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At least 19 recordsLinked to original sources
PubMed1977

Autonomic hyperreflexia: intraoperative control with pentolinium tartrate.

Autonomic hyperreflexia (AH) is a clinical syndrome associated with the development of severe hypertension. It usually occurs in patients with high-level chronic spinal cord injury, and in response to stimuli associated with the distension of a hollow viscus. Protection against AH by the prophylactic use of pentolinium tartrate (Ansolysen) in doses of 10-15 mg was evaluated in a controlled study of unanaesthetized patients who were either quadriplegic or paraplegic and who were undergoing rectal and bladder surgical procedures. When compared with the control group, the systolic and diastolic arterial pressures during operation were significantly less (P less than 0.05) and remained near normal in the pretreated patients. The use of pentolinium to prevent or control AH during surgical procedures in patients with chronic spinal cord damage is a simple alternative to spinal or general anaesthesia.

Adult↗
PubMed1979

Effects of delta 9-tetrahydrocannabinol, 2.4-dinitrophenol and pentolinium tartrate on behavioural thermoregulation in mice.

1 A new apparatus in which mice are allowed to shuttle between the warm and cool parts of a continuous oval tunnel has been designed for the measurement of drug effects on behavioural thermoregulation.2 The length of time that untreated mice spent in the warmer part of the apparatus (tunnel wall temperature 38 degrees C) was found to be inversely related to the temperature of the cooler part (wall temperature 18 degrees , 24 degrees or 30 degrees C).3 Mice treated with 2,4-dinitrophenol at a dose known to be hyperthermic at an ambient temperature of 32 degrees C (20 mg/kg s.c.) spent an increased length of time in the cooler part of the apparatus (wall temperature 18 degrees C) and did not exhibit any change in rectal temperature.4 Mice treated with pentolinium tartrate at a dose known to be hypothermic at room temperature (5.0 mg/kg i.v.) spent a decreased length of time in the cooler part of the apparatus (wall temperature 24 degrees C) and did not exhibit any change in rectal temperature.5 It is concluded from the above results that the apparatus can be used to measure drug effects on behavioural thermoregulation.6 In experiments of 30 min duration, mice treated with Delta(9)-tetrahydrocannabinol (Delta(9)-THC) at doses known to be hypothermic and to lower oxygen consumption at room temperature (20 mg/kg i.p. or 2.0 mg/kg i.v.) spent a longer time in the warmer part of the apparatus between 15 and 30 min after injection. Rectal temperatures measured 30 min after injection were only slightly less than those of control mice. In these experiments the wall temperature of the cool tunnel was 24 degrees C.7 In experiments of 15 min duration, mice treated with Delta(9)-THC (20 mg/kg) and then placed in the apparatus spent more time in the cooler part of the apparatus (wall temperature 24 degrees C) and exhibited a large fall in rectal temperature.8 It is concluded that immediately after injection of Delta(9)-THC the mice do not attempt to oppose drug-induced falls in deep body temperature by moving into a warm environment and that only later do the animals demonstrate a preference for a warm environment.

Animals↗
PubMed1986

Pressor resistance to vasopressin in sodium depletion, potassium depletion, and cirrhosis.

Resistance to the pressor effects of angiotensin II, but not norepinephrine, has been observed in sodium depletion, potassium depletion, and cirrhosis. We tested the response to arginine vasopressin (AVP) in each of these conditions. Male Sprague-Dawley rats were made sodium depleted with furosemide and a low-sodium diet for 3 days, potassium depleted by feeding a low-potassium diet for 14-21 days, or cirrhotic by inhalation of carbon tetrachloride for 8 wk. In conscious rats, the pressor response to graded doses of AVP was reduced in sodium depletion by 27-43% compared with control rats. Sodium-depleted rats were also found to have enhanced baroreceptor reflexes, since the decrease in heart rate for a given increase in mean arterial pressure was greater than in control rats. When the ganglionic blocker pentolinium tartrate was given to sodium-depleted rats the pressor response to AVP was restored to control levels. In potassium-depleted rats the pressor response to AVP was 21-52% lower than that in controls, whereas cirrhotic rats also had a blunted response to AVP (14-41% lower than control). However, there was no evidence in either of these two states of enhanced baroreceptor activity, and pretreatment with pentolinium tartrate did not restore the pressor response to normal. Therefore, although resistance to the pressor effect of AVP was found in all three conditions, the mechanism of this effect was different in sodium depletion compared with potassium depletion and cirrhosis. We conclude that resistance to the pressor action of AVP in sodium depletion was secondary to resetting of the baroreceptors.

Animals↗
PubMed1988

Effect of ganglion blockade with pentolinium on circulating neuropeptide Y levels in conscious rats.

The vasoconstrictor peptide, neuropeptide Y (NPY), is present in perivascular noradrenergic neurons of all mammals studied and may be important in the regulation of blood pressure. High plasma levels of NPY have been measured in the rat. To investigate partially the source and factors controlling the release of the circulating peptide, the effect of pentolinium tartrate administration has been studied in conscious rats. Pentolinium given as a bolus (5 mg/kg) followed by an infusion of a further 5 mg/kg/30 min produced a highly significant reduction in blood pressure of more than 40 mm Hg, when compared to either basal values or control animals treated with saline. Pentolinium treatment resulted in significantly lower plasma neuropeptide Y levels (31.0 +/- 6.7 fmol/ml) compared with those of control animals (78.6 +/- 8.2 fmol/ml). Circulating catecholamines were also significantly reduced in those animals receiving pentolinium. These results are compatible with circulating NPY arising from the sympathetic nervous system, with release being controlled by the mechanisms already established for catecholamines.

Animals↗
PubMed1990

Blood pressure in streptozotocin-treated Brattleboro and Long-Evans rats.

The diabetogenic agent streptozotocin (STZ) was injected intraperitoneally in Long-Evans and arginine vasopressin (AVP)-deficient Brattleboro rats. Twenty-eight days later both strains had a bradycardia and systolic hypotension; STZ-treated Brattleboro rats also had diastolic hypotension. The vasopressin (V1-receptor) antagonist, d(CH2)5[Tyr(Et)]DAVP, had no effect on resting blood pressure (BP) or heart rate (HR) in either strain of rat, indicating the relative maintenance of diastolic BP in STZ-treated Long-Evans rats was not dependent on acute vascular actions of AVP. Captopril caused a modest hypotension in all groups of rats, indicating that BP was not differentially dependent on the renin-angiotensin system in the different groups. In the presence of captopril and the ganglion blocker, pentolinium tartrate, the AVP-mediated recovery in BP was impaired in STZ-treated Long-Evans rats. During administration of d(CH2)5[Tyr(Et)]DAVP and pentolinium, the angiotensin II (ANG II)-mediated BP recovery was smaller in both groups of STZ-treated rats, indicating that this abnormality was not likely to be caused by inhibition of renin release by AVP. The abnormalities in ANG II- and AVP-mediated recovery were prevented by insulin treatment.

Animals↗
PubMed1976

Hemodynamic response to ganglionic blockade with pentolinium during N2O-halothane anesthesia in man.

Hemodynamic and blood-gas variables were studied before and after pentolinium tartrate administration in six patients anesthetized with nitrous oxide-halothane and maintained at PaCO2 35-40 torr. Measurements were made prior to induction of anesthesia; before and 10, 20, and 60 minutes after administration of pentolinium (0.3 mg/kg); 15 minutes after return of arterial blood pressure to control values. Mean arterial blood pressure (MAP) was significantly decreased at 20 (P less than 0.02) and 60 (P less than 0.001) minutes, in association with significant decreases in systemic vascular resistance (SVR) (P less than 0.05 and P less than 0.005). At 60 minutes MAP was significantly lower than that at 10 minutes (P less than 0.01). Cardiac output (CO) was increased (P less than 0.05) after 10 minutes secondary to a significant increase in heart rate. Neither variable changes significantly thereafter. CO and HR were significantly lower (P less than 0.01) 60 minutes after pentolinium than at 10 minutes; both returned to 10-minute values after intravenous administration of atropine. Changes in stroke volume (SV) and mean right atrial pressure (MRAP) were not significant. Whole-body O2 uptake (VO2) was not significantly altered by pentolinium. However, a substantial diminution of myocardial O2 consumption (MVO2) was deduced from a significant decrease in the heart rate-arterial systolic pressure produce (HR X ASP). Fifteen minutes after return of MAP to control levels, SVR was 11.5 per cent lower, while CO was still significantly higher (P less than 0.02) than control values. Following ganglionic blockade with pentolinium during halothane-N2O anesthesia, HR is a valuable index of changes in CO, while the HR X ASP index may be utilized to evaluate changes in MVO2. Assessment of myocardial performance during controlled hypotension is possible by the use of routinely available measurements.

Adolescent↗