scholarly journals Hemodynamic changes following accidental infiltration of a high dose of vasopressin

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052095949
Author(s):  
Jae Won Kim ◽  
Goo Kim ◽  
Tae Woo Kim ◽  
Woong Han ◽  
Mo Se Kim ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Systemic Effects ◽  
High Dose ◽  
Gynecological Surgery ◽  
Peripheral Perfusion ◽  
Robot Assisted ◽  
Hemodynamic Changes ◽  
Angiotensin System ◽  
Local Infiltration ◽  
Life Threatening

Vasopressin local infiltration is useful in gynecological surgery because it can reduce hemorrhage. Depending on the activities of the sympathetic system and the renin–angiotensin system, reactions to vasopressin may differ and predicting its systemic effects is difficult. Because life-threatening complications can occur, infiltration with vasopressin should be administered with caution. A 42-year-old female patient was diagnosed with uterine leiomyomas. During a robot-assisted laparoscopic myomectomy, 50 U of vasopressin, which is ten-times the recommended dose, was accidentally infiltrated. Subsequently, bradycardia with a heart rate of 25 bpm occurred, which recovered within 3 minutes. Peripheral perfusion indices and the diameter of the radial and brachial arteries also decreased markedly and recovered within 1 hour. The surgery was concluded without additional events. The patient was discharged 2 days later with no abnormal findings. Because vasopressin infiltration can cause life-threatening complications, it is necessary to determine the extent of patient reactions to vasopressin using measures such as the peripheral perfusion index or radial and brachial artery diameters. These measures may also help to predict the occurrence of complications.

Karl D. Nolph State of the Art Lecture: Feasible and Future Options for Salvation of the Peritoneal Membrane

2009 ◽  
Vol 29 (2_suppl) ◽  
pp. 195-197 ◽  
Author(s):  
Raymond T. Krediet ◽  
Annemieke M. Coester ◽  
Inna Kolesnyk ◽  
Marijke de Graaff ◽  
Machteld M. Zweers ◽  
...  
Keyword(s):  
Degradation Products ◽  
Experimental Studies ◽  
Renin Angiotensin System ◽  
Polyol Pathway ◽  
Dietary Sodium ◽  
High Dose ◽  
Peritoneal Membrane ◽  
Angiotensin System ◽  
Advanced Glycosylation End Products ◽  
Osmotic Agents

A review is given of the various available strategies that can be used to protect the peritoneal membrane. A discussion of experimental studies on approaches that are still experimental, but that might be applied in patients in the future, follows. The currently available approaches include dietary sodium restriction, use of high-dose loop diuretics and of inhibitors of the renin–angiotensin system. All should preferably be combined with a dialysis prescription aimed at reducing the patient's exposure to glucose and its degradation products. The experimental studies indicate favorable effects of combining osmotic agents, together with drugs that interfere with the polyol pathway and the formation of advanced glycosylation end-products.

Drug-Induced Electrolyte Disorders

1983 ◽  
Vol 17 (3) ◽  
pp. 175-185 ◽  
Author(s):  
Amin A. Nanji
Keyword(s):  
Parathyroid Hormone ◽  
Renin Angiotensin System ◽  
Renal Tubules ◽  
Electrolyte Disorders ◽  
Drug Induced ◽  
Sodium Potassium ◽  
Angiotensin System ◽  
Life Threatening ◽  
Calcium Magnesium ◽  
Pharmacologic Agents

A wide variety of pharmacologic agents have been implicated in a number of electrolyte disorders. The present review focuses on abnormalities of sodium, potassium, calcium, magnesium, and phosphate. Several mechanisms are involved in the pathogenesis of these disorders. These involve stimulation and modulation of other hormones (e.g., antidiuretic hormone, renin-angiotensin system, parathyroid hormone), damage to renal tubules, and, in some cases, a combination of factors. Recognition of these abnormalities is important because their presence may be life threatening or may aggravate the side effects of the drug itself.

scholarly journals ERAP1 and ERAP2 Enzymes: A Protective Shield for RAS against COVID-19?

2021 ◽  
Vol 22 (4) ◽  
pp. 1705
Author(s):  
Silvia D’Amico ◽  
Patrizia Tempora ◽  
Valeria Lucarini ◽  
Ombretta Melaiu ◽  
Stefania Gaspari ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Prognostic Factors ◽  
Mhc Class I ◽  
Antigen Processing ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Inflammatory Conditions ◽  
Protective Shield ◽  
Life Threatening ◽  
Mhc Class I Antigen

Patients with coronavirus disease 2019 (COVID-19) have a wide variety of clinical outcomes ranging from asymptomatic to severe respiratory syndrome that can progress to life-threatening lung lesions. The identification of prognostic factors can help to improve the risk stratification of patients by promptly defining for each the most effective therapy to resolve the disease. The etiological agent causing COVID-19 is a new coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that enters cells via the ACE2 receptor. SARS-CoV-2 infection causes a reduction in ACE2 levels, leading to an imbalance in the renin-angiotensin system (RAS), and consequently, in blood pressure and systemic vascular resistance. ERAP1 and ERAP2 are two RAS regulators and key components of MHC class I antigen processing. Their polymorphisms have been associated with autoimmune and inflammatory conditions, hypertension, and cancer. Based on their involvement in the RAS, we believe that the dysfunctional status of ERAP1 and ERAP2 enzymes may exacerbate the effect of SARS-CoV-2 infection, aggravating the symptomatology and clinical outcome of the disease. In this review, we discuss this hypothesis.

scholarly journals Improved renal cancer prognosis among users of drugs targeting renin-angiotensin system

2021 ◽  
Author(s):  
Tommi Eskelinen ◽  
Thea Veitonmäki ◽  
Andres Kotsar ◽  
Teuvo L. J. Tammela ◽  
Antti Pöyhönen ◽  
...  
Keyword(s):  
Ace Inhibitors ◽  
Renin Angiotensin System ◽  
Metastatic Tumor ◽  
Drug Group ◽  
High Dose ◽  
Defined Daily Dose ◽  
Prescription Database ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Tumor Extent

Abstract Purpose We explored renal cell cancer (RCC) survival among users of antihypertensive medication as hypertension is proposed to be a risk factor for RCC and ACE-inhibitors and angiotensin receptor blockers (ARBs) have been associated with improved prognosis of RCC. Methods Finnish cohort of 13,873 participants with RCC diagnosed between 1995–2012 was formed from three national databases. RCC cases were identified from Finnish Cancer Registry, medication usage from national prescription database and co-morbidities from Care Registry of Healthcare. Logistic regression was used to calculate odds ratios for metastatic tumor extent at the time of diagnosis. Risk of RCC specific death after diagnosis was analyzed using Cox regression adjusted for tumor clinical characteristics. Results A total of 5,179 participants died of RCC during the follow-up. No risk association was found for metastatic tumor extent for any drug group. ACE-inhibitors, but no other drug group were associated with decreased risk of RCC specific death overall (HR 0.88, 95% CI 0.82–0.95) compared to non-users. In time-dependent analysis high-dose use of ACE-inhibitors (392 Defined Daily Dose (DDD)/year), HR 0.54, 95% CI 0.45–0.66) and ARBs (786.1 DDD/year, HR 0.66, 95% CI 0.50–0.87) associated with improved RCC survival. No information of TNM-classification or tobacco smoking was available. Conclusion ACE-inhibitors and ARBs in high dose associated with improved RCC specific survival. This may reflect overall benefit of treating hypertension with medication targeting renin-angiotensin system (RAS) system among RCC patients. Further studies are needed to explore the role of RAS in RCC.

Effect of losartan and enalapril on renal adaptation sodium restriction in rat

1994 ◽  
Vol 267 (2) ◽  
pp. F281-F288 ◽  
Author(s):  
B. Jover ◽  
D. Saladini ◽  
N. Nafrialdi ◽  
M. Dupont ◽  
A. Mimran
Keyword(s):  
Sodium Excretion ◽  
Combined Treatment ◽  
Renin Angiotensin System ◽  
Systolic Arterial Pressure ◽  
Dietary Sodium ◽  
High Dose ◽  
Angiotensin System ◽  
Low Sodium ◽  
Renal Adaptation ◽  
Microsphere Method

The influence of losartan (10 or 30 mg.kg-1.day-1), enalapril (10 mg.kg-1.day-1), and combined treatment by losartan and enalapril on the renal adaptation to dietary sodium withdrawal was assessed in normal rats. Treatments were given by gavage for 3 days before and during the 6-day period of low-sodium (LS) diet. Cumulative sodium excretion during LS was similar in untreated and low-dose losartan groups (0.62 +/- 0.07 and 0.75 +/- 0.07 mmol/6 days), whereas it was significantly increased in groups treated by the high dose of losartan and enalapril alone or combined with both doses of losartan (1.38 +/- 0.16, 1.50 +/- 0.10, 1.37 +/- 0.16, and 1.12 +/- 0.03 mmol/6 days, respectively). A decrease in conscious systolic arterial pressure was observed in all treated groups in response to LS. At the end of LS, conscious renal blood flow (microsphere method) was similarly increased in all treated groups. Creatinine clearance decreased to a similar extent with both doses of losartan, whereas a further reduction was observed with enalapril given alone or combined with losartan. These results demonstrate that the enalapril-induced disturbance in the response of renal sodium excretion to LS is mainly related to angiotensin-mediated mechanisms. However, non-angiotensin-related actions of enalapril may contribute to the deterioration of renal function in sodium-restricted animals. In addition, a high dose of losartan is required to impair renal sodium conservation, thus suggesting that the tubular renin-angiotensin system may play a crucial role in the renal adaptation to dietary sodium withdrawal.

Functional evidence for subfornical organ-intrinsic conversion of angiotensin I to angiotensin II

1999 ◽  
Vol 276 (6) ◽  
pp. R1630-R1638 ◽  
Author(s):  
Matthias Rauch ◽  
Herbert A. Schmid
Keyword(s):  
Water Intake ◽  
Renin Angiotensin System ◽  
Subfornical Organ ◽  
Electrophysiological Recording ◽  
High Dose ◽  
Ang Ii ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Subcutaneous Injections

Using extracellular electrophysiological recording in an in vitro slice preparation, we investigated whether ANG I can be locally converted to the functionally active ANG II within the rat subfornical organ (SFO). ANG I and ANG II (10−8–10−7M) excited ∼75% of all neurons tested with both peptides ( n = 25); the remainder were insensitive. The increase in firing rate and the duration and the latency of the responses of identical neurons, superfused with equimolar concentrations of ANG I and ANG II, were not different. The threshold concentrations of the ANG I- and ANG II-induced excitations were both 10−9M. Inhibition of the angiotensin-converting enzyme by captopril (10−4M; n = 8) completely blocked the ANG I-induced excitation, a 10-fold lower dose was only effective in two of four neurons. The AT1-receptor antagonist losartan (10−5M; n = 6) abolished the excitation caused by ANG I and ANG II. Subcutaneous injections of equimolar doses of ANG I and ANG II (200 μl; 2 × 10−4M) in water-sated rats similarly increased water intake by 2.4 ± 0.5 ( n = 16) and 2.7 ± 0.4 ml ( n = 20) after 1 h, respectively. Control rats receiving saline drank 0.07 ± 0.06 ml under these conditions. Pretreatment with a low dose of captopril (2.3 × 10−3M) 10 min before the injection of ANG I caused a water intake of 2.8 ± 0.5 ml ( n = 10), whereas a high dose of captopril (4.6 × 10−1M) suppressed the dipsogenic response of ANG I entirely ( n = 11). These data provide direct functional evidence for an SFO-intrinsic renin-angiotensin system (RAS) and underline the importance of the SFO as a central nervous interface connecting the peripheral with the central RAS.

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