ABSTRACT
Coronary blood flow, cardiac work and metabolism were studied in dogs under sodium nitroprusside (SNP) and trimetaphan (TMP) deliberate hypotension (20% and 40% mean pressure decrease from baseline). Regarding the effects of drug-induced hypotension on coronary blood flow, aortic and coronary sinus metabolic data (pH, pO2, pCO2) we could confirm that nitroprusside hypotension could be safely used to 30% mean blood pressure decrease from control, trimetaphan hypotension to 20% mean blood pressure decrease. Cardiac work was significantly reduced during SNP hypotension. Myocardial O2 consumption and O2 availability were directly dependent on the coronary perfusion. Careful invasive monitoring of the blood pressure, blood gases and of the ECG ST-T segment is mandatory.
Subject(s)
Hemodynamics/drug effects , Hypotension, Controlled , Myocardium/metabolism , Animals , Blood Gas Analysis , Blood Pressure/drug effects , Dogs , Nitroprusside/pharmacology , Oxygen Consumption/drug effects , Trimethaphan/pharmacologyABSTRACT
Atropine sulphate or atropine-methyl-bromide were administered to cats intravenously in a dose of 0.0115 mmol/kg (i.e 4 mg/kg). Electrocorticogram changes were studied. Atropine sulphate caused the classical shift of the electrocorticogram from high-frequency-low-voltage pattern to a low-frequency-high-voltage pattern. We observed no changes of the electrocorticogram after the administration of atropine-methyl-bromide.
Subject(s)
Electroencephalography , Parasympatholytics/poisoning , Animals , Atropine/poisoning , Atropine Derivatives/poisoning , Cats , MaleABSTRACT
The nitrous oxide withdrawal syndrome in mice was used as an experimental model to examine some of the factors which may play a role in postanesthetic excitation. Predisposition to nitrous oxide withdrawal convulsions as judged by duration of susceptibility was decreased significantly after pretreatment with the cholinesterase inhibitors, physostigmine and galanthamine, or with the opiate receptor blocking agent naloxone. Results are discussed in relation to the central anticholinergic syndrome, endorphin release, and disturbances which follow nitrous oxide anesthesia in humans and animals.
Subject(s)
Brain/physiopathology , Endorphins/physiology , Nitrous Oxide/adverse effects , Parasympathetic Nervous System/physiopathology , Substance Withdrawal Syndrome/physiopathology , Animals , Galantamine/pharmacology , Humans , Male , Mice , Naloxone/pharmacology , Physostigmine/pharmacology , Seizures/chemically induced , Seizures/physiopathologyABSTRACT
The autoregulation of myocardial blood flow was studied under: (a) haemorrhagic hypotension (mean pressure decrease 40% from baseline); (b) drug-induced hypotension with sodium nitroprusside or trimetaphan (40% pressure decrease); (c) drug-induced hypotension (40% pressure decrease) after moderate blood loss of 20%. Dogs were used in experiments under general anaesthesia with sodium thiopentone and artificially ventilated with N2O/O2 (70%, 30%) and pancuronium. Under haemorrhagic hypotension, the flow was pressure-dependent from the beginning. During nitroprusside hypotension, there was autoregulation of coronary flow to the level of mean pressure decrease 30% from control. Under trimetaphan, a constant flow persisted to the level of mean pressure decrease 20% from the baseline. Identical changes were seen during drug-induced hypotension after moderate blood loss (20%). Central venous pressure, cardiac output, left ventricular stroke work and minute work changes are demonstrated. Blood gas data pH, PO2, PCO2 in the aortic and coronary sinus under drug-induced hypotension are compared with control groups. There is a level of autoregulation of myocardial blood flow under hypotension. This level can be unfavourably changed in cases with hypertension and coronary obstructive diseases.
