Type II tooth cusp occurrence asymmetry in a human monozygotic twin pair.

A Type II tooth cusp occurrence asymmetry proposed for human twins in 1974 but not observed until recently was described in a female monozygotic twin pair.

Effect of naftidrofuryl oxalate (Praxilene) on blood flow in the experimental saphenous flap model.

Intravenous administration of naftidrofuryl oxalate (Praxilene) in the dog has shown a significant increase in blood flow into an experimental saphenous flap model (64% p less than 0.05). Further study is needed to show whether a similar increase in blood flow could be produced in an ischaemic flap.

Oculocardiac reflex from the empty orbit.

Two cases of profound bradycardia (one progressing to asystole) during orbital surgery where the relevant eye had been removed years earlier are reported. Cessation of stimulation was followed by recovery of heart rate. Intravenous atropine prevented further bradycardia.

The effect of temperature on blood flow in island and free skin flaps: an experimental study.

Skin blood flow is especially susceptible to temperature change, as the skin has an important role in body thermoregulation. The effect of temperature on blood flow in an experimental skin flap model in the dog has been measured using an electromagnetic flowmeter. the flap blood flow varied directly with temperature. In the range 22 degrees C-38 degrees C, this relationship was linear, the increase in the flap blood flow being 3.41% per degree Celsius. However, outside this temperature range the change was much greater.

Effect of nitrous oxide on the cardiovascular system and coronary circulation of the dog.

A comparison was made in seven dogs anaesthetized with pentobarbitone of cardiovascular measurements during ventilation with 65-70% nitrous oxide in oxygen and ventilation with 65-70% nitrogen in oxygen. The substitution of nitrous oxide for nitrogen was found to be associated, after 15 min, with a significant decrease in cardiac output and significant increases in right atrial and left ventricular end-diastolic pressure and systemic vascular resistance. There was no significant change in mean coronary artery flow, coronary vascular resistance or myocardial oxygen consumption.

Response of mean and phasic coronary arterial blood flow to graded hypercapnia in dogs.

An electromagnetic flow meter was used to assess the changes in coronary blood flow in response to four levels of increased PaCO2 in six dogs. Mean, diastolic and systolic flow all increased during hypercapnia, the increase being maximal at mean PaCO2 11.3 KPa. Mean and diastolic coronary vascular resistances decreased progressively as PaCO2 increased, but systolic resistance, although decreasing with the lower levels of hypercapnia, returned to control at the greatest PaCO2. Although the oxygen available to the myocardium was increased markedly during hypercapnia, coronary sinus PO2 increased also, reflecting a reduction in myocardial oxygen extraction; thus myocardial oxygen consumption was unchanged. Cardiac output was increased significantly only at the greatest PaCO2. Total body oxygen handling was not altered significantly.

The effects of ketamine on the canine coronary circulation.

Systemic and coronary haemodynamic measurements have been made in six healthy greyhounds anaesthetized with trichloroethylene. The administration of ketamine in bolus doses of 5 mg/kg, 10 mg/kg and 5 mg/kg followed by an infusion 0.1 mg/kg/min was found to be accompanied by a decrease in arterial pressure and an increase in cardiac output produced by an increase (84%) in stroke volume. Coronary blood flow increased greatly as did myocardial oxygen consumption and there was no change in myocardial oxygen extraction.

Effect of hypotension induced with sodium nitroprusside on canine coronary arterial flow.

In seven dogs anaesthetized with pentobarbitone, coronary and pulmonary artery blood flows were measured using electromagnetic flow meters. The infusion of a 0.01% solution of sodium nitroprusside caused an initial small increase in mean coronary artery flow which returned to control as the arterial pressure decreased. No changes were noted in cardiac output nor were further changes observed in coronary flow. Heart rate was increased consistently during the hypotension and left ventricular dp/dt max was reduced as were coronary and total peripheral resistances. There were no significant changes in myocardial or total body oxygen extraction or consumption.

Canine coronary blood flow responses to hypoxaemia: the influence of halothane.

Electromagnetic flow meters were used to measure blood flow in the coronary and pulmonary arteries of six anaesthetized dogs following thoracotomy. Halothane 1% (v/v) caused a reduction in arterial pressure, coronary artery flow, cardiac output and myocardial and total body oxygen consumption and an increase in coronary vascular resistance. Hypoxaemia caused large increases in coronary artery flow during both cardiac systole and diastole, but not until PaO2 was less than 5.3 kPa. This response was not influenced by the presence of halothane. Although myocardial oxygen availability and consumption were maintained during hypoxaemia, total body oxygen availability and consumption were markedly reduced.

The combined effect of halothane-induced hypotension and hypocapnia on canine myocardial blood-flow and oxygen consumption.

In eleven intact mechanically ventilated dogs anaesthetized with pentobarbitone, mean arterial pressure was reduced to 55% of the control value by ventilating with 1-1.5% halothane. At normocapnia this resulted in decreases in myocardial blood-flow and oxygen consumption to 47% and 55% of their respective control values and an increase in myocardial vascular resistance to 123% of control value. When hypocapnia (mean PaCO2=26 mm Hg) was superimposed on hypotension, myocardial blood-flow was further decreased to 38% of control value whereas oxygen consumption did not alter significantly. When halothane was discontinued, allowing recovery from hypotension, the rate of recovery of myocardial blood-flow and cardiac output was much slower than that of arterial pressure.