Search PubMed⌕ Search

Biomedical subjects

D M Philbin

Publications and source records attributed to D M Philbin.

At least 73 records · Page 4Linked to original sources
PubMed1981

Renal function and stress response during halothane or fentanyl anesthesia.

The effects of anesthesia on hormonal stress response and renal function were measured before institution of cardiopulmonary bypass in two groups of patients undergoing elective coronary artery surgery. Group 1 (10 patients) received fentanyl, 100 microgram/kg, and N2O/O2; group 2 (12 patients) received halothane and N2O/O2. Patients in group 1 showed no significant changes in plasma levels of vasopressin, renin, or aldosterone during anesthesia or operation. This same group, however, demonstrated significant decreases in plasma levels of cortisol (8.4 +/- 1 to 4.2 +/- 1 microgram%, p less than 0.01), epinephrine (260 +/- 72 to 97 +/- 28 pg/ml, p less than 0.05), and norepinephrine (715 +/- 177 to 322 +/- 46 pg/ml, p less than 0.05) during operation. This was accompanied by an increase in urine volume (2.1 +/- 0.8 to 7.6 +/- 2 ml/min, p less than 0.05), a decrease in urine osmolality (610 +/- 82 to 166 +/- 60 mOsm/kg, p less than 0.01), and urine Na+ (54 +/- 12 to 16 +/- 4 meq/L, p less than 0.01) and no change in creatinine clearance. In contrast, in the group 2 patients during operation plasma levels of cortisol (11.7 +/- 2 to 31.1 +/- 2 microgram%, p less than 0.01), aldosterone (60 +/- 14 to 106 +/- 2 pg/ml, p less than 0.01), and vasopressin (10.4 +/- 1 to 23.3 +/- 3 pg/ml, p less than 0.01) all increased. This was accompanied by a significant decrease in creatinine clearance (148 +/- 52 to 92 +/- 12 ml/min/m2, p less than 0.05). The data demonstrate that high dose fentanyl anesthesia can significantly attenuate the hormonal stress response to operation and preserve renal function. They also suggest that decreases in renal function observed with anesthesia and operation may be a reflection of the hormonal changes associated with surgical stimulation.

Aldosterone↗
PubMed1980

Water metabolism and antidiuretic hormone (ADH) response following thermal injury.

ADH has been implicated in the development of a positive water balance in thermal injury. However, the association of plasma ADH levels to the hemodynamic response and water and electrolyte balance of early thermal injury has not been defined. Plasma ADH was measured by radioimmunoassay in 13 patients with greater than 15% body surface area burns. In three patients frequent hemodynamic measurements were also made. Large individual variations of ADH were noted, but in general the ADH levels peaked early in the postburn period and declined thereafter. The highest mean ADH value was on day 2 (53.8 = 27 pg/ml); the lowest value on day 7 (13.4 +/- 8 pg/ml). Urine electrolytes demonstrated wide variation (Na+, 2 to 236 mEq/L; K+, 2 to 228 mEq/L) as did serum (261--331 mOsm/kg) and urine (557--785 mOsm/kg) osmolalities. No correlation was noted between ADH levels and osmolalities or hemodynamic variables. These data suggest that ADH response following burns is a stress response producing levels beyond the physiologic range for an antidiuretic effect and that the osmolar, hypovolemic, and hypotensive feedback loops are not involved: ADH seems to act as a vasoconstrictor and to have no significant effect on quality or quantity of urine. We conclude that the positive water balance following burns is not ADH mediated.

Adult↗
PubMed1980

[Antidiuretic hormone, the renin-angiotensin system and anesthesia].

The authors, on the basis of the literature and their own studies, envisage the behaviour of the renin-angiotensin system and of ADH during anesthesia. With regard to renin-angiotensin, it would seem that the changes reported in the past are due to the surgical procedure itself or result form haemodynamic changes but that no anesthetic has a direct effect upon the secretion of renin. For ADH, three concepts must be borne in mind: not only is secretion not influenced by anesthetics, but on the contrary anaesthesia decreases the "vasopressin" response to surgical stress. By contrast, the surgical procedure may induce the secretion of ADH responsible for coronary vasoconstriction. Finally, at high doses, ADH would appear to have an inverse antinatriuretic effect resulting in a sodium diuresis.

Anesthesia↗
PubMed1980

The effects of anesthesia on antidiuretic hormone.

Arginine vasopressin, the antidiuretic hormone in man, in low concentrations increases reabsorption of water in the collecting ducts of the kidney, producing a concentrated urine. It is also a potent vasoconstrictor because of its direct effect on arteriolar smooth muscle, particularly the splanchnic, renal, and coronary vascular beds. This appears to be a dose-dependent response. In very high concentrations it is capable of producing a diuresis with increased urinary sodium excretion. The preponderance of evidence today has failed to show any significant increase in antidiuretic hormone levels with anesthesia alone, provided significant hemodynamic changes do not occur. It seems unlikely, then, that the inhalation anesthetics or high-dose narcotic anesthesia are a direct stimulus to ADH release. If a decrease in urine flow does occur, it is more likely caused by either the renal hemodynamic effects of the anesthetic or a secondary release of ADH. Surgical stimulation is capable of significantly increasing ADH levels. This apparently is a stress response that can be attenuated by the depth of anesthesia. Such a response to operation may produce ADH levels that can indeed decrease urinary flow, but more importantly may succeed in achieving levels that can exert a significant vasopressor effect. In unusual circumstances, vasopressin levels can occur that are capable of producing a diuresis and increased urine sodium excretion.

Anesthesia↗
PubMed1979

Fentanyl-oxygen anaesthesia for coronary artery surgery: cardiovascular and antidiuretic hormone responses.

This study demonstrates that large doses of fentanyl, as the sole anaesthetic with ventilation with oxygen, produces complete anaesthesia and minimal changes in cardiovasuclar dynamics in patients with coronary artery disease. It also indicates that high dose fentanyl anaesthesia blocks the increase in plasma anti-diuretic hormone and cardiovascular dynamics which are so common with morphine and other anaesthetic techniques during tracheal intubation and surgical stimulation in patients with coronary artery disease. Our findings suggest that fentanyl-oxygen anaesthesia is an attractive technique in patients with coronary artery disease.

Anesthesia, Intravenous↗
PubMed1979

Comparative haemodynamic effects of tubocurarine and metocurine in the dog.

On accout of its histamine releasing and ganglion blocking properties tubocurarine is known to have significant haemodynamic effects. Methylation of the compound produces metocurine and should decrease both histamine release and ganglionic blockade. The haemodynamic effects of these two compounds were compared in 10 mongrel dogs anaesthetized with chloralose and morphine. Haemodynamic measurements were made 2 min before and 2, 5, 10 and 20 min after administration of the drugs. Each animal received three doses of each drug with a 2-h rest period between doses: tubocurarine 0.35 (muscle twitch ED95), 0.7 and 1.4 mg kg-1 and metocurine 0.2 (2 x ED95), 0.4 and 0.8 mg kg-1. All doses of tubocurarine produced an increase in heart rate (212, 197 and 212% of control respectively). The mean arterial pressure decreased significantly with 0.7 mg kg-1 (48% of control; P less than 0.05). Metocurine produced no significant haemodynamic effects except for the largest dose (8 x ED95). The data suggest that the haemodynamic margin of safety with metocurine in the dog is eight times that of tubocurarine.

Animals↗
PubMed1979

Plasma vasopressin levels and urinary flow during cardiopulmonary bypass in patients with valvular heart disease: effect of pulsatile flow.

The effect of pulsatile flow on plasma vasopressin levels during cardiopulmonary bypass (CPB) was studied in 20 patients undergoing open valve replacement. Routine bypass was used in 10 patients and the AVCO pulsatile bypass pump was utilized in the other 10. In Group I (nonpulsatile) during CPB, the vasopressin level was markedly elevated (3.1 +/- 2 to 80 +/- 22 pg/ml) as was urine flow (0.6 +/- 0.2 to 5.9 +/- 2 ml/min) and urine Na+ concentration (69 +/- 19 to 116 +/- 7 mEq/L). In Group II (pulsatile) during CPB, the vasopressin level (3.8 +/- 3 to 54 +/- 14 pg/ml), urine flow (0.6 +/- 0.1 to 16.2 +/- 4.8 ml/min), and urine Na+ concentrations (61 +/- 13 to 97 +/- 10 mEq/L) were also elevated. The rise in vasopressin and urine Na+ was less in the pulsatile group (p less than 0.05) whereas the urine flow was higher (p less than 0.05). To maintain comparable blood pressure, the pulsatile flow group required significantly higher flows (4.5 +/- 0.2 compared to 3.8 +/- 0.2; p less than 0.05). These data suggest that CPB produces a marked vasopressin stress response which is beyond the physiological range for an antidiuretic effect on the kidney. At these levels vasopressin can exert a vasopressor effect to maintain resistance and affect renal blood flow, as well as producing an Na+ diuresis. The addition of pulsatile flow creates a more physiological situation attenuating the vasopressin response and producing a decrease in systemic resistance and a less pronounced Na+ diuresis.

Arginine Vasopressin↗
PubMed1978

Plasma vasopressin levels during cardiopulmonary bypass with and without profound haemodilution.

In cardiopulmonary bypass the effect on plasma vasopressin levels of the addition of whole blood to the pump priming solution was measured. Six patients (Group I) had blood added to the lactated Ringer's solution for the prime, and six patients (Group II) had only lactated Ringer's solution. Neither group had significant changes in plasma vasopressin levels until surgical stimulation occurred. Comparable significant elevations occurred during bypass in both groups. Greater decreases in haematocrit and urinary K+ and greater increases in urinary Na+ occurred in Group II. The degree of haemodilution does not appear to effect plasma vasopressin levels but may alter the degree of electrolyte shift.

Cardiopulmonary Bypass↗
PubMed1977

Antidiuretic hormone levels during cardiopulmonary bypass.

The effect of CPB on plasma ADH levels, urine flow, and urine osmolality was studied in nine patients. All patients received morphine, 1 mg. per kilogram, and 50 per cent nitrous oxide-50 per cent oxygen for anesthesia. CPB utilized a Travenol disposable bubble oxygenator and the prime consisted of 3 L. of Ringer's lactate. Measurements were made prior to induction of anesthesia , at 30 minutes following surgical incision, and at 15, 30, and 45 minutes during CPB. There were no statistically significant changes in mean arterial BP, cardiac index, serum sodium, or serum osmolality in any period. Urine flow increased from 0.99 +/- 0.3 ml. per minute to a high of 6.13 +/- 2.0 ml. per minute at 30 minute at 30 minutes on CPB (P less than 0.02). Urine osmolality declined from a control value of 691 +/- 142 mOsm. per kilogram to a low of 425 +/- 48 mOsm. per kilogram at 45 minutes on CPB (p less than 0.05). ADH levels rose from a control value of 4.3 +/- 1.5 to 13.0 +/- 3.3 pg. per milliliter with surgical stimulatiion (p less than 0.05). During CPB the ADH levels rose to a peak of 23.7 +/- 3.6 pg. per milliliter at 30 minutes (p less than 0.01) and were declining at 45 minutes. These data suggest that the stress of CPB results in an outpouring of ADH (or vasopressin) to function as a pressor to produce an increase in peripheral resistance. The ADH concentrations far exceed those required for normal physiologic control of water excretion and the urineflow will thus vary more with the hemodynamic changes than with the ADH levels.

Aged↗
PubMed1976

Radioimmunoassay of antidiuretic hormone during morphine anaesthesia.

The effect of morphine anaesthesia on plasma antidiuretic hormone levels was studied in seven adult patients. Measurements of ADH showed no significant change with morphine and 50 per cent nitrous oxide. Significant elevation occurred with surgical stimulation as previously reported. Changes in urine flow with high doses of morphine are then not ADH related.

Aged↗
PubMed1976

Lack of beta-adrenergic activity of isoflurane in the dog: a comparison of circulatory effects of halothane and isoflurane after propranolol administration.

The studies were undertaken to determine whether isoflurance inhalation is associated with a degree of beta-adrenergic action that is potentially important in clinical situations, and to compare the circulatory tolerance to isoflurane and halothane in dogs following beta blockade. We measured arterial and pulmonary artery pressure, left and right ventricular filling pressure, heart rate and cardiac output, and derived stroke volume and systemic and pulmonary vascular resistances in 13 mongrel dogs. The haemodynamic response to 1 MAC and 2 MAC isoflurane was studied in seven dogs and was similar before and after propranolol 0.1mg/kg i.v. In six dogs, propranolol 0.5mg/kg caused no significant changes in the circulatory response to 1 MAC and 2 MAC isoflurane or 1 MAC halothane. However, in three dogs, administration of 2 MAC halothane after propranolol 0.5mg/kg resulted in such profound circulatory depression as to preclude further study. These data suggest that (a) isoflurane possesses no clinically important beta-adrenergic stimulating activity; (b) there is no adverse drug interaction upon the circulation with the combination of isoflurane and propranolol; (c) in the presence of moderated profound beta-adrenergic blockade, 2 MAC isoflurane may be tolerated better than 2 MAC halothane.

Adrenergic beta-Agonists↗