pituitrin and Vascular-Diseases

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins

Topics: 5-Hydroxytryptophan; Acanthosis Nigricans; Carcinoid Tumor; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Dermatomyositis; Endocrine System Diseases; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Neoplasms; Neuromuscular Diseases; Osteoarthropathy, Secondary Hypertrophic; Peripheral Nervous System Diseases; Polycythemia; Puberty, Precocious; Syndrome; Toxins, Biological; Vascular Diseases; Vasopressins; Zollinger-Ellison Syndrome

Gastrointestinal blood flow can be compromised during and after cardiopulmonary bypass. Endothelin has been shown to be involved in the intestinal microcirculatory disturbance of sepsis. The aim of the present study was to analyze the involvement of the endothelin system on intestinal blood flow regulation during cardiopulmonary bypass and the effect of vasopressin given during cardiopulmonary bypass.. A total of 24 pigs were studied in 4 groups (n = 6): group I, sham; group II, ischemia/reperfusion with 1 hour of superior mesenteric artery occlusion; group III, cardiopulmonary bypass for 1 hour; and group IV, 1 hour of cardiopulmonary bypass plus vasopressin administration, maintaining the baseline arterial pressure. All the pigs were reperfused for 90 minutes. During the experiment, the hemodynamics and jejunal microcirculation were measured continuously. The jejunal mucosal expression of endothelin-1 and its receptor subtypes A and B were determined using polymerase chain reaction.. During cardiopulmonary bypass, superior mesenteric artery flow was preserved but marked jejunal microvascular impairment occurred compared with baseline (mucosal capillary density, 192.2 ± 5.4 vs 150.8 ± 5.1 cm/cm(2); P = .005; tissue blood flow, 501.7 ± 39.3 vs 332.3 ± 27.9 AU; P = .025). The expression of endothelin-1 after cardiopulmonary bypass (3.2 ± 0.4 vs 12.2 ± 0.8 RQ, P = .006) and endothelin subtype A (0.7 ± 0.2 vs 2.4 ± 0.6 RQ; P = .01) was significantly increased compared to the sham group. Vasopressin administration during cardiopulmonary bypass led to normal capillary density (189.9 ± 3.9 vs 178.0 ± 6.3; P = .1) and tissue blood flow (501.7 ± 39.3 vs 494.7 ± 44.4 AU; P = .4) compared with baseline. The expression of endothelin-1 (3.2 ± 0.4 vs 1.8 ± 0.3 RQ; P = .3) and endothelin subtype A (0.7 ± 0.2 vs 0.9 ± 0.2 RQ; P = .5) was not different from the sham group.. Cardiopulmonary bypass leads to microvascular impairment of jejunal microcirculation, which is associated with the upregulation of endothelin-1 and endothelin subtype A. The administration of vasopressin minimizes these cardiopulmonary bypass-associated alterations.

Topics: Animals; Biopsy; Blood Flow Velocity; Capillaries; Cardiopulmonary Bypass; Endothelin-1; Ischemia; Jejunum; Mesenteric Artery, Superior; Mesenteric Ischemia; Microcirculation; Models, Animal; Real-Time Polymerase Chain Reaction; Receptor, Endothelin A; Receptor, Endothelin B; Regional Blood Flow; RNA, Messenger; Splanchnic Circulation; Sus scrofa; Time Factors; Vascular Diseases; Vasopressins

Topics: Angiotensins; Arteries; Arteriosclerosis; Body Temperature Regulation; Endothelins; Energy Metabolism; Epinephrine; Hemostasis; Humans; Nitric Oxide; Prostaglandins; Ultrasonography; Vascular Diseases; Vasopressins

Adult patients with hypopituitarism are treated by the replacement of deficient hormones, although GH has not been substituted until March 2006 in Japan except for clinical trial. This study examines which hormonal status influences the prevalence of vascular risk disorders in hypopituitary adults. A sample of 263 adult patients with hypopituitarism was studied, among whom there were various hormonal status such as no deficiency, treated or untreated deficiency of each pituitary hormone. Analysis of adult patients with hypopituitarism showed that hypertension was more prevalent in the older than in younger patients and in male than in female patients. Hypercholesterolemia and hypertriglyceridemia were more prevalent in patients with TSH deficiency even with thyroxine substitution than those without TSH deficiency. Both obesity and hypertension were less prevalent in patients with treated ACTH deficiency than those without ACTH deficiency. Obesity was more prevalent in patients with treated vasopressin deficiency than those without vasopressin deficiency. These results provide evidence that glucocorticoid substitution in ACTH deficient adults was favorable to prevent obesity and hypertension but that the thyroxine substitution in TSH deficient adults appeared rather insufficient to prevent hyperlipidemia.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Age Distribution; Aged; Aged, 80 and over; Female; Hormone Replacement Therapy; Humans; Hypercholesterolemia; Hypertension; Hypertriglyceridemia; Hypopituitarism; Male; Middle Aged; Obesity; Prevalence; Risk Factors; Sex Distribution; Thyrotropin; Thyroxine; Vascular Diseases; Vasopressins

Topics: Adrenal Gland Neoplasms; Catecholamines; Humans; Male; Middle Aged; Pheochromocytoma; Shock; Vascular Diseases; Vascular Resistance; Vasopressins

Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by ARN. An additional 45 neurosecretory neurons (29 AVP and 16 Oxy neurons) were tested for their responses to RVO and/or RAO. RVO inhibited 42% of the putative AVP neurons and 13% of the putative Oxy neurons. On the other hand, RAO excited 33% of the AVP and 9% of the Oxy neurons. No AVP or Oxy neurons were found to be excited by RVO or inhibited by RAO. These data indicate that sensory information originating in renal receptors alters the activity of AVP and Oxy neurons in the PVH and suggest that these renal receptors contribute to the hypothalamic control of AVP and Oxy release into the circulation.

Topics: Afferent Pathways; Animals; Arterial Occlusive Diseases; Cardiovascular System; Constriction, Pathologic; Electric Stimulation; Kidney; Male; Neurons; Neurosecretory Systems; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; Renal Artery; Renal Veins; Vascular Diseases; Vasopressins

Topics: Angiography; Angioplasty, Balloon; Animals; Arteries; Dogs; Rabbits; Vascular Diseases; Vasoconstriction; Vasopressins

Catheter dislodgement is a major cause of technical failures in intraarterial vasopressin therapy for gastrointestinal bleeding. Ten such cases were observed in the past five years. In seven patients catheter dislodgement led to recurrent bleeding during vasopressin infusion. In one patient aortic infusion of vasopressin caused recurrent bleeding and reversible acrocyanosis of the feet, and in two patients vasopressin infusion into the left renal artery resulted in chest pain and hematuria. Catheter dislodgement should be suspected if bleeding that was initially controlled recurs during vasopressin infusion.

Topics: Adolescent; Angiography; Aorta, Abdominal; Catheterization; Celiac Artery; Female; Gastrointestinal Hemorrhage; Heart Valve Prosthesis; Humans; Infusions, Parenteral; Male; Middle Aged; Peptic Ulcer Hemorrhage; Postoperative Complications; Spinal Injuries; Vascular Diseases; Vasopressins

Topics: Angiotensin II; Animals; Arteries; Blood Pressure; Capillary Permeability; Humans; Hypertension, Malignant; Necrosis; Renin; Vascular Diseases; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Alkalosis; Autoimmune Diseases; Bone Diseases; Carcinoma, Bronchogenic; Cushing Syndrome; Endocrine System Diseases; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Lung Neoplasms; Metabolic Diseases; Neoplasm Metastasis; Neurologic Manifestations; Neuromuscular Diseases; Skin Diseases; Skin Manifestations; Vascular Diseases; Vasopressins

Topics: Animals; Blood Pressure; Body Weight; Desoxycorticosterone; Heart; Hypertension; In Vitro Techniques; Male; Nephrectomy; Norepinephrine; Perfusion; Potassium; Rats; Sodium Chloride; Tail; Vascular Diseases; Vascular Resistance; Vasopressins

Topics: Cornea; Corneal Opacity; Eye Injuries; Heparin Antagonists; Histamine H1 Antagonists; Humans; Protamines; Vascular Diseases; Vasopressins

Topics: Afibrinogenemia; Autonomic Nervous System Diseases; Bone Diseases; Carcinoma, Bronchogenic; Collagen Diseases; Cushing Syndrome; Endocrine System Diseases; Fibrinolysis; Hematologic Diseases; Humans; Hypercalcemia; Lung Neoplasms; Muscular Diseases; Neurologic Manifestations; Osteoarthropathy, Secondary Hypertrophic; Pathology; Peripheral Nervous System Diseases; Spinal Cord; Thrombophlebitis; Vascular Diseases; Vasopressins

Topics: Animals; Aortic Diseases; Atropine; Dogs; Electrocardiography; Epinephrine; Heart Auscultation; Heart Sounds; Hemodynamics; Hemorrhage; Histamine; Infusions, Parenteral; Isoproterenol; Methoxamine; Myocardial Infarction; Norepinephrine; Pharmacology; Phenylephrine; Phonocardiography; Pulmonary Artery; Research; Respiration; Vascular Diseases; Vasopressins; Venae Cavae; Veratrine

Topics: Angiotensins; Blood Pressure Determination; Central Nervous System Stimulants; Heart Arrest; Heart Failure; Humans; Hypotension; Pharmacology; Postoperative Care; Postoperative Complications; Shock; Sympathomimetics; Toxicology; Vascular Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Blood Vessels; Humans; Vascular Diseases; Vasoconstrictor Agents; Vasopressins