the endoscrotal structures. Boys younger than 10 years old are usually involved in 60–90% of all cases. Diagnosis is made after exclusion of other causes of acute scrotum. We present a case of a 7-year old boy, who was admitted to the Emergency Department due to development of scrotal edema and erythema over the last 48 hours, which extended to the base of the penis. The patient mentioned that he first noticed the erythema on the anterior surface of the right hemiscrotum, which gradually extended. Physical examination did not reveal presence of pathology involving the endoscrotal structures, indicative of need for urgent surgical intervention. Transillumination was negative for blue dot sign. Ultrasonographic examination of the scrotum documented the homogeneity of the testicular parenchyma, while color Doppler revealed the presence of fountain’s sign (equal arterial blood supply to both testicles). Conservative strategy was followed and the patient gradually improved within the next three days. In conclusion, meticulous physical examination along with ultrasonographic examination of the suffering scrotum, especially with the highlighting of fountain’s sign with color Doppler, document the diagnosis of AISE. Thus, need for urgent surgical investigation of the suffering scrotum due to diagnostic doubt is limited.

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